- About
- Home
- Introduction
- Statistics
- Programs
- Dignet
- Gene
- GenePair
- BioSummarAI
- Help & Docs
- Documents
- Help
- FAQs
- Links
- Acknowledge
- Disclaimer
- Contact Us
Gene Information
Gene symbol: TGFB1
Gene name: transforming growth factor, beta 1
HGNC ID: 11766
Synonyms: CED, TGFbeta
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1386312 | Type 1, insulin-dependent diabetes mellitus (IDDM) appears to result from a T cell-dependent destruction of insulin-producing pancreatic beta cells. |
| 2 | 1386312 | By polymerase chain reaction (PCR), I.S. 2.15 T cells contain mRNA species encoding for the potentially immunosuppressive cytokines, interleukin-10 (IL-10) and transforming growth factor-beta (TGF-beta). |
| 3 | 1466796 | In other experimental autoimmune diseases there is evidence that CD8+ T cells can be protective and that these cells may mediate this protection by the synthesis of transforming growth factor-beta. |
| 4 | 1503634 | Of the different cytokines which are present in the synovial fluid or produced by cells in the synovial tissue, most are presumed to have originated in macrophages/monocytes such as IL-1, IL-6, IL-8, TNF-alpha and TGF-beta. |
| 5 | 1572403 | Effects of platelet-contained growth factors (PDGF, EGF, IGF-I, and TGF-beta) on DNA synthesis in porcine aortic smooth muscle cells in culture. |
| 6 | 1572403 | Platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I), and transforming growth factor-beta (TGF-beta) are potent mitogens present in human platelets. |
| 7 | 1572403 | Effects of the other three growth factors on DNA synthesis were only stimulatory; their maximally effective concentrations were 20 ng/ml for PDGF (eightfold over the basal), 40 ng/ml for EGF (six-fold increase), and 20 ng/ml for IGF-I (fourfold increase). |
| 8 | 1572403 | When PDGF, EGF, and IGF-I were added at submaximally effective concentrations, their effects were additive. |
| 9 | 1572403 | TGF-beta at 1 ng/ml inhibited at least 50% of the effects of 20 ng/ml EGF and of 10 ng/ml IGF-I, whereas inhibition of the effect of 10 ng/ml PDGF required 10 ng/ml of TGF-beta. |
| 10 | 1572403 | The concentration of TGF-beta needed to inhibit 50% of the combined effect of EGF, IGF-1, and PDGF was 5 ng/ml. |
| 11 | 1572403 | Effects of platelet-contained growth factors (PDGF, EGF, IGF-I, and TGF-beta) on DNA synthesis in porcine aortic smooth muscle cells in culture. |
| 12 | 1572403 | Platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I), and transforming growth factor-beta (TGF-beta) are potent mitogens present in human platelets. |
| 13 | 1572403 | Effects of the other three growth factors on DNA synthesis were only stimulatory; their maximally effective concentrations were 20 ng/ml for PDGF (eightfold over the basal), 40 ng/ml for EGF (six-fold increase), and 20 ng/ml for IGF-I (fourfold increase). |
| 14 | 1572403 | When PDGF, EGF, and IGF-I were added at submaximally effective concentrations, their effects were additive. |
| 15 | 1572403 | TGF-beta at 1 ng/ml inhibited at least 50% of the effects of 20 ng/ml EGF and of 10 ng/ml IGF-I, whereas inhibition of the effect of 10 ng/ml PDGF required 10 ng/ml of TGF-beta. |
| 16 | 1572403 | The concentration of TGF-beta needed to inhibit 50% of the combined effect of EGF, IGF-1, and PDGF was 5 ng/ml. |
| 17 | 1572403 | Effects of platelet-contained growth factors (PDGF, EGF, IGF-I, and TGF-beta) on DNA synthesis in porcine aortic smooth muscle cells in culture. |
| 18 | 1572403 | Platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I), and transforming growth factor-beta (TGF-beta) are potent mitogens present in human platelets. |
| 19 | 1572403 | Effects of the other three growth factors on DNA synthesis were only stimulatory; their maximally effective concentrations were 20 ng/ml for PDGF (eightfold over the basal), 40 ng/ml for EGF (six-fold increase), and 20 ng/ml for IGF-I (fourfold increase). |
| 20 | 1572403 | When PDGF, EGF, and IGF-I were added at submaximally effective concentrations, their effects were additive. |
| 21 | 1572403 | TGF-beta at 1 ng/ml inhibited at least 50% of the effects of 20 ng/ml EGF and of 10 ng/ml IGF-I, whereas inhibition of the effect of 10 ng/ml PDGF required 10 ng/ml of TGF-beta. |
| 22 | 1572403 | The concentration of TGF-beta needed to inhibit 50% of the combined effect of EGF, IGF-1, and PDGF was 5 ng/ml. |
| 23 | 1572403 | Effects of platelet-contained growth factors (PDGF, EGF, IGF-I, and TGF-beta) on DNA synthesis in porcine aortic smooth muscle cells in culture. |
| 24 | 1572403 | Platelet-derived growth factor (PDGF), epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I), and transforming growth factor-beta (TGF-beta) are potent mitogens present in human platelets. |
| 25 | 1572403 | Effects of the other three growth factors on DNA synthesis were only stimulatory; their maximally effective concentrations were 20 ng/ml for PDGF (eightfold over the basal), 40 ng/ml for EGF (six-fold increase), and 20 ng/ml for IGF-I (fourfold increase). |
| 26 | 1572403 | When PDGF, EGF, and IGF-I were added at submaximally effective concentrations, their effects were additive. |
| 27 | 1572403 | TGF-beta at 1 ng/ml inhibited at least 50% of the effects of 20 ng/ml EGF and of 10 ng/ml IGF-I, whereas inhibition of the effect of 10 ng/ml PDGF required 10 ng/ml of TGF-beta. |
| 28 | 1572403 | The concentration of TGF-beta needed to inhibit 50% of the combined effect of EGF, IGF-1, and PDGF was 5 ng/ml. |
| 29 | 1597472 | The 260-kDa transforming growth factor (TGF)-beta binding protein in rat glomeruli is a complex comprised of 170- and 85-kDa TGF-beta binding proteins. |
| 30 | 1660827 | Analyses of fetal liver from the last one-third of gestation demonstrated the presence of specific mRNAs for the transforming growth factors (TGFs) TGF-alpha and TGF-beta. |
| 31 | 1660827 | TGF-alpha, a homologue of epidermal growth factor (EGF), acts through EGF receptors. |
| 32 | 1660827 | Levels of mRNA for TGF-alpha increased dramatically postnatally, whereas EGF receptor number increased just before term. |
| 33 | 1660827 | Other analyses demonstrated increases in tyrosine kinase activities of the insulin receptor, EGF receptor, and insulinlike growth factor I receptor as term approached. |
| 34 | 1660827 | TGF-beta was a potent inhibitor of fetal hepatocyte proliferation in culture, whereas insulin potentiated fetal hepatocyte growth above "mitogen-independent" levels. |
| 35 | 1660827 | Analyses of fetal liver from the last one-third of gestation demonstrated the presence of specific mRNAs for the transforming growth factors (TGFs) TGF-alpha and TGF-beta. |
| 36 | 1660827 | TGF-alpha, a homologue of epidermal growth factor (EGF), acts through EGF receptors. |
| 37 | 1660827 | Levels of mRNA for TGF-alpha increased dramatically postnatally, whereas EGF receptor number increased just before term. |
| 38 | 1660827 | Other analyses demonstrated increases in tyrosine kinase activities of the insulin receptor, EGF receptor, and insulinlike growth factor I receptor as term approached. |
| 39 | 1660827 | TGF-beta was a potent inhibitor of fetal hepatocyte proliferation in culture, whereas insulin potentiated fetal hepatocyte growth above "mitogen-independent" levels. |
| 40 | 1671798 | The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. |
| 41 | 1671798 | Pituitary hormones and hypothalamic releasing factors, such as human ACTH (10 nM), beta-endorphin (10 nM), beta-lipotropin (10 nM), alpha-MSH (10 nM), gamma 3-MSH (10 nM), ovine luteinizing hormone (10 ng/ml), ovine follicle-stimulating hormone (10 ng/ml), ovine thyroid-stimulating hormone (10 ng/ml), rat growth hormone (10 ng/ml), rat prolactin (10 ng/ml), rat corticotropin-releasing factor (10 nM), luteinizing hormone-releasing factor (10 nM), thyrotropin-releasing factor (10 nM), human growth hormone-releasing factor (10 nM), and somatostatin (10 nM), have no significant effects on aromatase activity. |
| 42 | 1671798 | Porcine inhibin A (10 ng/ml) and porcine activin AB (10 ng/ml), two ovarian hormones with structural transforming homology to transforming growth factor-beta, also have no effect on aromatase activity. |
| 43 | 1671798 | Although basic fibroblast growth factor (1-100 ng/ml), acidic fibroblast growth factor (1 ng/ml), epidermal growth factor (1 ng/ml), platelet-derived growth factor (1 ng/ml), tumor necrosis factor (1 ng/ml), and transforming growth factor-beta 1 (1 ng/ml) have no effect on basal aromatase activity in human skin fibroblasts, all of these growth factors inhibited the ability of dibutyryladenosine 3',5'-cyclic monophosphate to stimulate aromatase activity. |
| 44 | 1671798 | In contrast, both insulin (100 pg/ml-10 ng/ml) and insulin-like growth factor-1 (1-100 ng/ml) had no effect on cAMP-stimulated aromatase but potentiated the action of dexamethasone (100 nM). |
| 45 | 1671798 | On the basis of the results presented here, it is interesting to speculate that the hyperandrogenism that is often associated with insulin resistance may be due to a combination of growth factor-mediated inhibition of aromatase activity and the failure of peripheral tissues to respond to insulin and metabolize androgens to estrogens. |
| 46 | 1671798 | The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. |
| 47 | 1671798 | Pituitary hormones and hypothalamic releasing factors, such as human ACTH (10 nM), beta-endorphin (10 nM), beta-lipotropin (10 nM), alpha-MSH (10 nM), gamma 3-MSH (10 nM), ovine luteinizing hormone (10 ng/ml), ovine follicle-stimulating hormone (10 ng/ml), ovine thyroid-stimulating hormone (10 ng/ml), rat growth hormone (10 ng/ml), rat prolactin (10 ng/ml), rat corticotropin-releasing factor (10 nM), luteinizing hormone-releasing factor (10 nM), thyrotropin-releasing factor (10 nM), human growth hormone-releasing factor (10 nM), and somatostatin (10 nM), have no significant effects on aromatase activity. |
| 48 | 1671798 | Porcine inhibin A (10 ng/ml) and porcine activin AB (10 ng/ml), two ovarian hormones with structural transforming homology to transforming growth factor-beta, also have no effect on aromatase activity. |
| 49 | 1671798 | Although basic fibroblast growth factor (1-100 ng/ml), acidic fibroblast growth factor (1 ng/ml), epidermal growth factor (1 ng/ml), platelet-derived growth factor (1 ng/ml), tumor necrosis factor (1 ng/ml), and transforming growth factor-beta 1 (1 ng/ml) have no effect on basal aromatase activity in human skin fibroblasts, all of these growth factors inhibited the ability of dibutyryladenosine 3',5'-cyclic monophosphate to stimulate aromatase activity. |
| 50 | 1671798 | In contrast, both insulin (100 pg/ml-10 ng/ml) and insulin-like growth factor-1 (1-100 ng/ml) had no effect on cAMP-stimulated aromatase but potentiated the action of dexamethasone (100 nM). |
| 51 | 1671798 | On the basis of the results presented here, it is interesting to speculate that the hyperandrogenism that is often associated with insulin resistance may be due to a combination of growth factor-mediated inhibition of aromatase activity and the failure of peripheral tissues to respond to insulin and metabolize androgens to estrogens. |
| 52 | 1698682 | Fibroblast growth factors, platelet-derived growth factor, and calcium acted as mitogens for parathyroid endothelial cells, whereas transforming growth factor beta inhibited proliferation. |
| 53 | 1712736 | At sites of vascular injuries, degranulating platelets release PDGF, IGF-I, EGF, and TGF-beta. |
| 54 | 1712736 | Macrophages and neutrophiles drawn into the ischaemic or injured areas synthesise and release TGF-alpha, TGF-beta, and PDGF, and wounded endothelial cells secrete FGF. |
| 55 | 1712736 | Clinical correlations suggest that peptide growth factors in the vitreous such as IGF-I and bFGF may promote diabetic retinopathy. |
| 56 | 1712736 | At sites of vascular injuries, degranulating platelets release PDGF, IGF-I, EGF, and TGF-beta. |
| 57 | 1712736 | Macrophages and neutrophiles drawn into the ischaemic or injured areas synthesise and release TGF-alpha, TGF-beta, and PDGF, and wounded endothelial cells secrete FGF. |
| 58 | 1712736 | Clinical correlations suggest that peptide growth factors in the vitreous such as IGF-I and bFGF may promote diabetic retinopathy. |
| 59 | 1768735 | The objective of this study was to determine whether transforming growth factor beta (TGF-beta) can inhibit the destruction of islet cells by either spleen cells from acutely diabetic BB/Wor rats, or by the cytokines tumor necrosis factor (TNF) and interferon gamma (IFN-gamma). |
| 60 | 1768735 | Similarly, TNF and IFN-gamma have been shown to act synergistically to destroy islet cell monolayers. |
| 61 | 1768735 | TGF-beta (10 ng/ml) was also shown to significantly inhibit the TNF and IFN-gamma-induced lysis of islet cell monolayers. |
| 62 | 1768735 | The objective of this study was to determine whether transforming growth factor beta (TGF-beta) can inhibit the destruction of islet cells by either spleen cells from acutely diabetic BB/Wor rats, or by the cytokines tumor necrosis factor (TNF) and interferon gamma (IFN-gamma). |
| 63 | 1768735 | Similarly, TNF and IFN-gamma have been shown to act synergistically to destroy islet cell monolayers. |
| 64 | 1768735 | TGF-beta (10 ng/ml) was also shown to significantly inhibit the TNF and IFN-gamma-induced lysis of islet cell monolayers. |
| 65 | 1851759 | Novel 150- and 180-kDa glycoproteins that bind transforming growth factor (TGF)-beta 1 but not TGF-beta 2 are present in several cell lines. |
| 66 | 1933739 | In vivo experimental findings suggest that combinations of PDGF and insulin applied topically to wounds may increase the rate of wound repair in diabetics. |
| 67 | 1933739 | The ability of TGF-beta to promote collagen formation may also relate to a metabolic condition such as osteoporosis, in which inadequate formation of collagen or other components of the bone matrix may contribute to pathogenesis. |
| 68 | 2029849 | TGF-beta localization was observed exclusively in photoreceptors in all adult non-diabetic and non-insulin dependent diabetic eyes, and 4 of 6 insulin dependent eyes. |
| 69 | 2029849 | Chondroitinase ABC digestion of sections prior to immunohistochemistry did not reduce TGF-beta immunoreactivity, suggesting that binding was not to glycosaminoglycans in the interphotoreceptor matrix. |
| 70 | 2029849 | TGF-beta localization was observed exclusively in photoreceptors in all adult non-diabetic and non-insulin dependent diabetic eyes, and 4 of 6 insulin dependent eyes. |
| 71 | 2029849 | Chondroitinase ABC digestion of sections prior to immunohistochemistry did not reduce TGF-beta immunoreactivity, suggesting that binding was not to glycosaminoglycans in the interphotoreceptor matrix. |
| 72 | 2539392 | TGF-beta significantly increased the production of collagen and fibronectin by glomerular mesangial cells whereas only fibronectin production was augmented in glomerular epithelial cells. |
| 73 | 2562644 | The diabetic rat as an impaired wound healing model: stimulatory effects of transforming growth factor-beta and basic fibroblast growth factor. |
| 74 | 2562644 | A single injection into sponges 3 days postimplantation of basic fibroblast growth factor, transforming growth factor-beta, or vehicle only, was evaluated at 7 and 9 days postimplantation. |
| 75 | 2562644 | The diabetic rat as an impaired wound healing model: stimulatory effects of transforming growth factor-beta and basic fibroblast growth factor. |
| 76 | 2562644 | A single injection into sponges 3 days postimplantation of basic fibroblast growth factor, transforming growth factor-beta, or vehicle only, was evaluated at 7 and 9 days postimplantation. |
| 77 | 3255729 | Growth factors bFGF and TGB beta accelerate the rate of wound repair in normal and in diabetic rats. |
| 78 | 3255729 | The effects of basic fibroblast growth factor (bFGF) and transforming growth factor beta (TGF beta) on the rate of wound repair in both normal and streptozotocin-induced diabetic rats were investigated using two model systems of wound repair, namely incisional wounding and subcutaneous implantation of polyvinyl alcohol (PVA) sponges. |
| 79 | 3865880 | There are two different classes of humoral growth factors for arterial smooth muscle and endothelial cells that age of potential relevance for the development of macrovascular disease inn diabetes mellitus: hormones (growth hormone, insulin like growth factor I and II, insulin) and locally released growth factors of platelet origin. |
| 80 | 3865880 | Human platelets contain at least six growth peptides or proteins that all stimulate in vitro growth of arterial wall cells: platelet derived growth factor, epidermal growth factor, platelet derived endothelial cell mitogen, endothelial growth factor, diabetic serum growth factor (DSGF), transforming growth factor-beta. |
| 81 | 7485382 | Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E. |
| 82 | 7485382 | Immunohistological studies using monoclonal antibodies showed that infiltrating MNC consisted mainly of CD4+ T cells ( > 75% of leukocytes) plus smaller numbers of macrophages and CD8+ T cells. |
| 83 | 7485382 | These cells displayed evidence of immune activation with expression of receptors for interleukin-2 (IL-2R) plus Th1 cytokines; dense labeling for IFN-gamma and tumor necrosis factor-alpha, plus lesser amounts of IL-2, was observed. |
| 84 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 85 | 7485382 | By contrast, at 10 weeks, pancreatic tissues from NOD mice fed insulin showed considerably less insulitis, and the residual MNC, although still largely CD4+ T cells plus macrophages, showed dense labeling for IL-4, IL-10, prostaglandin-E, and transforming growth factor-beta and an absence of IL-2, IFN-gamma or tumor necrosis factor-alpha Taken together with our previous findings, these data indicate that oral administration of insulin affects the development of diabetes in NOD mice through the generation of cells that elaborate immunoregulatory cytokines within the target organ and shift the balance from a Th1 to a Th2 pattern of cytokine expression. |
| 86 | 7485382 | Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E. |
| 87 | 7485382 | Immunohistological studies using monoclonal antibodies showed that infiltrating MNC consisted mainly of CD4+ T cells ( > 75% of leukocytes) plus smaller numbers of macrophages and CD8+ T cells. |
| 88 | 7485382 | These cells displayed evidence of immune activation with expression of receptors for interleukin-2 (IL-2R) plus Th1 cytokines; dense labeling for IFN-gamma and tumor necrosis factor-alpha, plus lesser amounts of IL-2, was observed. |
| 89 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 90 | 7485382 | By contrast, at 10 weeks, pancreatic tissues from NOD mice fed insulin showed considerably less insulitis, and the residual MNC, although still largely CD4+ T cells plus macrophages, showed dense labeling for IL-4, IL-10, prostaglandin-E, and transforming growth factor-beta and an absence of IL-2, IFN-gamma or tumor necrosis factor-alpha Taken together with our previous findings, these data indicate that oral administration of insulin affects the development of diabetes in NOD mice through the generation of cells that elaborate immunoregulatory cytokines within the target organ and shift the balance from a Th1 to a Th2 pattern of cytokine expression. |
| 91 | 7485382 | Suppression of insulitis in non-obese diabetic (NOD) mice by oral insulin administration is associated with selective expression of interleukin-4 and -10, transforming growth factor-beta, and prostaglandin-E. |
| 92 | 7485382 | Immunohistological studies using monoclonal antibodies showed that infiltrating MNC consisted mainly of CD4+ T cells ( > 75% of leukocytes) plus smaller numbers of macrophages and CD8+ T cells. |
| 93 | 7485382 | These cells displayed evidence of immune activation with expression of receptors for interleukin-2 (IL-2R) plus Th1 cytokines; dense labeling for IFN-gamma and tumor necrosis factor-alpha, plus lesser amounts of IL-2, was observed. |
| 94 | 7485382 | MNC lacked labeling for IL-4, IL-10, prostaglandin-E, or transforming growth factor-beta. |
| 95 | 7485382 | By contrast, at 10 weeks, pancreatic tissues from NOD mice fed insulin showed considerably less insulitis, and the residual MNC, although still largely CD4+ T cells plus macrophages, showed dense labeling for IL-4, IL-10, prostaglandin-E, and transforming growth factor-beta and an absence of IL-2, IFN-gamma or tumor necrosis factor-alpha Taken together with our previous findings, these data indicate that oral administration of insulin affects the development of diabetes in NOD mice through the generation of cells that elaborate immunoregulatory cytokines within the target organ and shift the balance from a Th1 to a Th2 pattern of cytokine expression. |
| 96 | 7508064 | Moreover, they were hyperresponsive to many growth factors such as calf serum, epidermal growth factor (EGF), platelet-derived growth factor (PDGF), transforming growth factor beta 1 (TGF beta 1), and insulin. |
| 97 | 7508064 | Additive effects were observed for EGF and PDGF or EGF and insulin. |
| 98 | 7510100 | The stimulatory cytokines include interleukin-1 (IL-1), interferon-gamma (IFN-gamma), tumour necrosis factor-alpha (TNF-alpha) and migration inhibitory factor. |
| 99 | 7510100 | A number of cytokines, including IL-4, IL-10 and transforming growth factor-beta, can down regulate the induction of NO synthase in macrophages. |
| 100 | 7538809 | The levels of mRNA coding for transforming growth factor-beta 1, tenascin, and laminin B1 increased 1.9-, 2.0-, and 1.7-fold, respectively, whereas platelet-derived growth factor (PDGF)-B, alpha 1(IV) collagen, 72-kd collagenase, alpha-smooth muscle actin, and beta-actin mRNA remained stable in the diabetic mice. |
| 101 | 7538809 | There was no increase in cell number per glomerulus after the onset of diabetes, a finding consistent with stable PDGF-B and alpha-smooth muscle actin mRNA levels. |
| 102 | 7538809 | These findings provide evidence that increased glomerular transforming growth factor-beta 1, but not PDGF-B, mRNA is associated with the up-regulation of tenascin and laminin expression after advanced glycosylation endproduct accumulation, early after the onset of diabetes. |
| 103 | 7538809 | The levels of mRNA coding for transforming growth factor-beta 1, tenascin, and laminin B1 increased 1.9-, 2.0-, and 1.7-fold, respectively, whereas platelet-derived growth factor (PDGF)-B, alpha 1(IV) collagen, 72-kd collagenase, alpha-smooth muscle actin, and beta-actin mRNA remained stable in the diabetic mice. |
| 104 | 7538809 | There was no increase in cell number per glomerulus after the onset of diabetes, a finding consistent with stable PDGF-B and alpha-smooth muscle actin mRNA levels. |
| 105 | 7538809 | These findings provide evidence that increased glomerular transforming growth factor-beta 1, but not PDGF-B, mRNA is associated with the up-regulation of tenascin and laminin expression after advanced glycosylation endproduct accumulation, early after the onset of diabetes. |
| 106 | 7544540 | The amount of glomerular type IV collagen and tenascin but not laminin was increased by immunofluorescence microscopy. mRNA levels in microdissected glomeruli were measured by competetive reverse transcription-polymerase chain reaction and corrected for cell number. alpha 1-Chain type IV collagen and tenascin mRNAs were increased 3.2-fold and 1.8-fold, whereas laminin B1 mRNA levels were not. |
| 107 | 7544540 | Transforming growth factor-beta 1 mRNA levels were elevated 1.8-fold, but platelet-derived growth factor-B mRNA levels remained normal. |
| 108 | 7556948 | Proximal tubule cells and glomerular mesangial cells cultured in high glucose concentration express increased TGF-beta 1 mRNA and protein levels, and treatment with anti-TGF-beta antibodies results in prevention of the effects of high glucose to induce cellular hypertrophy and stimulate collagen biosynthesis. |
| 109 | 7556948 | We have also observed that the development of renal hypertrophy in the insulin-dependent diabetic BB rat and NOD mouse is associated with increased expression of TGF-beta 1 in the kidney and that short-term administration of antibodies capable of neutralizing the activity of TGF-beta in the streptozotocin mouse model of diabetes results in attenuation of whole kidney and glomerular hypertrophy and overexpression of mRNAs encoding matrix components. |
| 110 | 7556948 | Proximal tubule cells and glomerular mesangial cells cultured in high glucose concentration express increased TGF-beta 1 mRNA and protein levels, and treatment with anti-TGF-beta antibodies results in prevention of the effects of high glucose to induce cellular hypertrophy and stimulate collagen biosynthesis. |
| 111 | 7556948 | We have also observed that the development of renal hypertrophy in the insulin-dependent diabetic BB rat and NOD mouse is associated with increased expression of TGF-beta 1 in the kidney and that short-term administration of antibodies capable of neutralizing the activity of TGF-beta in the streptozotocin mouse model of diabetes results in attenuation of whole kidney and glomerular hypertrophy and overexpression of mRNAs encoding matrix components. |
| 112 | 7565477 | A variety of proinflammatory and vasoactive agents including thrombin, transforming growth factor beta, angiotensin II as well as mechanical forces enhance the renal synthesis of ET. |
| 113 | 7565477 | Two receptor subtypes, ETA and ETB, are widely expressed in the kidney, coupled to multiple intracellular signal transduction pathways that mediate distinct activities. |
| 114 | 7621107 | Increased synthesis of ECM components is stimulated by growth factors like transforming growth factor beta (TGF beta) (Derynck et al., 1984) and insulin-like growth factor I (IGF-I) (Moran et al., 1991). |
| 115 | 7621993 | We have previously reported that the mRNA levels of extracellular matrix (ECM) components including alpha 1(I), alpha 1(III), and alpha 1(IV) collagen chains, laminin B1 and B2 chains, and growth factors including tumor necrosis factor (TNF)-alpha, platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF)-beta, and basic fibroblast growth factor (FGF) all increase with age in diabetic glomeruli. |
| 116 | 7621993 | FR139317 attenuated the increases in glomerular mRNA levels of alpha 1(I) (P < 0.01), alpha 1(III) (P < 0.01), and alpha 1(IV) (P < 0.01) collagen chains, laminin B1 (P < 0.01) and B2 (P < 0.01) chains, TNF-alpha (P < 0.01), PDGF-B (P < 0.01), TGF-beta (P < 0.001) and basic FGF (P < 0.01) in diabetic rats. |
| 117 | 7725402 | Transforming growth factor beta and interferon gamma modulate the development of TH-1-mediated autoimmunity in susceptible and resistant strains of rats. |
| 118 | 7752595 | We found prominent mesangial cell proliferation at three days (4.34 +/- 2.24 PCNA + cells/glom vs. 1.6 +/- 0.74 in controls, P < 0.001) associated with increased alpha-actin expression. |
| 119 | 7752595 | PDGF B-chain mRNA was slightly increased at day one, and PDGF B-chain immunostaining was slightly increased at days one and six. |
| 120 | 7752595 | Insulin treatment prevented mesangial cell proliferation, actin expression, and macrophage infiltration, and normalized TGF-beta expression at 14 and 30 days. |
| 121 | 7752595 | These multiple cellular events preceded any detectable increases in glomerular gene expression or deposition of collagen I, IV or laminin. |
| 122 | 7759509 | We found a large induction of VEGF expression upon treatment of quiescent cells with serum, epidermal growth factor, transforming growth factor-beta 1, keratinocyte growth factor, or the proinflammatory cytokine tumor necrosis factor alpha, respectively. |
| 123 | 7810696 | In this study we evaluated the gene and protein expression of TGF-beta 1 in the kidney of two rodent models of spontaneous insulin-dependent diabetes mellitus [the biobreeding (BB) rat and the nonobese diabetic (NOD) mouse]. |
| 124 | 7819711 | Recently a plausible mechanism for the atherogenic activity of Lp(a) has been ascribed to the inhibiting effect of Lp(a) on plasminogen activation, thus decreasing plasmin formation which in turn reduces the activation of transforming growth factor beta, a potent inhibitor of smooth muscle cell proliferation. |
| 125 | 7822950 | Low-density lipoprotein stimulation of mesangial cell fibronectin synthesis: role of protein kinase C and transforming growth factor-beta. |
| 126 | 7822950 | In the present study we evaluated the effect of LDL on fibronectin synthesis in cultured rat mesangial cells (MCs) and the roles of protein kinase C (PKC) and transforming growth factor-beta (TGF-beta) in mediating this LDL action. |
| 127 | 7822950 | Low-density lipoprotein stimulation of mesangial cell fibronectin synthesis: role of protein kinase C and transforming growth factor-beta. |
| 128 | 7822950 | In the present study we evaluated the effect of LDL on fibronectin synthesis in cultured rat mesangial cells (MCs) and the roles of protein kinase C (PKC) and transforming growth factor-beta (TGF-beta) in mediating this LDL action. |
| 129 | 7850412 | Recently, the proteoglycan decorin was shown to neutralize TGF-beta. |
| 130 | 7850412 | Thus, decorin offers hope as a treatment for progressive kidney diseases caused by the overproduction of TGF-beta. |
| 131 | 7850412 | Recently, the proteoglycan decorin was shown to neutralize TGF-beta. |
| 132 | 7850412 | Thus, decorin offers hope as a treatment for progressive kidney diseases caused by the overproduction of TGF-beta. |
| 133 | 7866423 | Increases in the expression of heat-shock protein-70, basic fibroblast growth factor, N-ras, and c-myc, and decreases in transforming growth factor-beta occurred acutely after obstruction, suggesting that these changes may play a role in obstruction-induced bladder hypertrophy. |
| 134 | 7866423 | Removal of the obstruction induces apoptosis of urothelial and connective tissue elements in the bladder, accompanied by increases in transforming growth factor-beta and decreases in basic fibroblast growth factor genes, and a reversal of the bladder dysfunction. |
| 135 | 7866423 | Increases in the expression of heat-shock protein-70, basic fibroblast growth factor, N-ras, and c-myc, and decreases in transforming growth factor-beta occurred acutely after obstruction, suggesting that these changes may play a role in obstruction-induced bladder hypertrophy. |
| 136 | 7866423 | Removal of the obstruction induces apoptosis of urothelial and connective tissue elements in the bladder, accompanied by increases in transforming growth factor-beta and decreases in basic fibroblast growth factor genes, and a reversal of the bladder dysfunction. |
| 137 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 138 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 139 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 140 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 141 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 142 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 143 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 144 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 145 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 146 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 147 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 148 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 149 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 150 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 151 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 152 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 153 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 154 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 155 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 156 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 157 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 158 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 159 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 160 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 161 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 162 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 163 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 164 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 165 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 166 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 167 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 168 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 169 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 170 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 171 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 172 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 173 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 174 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 175 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 176 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 177 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 178 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 179 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 180 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 181 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 182 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 183 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 184 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 185 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 186 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 187 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 188 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 189 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 190 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 191 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 192 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 193 | 7875052 | Bimodal effect of transforming growth factor-beta on insulin secretion in MIN6 cells. |
| 194 | 7875052 | The effects of transforming growth factor-beta (TGF-beta) on insulin secretion were investigated using a glucose-responsive clonal cell line, MIN6. |
| 195 | 7875052 | One hundred pM TGF-beta stimulated insulin release during 0.5-24 h of incubation in the presence of 5.5 mM glucose, but not after 48 h; 1 nM TGF-beta also stimulated insulin release up to 2 h of exposure, but the effect was not seen after 6 h of exposure. |
| 196 | 7875052 | When cells were incubated with 25 mM glucose for 24 h, 100 pM TGF-beta significantly inhibited glucose-stimulated insulin release, whereas insulin release was not altered at 0 or 2.8 mM glucose. |
| 197 | 7875052 | On the contrary, forskolin- (10 microM) and tolbutamide- (40 microM) induced insulin release were not affected by TGF-beta. |
| 198 | 7875052 | TGF-beta affected neither the cell growth nor the cellular insulin content. |
| 199 | 7875052 | An addition of 1 microM nitrendipine abolished TGF-beta-induced insulin secretion at 5.5 mM glucose. |
| 200 | 7875052 | The presence study shows that TGF-beta exerts a bimodal effect on glucose-induced insulin secretion from MIN6 cells, depending on dose, time of exposure and concentrations of coexisting glucose. |
| 201 | 7937785 | We found that AGE induced an increase in glomerular extracellular matrix alpha 1(IV) collagen, laminin B1, and transforming growth factor beta 1 mRNA levels, as measured by competitive PCR, as well as glomerular hypertrophy. |
| 202 | 7951472 | Transforming growth factor beta (TGF-beta) inhibits the differentiation of human adipocyte precursor cells in primary culture. |
| 203 | 7951472 | In order to improve our understanding of the control of adipose tissue development in man by adipogenic and antiadipogenic factors we studied the effect of transforming growth factor beta (TGF beta) on the differentiation of human adipocyte precursor cells cultured in a serum-free medium. |
| 204 | 7951472 | Transforming growth factor beta (TGF-beta) inhibits the differentiation of human adipocyte precursor cells in primary culture. |
| 205 | 7951472 | In order to improve our understanding of the control of adipose tissue development in man by adipogenic and antiadipogenic factors we studied the effect of transforming growth factor beta (TGF beta) on the differentiation of human adipocyte precursor cells cultured in a serum-free medium. |
| 206 | 7956951 | Troglitazone prevents the inhibitory effects of inflammatory cytokines on insulin-induced adipocyte differentiation in 3T3-L1 cells. |
| 207 | 7956951 | Tumor necrosis factor (TNF) is implicated in wasting syndromes and insulin resistance in chronic infection and obese-linked diabetes. |
| 208 | 7956951 | TNF (10 ng/ml) inhibited adipocyte differentiation of 3T3-L1 cells, and in these TNF treated cells little insulin-stimulated glucose uptake was observed. |
| 209 | 7956951 | Treatment of 3T3-L1 cells with troglitazone (1-10 microM) partially prevented this inhibitory effect of TNF on adipogenesis, and enhanced expression of C/EBP alpha and GLUT4, even in the presence of TNF. |
| 210 | 7956951 | Troglitazone also prevented the inhibitory effects of interleukin-1, interleukin-6, and leukemia inhibitory factor, but not of transforming growth factor beta on adipocyte differentiation of 3T3-L1 cells. |
| 211 | 7967355 | RNA samples were reverse transcribed (RT) and subjected to polymerase chain reaction (PCR) amplication with specific 5' and 3' primers for rat transforming growth factor (TGF-beta 1) and beta-actin. |
| 212 | 7967355 | RT-PCR analysis revealed that glomerular TGF-beta 1 mRNA levels increased relative to beta-actin as early as 24 hours after the onset of hyperglycemia, reaching a plateau after 96 hours that was sustained at one and two weeks. |
| 213 | 7967355 | Intensive insulin treatment to normalize blood glucose levels attenuated the rise in glomerular and renal cortical TGF-beta 1 mRNA. |
| 214 | 7967355 | Normalization of blood glucose levels with insulin treatment attenuates the increase in TGF-beta 1 expression. |
| 215 | 7967355 | RNA samples were reverse transcribed (RT) and subjected to polymerase chain reaction (PCR) amplication with specific 5' and 3' primers for rat transforming growth factor (TGF-beta 1) and beta-actin. |
| 216 | 7967355 | RT-PCR analysis revealed that glomerular TGF-beta 1 mRNA levels increased relative to beta-actin as early as 24 hours after the onset of hyperglycemia, reaching a plateau after 96 hours that was sustained at one and two weeks. |
| 217 | 7967355 | Intensive insulin treatment to normalize blood glucose levels attenuated the rise in glomerular and renal cortical TGF-beta 1 mRNA. |
| 218 | 7967355 | Normalization of blood glucose levels with insulin treatment attenuates the increase in TGF-beta 1 expression. |
| 219 | 7967355 | RNA samples were reverse transcribed (RT) and subjected to polymerase chain reaction (PCR) amplication with specific 5' and 3' primers for rat transforming growth factor (TGF-beta 1) and beta-actin. |
| 220 | 7967355 | RT-PCR analysis revealed that glomerular TGF-beta 1 mRNA levels increased relative to beta-actin as early as 24 hours after the onset of hyperglycemia, reaching a plateau after 96 hours that was sustained at one and two weeks. |
| 221 | 7967355 | Intensive insulin treatment to normalize blood glucose levels attenuated the rise in glomerular and renal cortical TGF-beta 1 mRNA. |
| 222 | 7967355 | Normalization of blood glucose levels with insulin treatment attenuates the increase in TGF-beta 1 expression. |
| 223 | 7967355 | RNA samples were reverse transcribed (RT) and subjected to polymerase chain reaction (PCR) amplication with specific 5' and 3' primers for rat transforming growth factor (TGF-beta 1) and beta-actin. |
| 224 | 7967355 | RT-PCR analysis revealed that glomerular TGF-beta 1 mRNA levels increased relative to beta-actin as early as 24 hours after the onset of hyperglycemia, reaching a plateau after 96 hours that was sustained at one and two weeks. |
| 225 | 7967355 | Intensive insulin treatment to normalize blood glucose levels attenuated the rise in glomerular and renal cortical TGF-beta 1 mRNA. |
| 226 | 7967355 | Normalization of blood glucose levels with insulin treatment attenuates the increase in TGF-beta 1 expression. |
| 227 | 8011155 | Suppression can be adoptively transferred by CD8+ T lymphocytes which act by releasing TGF-beta and IL-4 following antigen-specific triggering. |
| 228 | 8013761 | The formation of islet-like cell clusters (ICCs) during a 6-day culture was stimulated two- to threefold by hepatocyte growth factor/scatter factor (HGF/SF) basic fibroblast growth factor (FGF)-2, and to a lesser extent by keratinocyte growth factor (FGF-7) and insulin-like growth factor-II (IGF-II). |
| 229 | 8013761 | The ICCs formed during HGF/SF stimulation consisted mainly of epithelial cells, whereas FGF-2-induced ICCs were predominantly nonepithelial. |
| 230 | 8013761 | Furthermore, although both FGF-2 and HGF/SF increased the total insulin content of the cultures, only HGF/SF increased the insulin content per DNA. |
| 231 | 8013761 | Quantitatively, HGF/SF stimulated a 2.3-fold increase in the proportion of insulin-positive cells and a 3-fold higher number of replicating beta-cells. |
| 232 | 8013761 | Blocking of the IGF-I receptor inhibited ICC formation but did not affect their insulin content. |
| 233 | 8013761 | Immunoneutralizing TGF-beta resulted in increased cell growth and insulin content, indicating the presence of an endogenous inhibitory TGF-beta activity in the model system. |
| 234 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 235 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 236 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 237 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 238 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 239 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 240 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 241 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 242 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 243 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 244 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 245 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 246 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 247 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 248 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 249 | 8094359 | Evaluations of glomerular mRNA levels encoding for PCNA, TNF-alpha, PDGF-A and -B chains, TGF-beta, IGF-I, bFGF, and EGF were made at 4, 12, and 24 wk after injection of STZ in Sprague-Dawley rats. |
| 250 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 251 | 8094359 | At 24 wk after STZ injection, mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF were increased 3.8-fold, (P < 0.01), 4.2-fold (P < 0.01), 4.0-fold (P < 0.01), 5.2-fold (P < 0.001), and 3.6-fold (P < 0.01), respectively, in the glomeruli of diabetic rats when compared with control rats. |
| 252 | 8094359 | In contrast, mRNA levels for IGF-I, PDGF-A chain, and EGF were not altered in glomeruli from diabetic and control rats throughout the experimental period. |
| 253 | 8094359 | Insulin treatment partially ameliorated the increase in mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF in the glomeruli of diabetic rats. |
| 254 | 8116045 | To investigate this new postulate independently of an IL-2-dependent mechanism, we utilized, as probes, two mammalian cell lines, distinguished by their sensitivity to growth inhibition by TGF-beta and resistance to IL-2: CCL-64 mink lung epithelial cells (CCL-64 cells) and A-549 human adenocarcinoma cells (A-549 cells). |
| 255 | 8171758 | Utilizing cDNA probes, the gene products sulfated glycoprotein-2 (SGP-2), transforming growth factor-beta (TGF-beta), beta-actin (beta-actin), N-ras and beta nerve growth factor (beta-NGF), were quantitated in bladders of male Sprague-Dawley rats at 1, 2, 4 and 6 weeks after induction of diabetes with streptozotocin (STZ). beta-actin and SGP-2 expression were transiently increased at 1 and 4 weeks after induction, respectively. |
| 256 | 8171758 | N-ras was reduced at all times compared with control rat bladders. |
| 257 | 8195682 | We have previously reported that the mRNA levels of endothelin (ET-1), tumor necrosis factor-alpha), (TNF-alpha), platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF-beta), and basic fibroblast growth factor (bFGF) all increased with age in diabetic rat glomeruli. |
| 258 | 8195682 | We have now assessed the effect of the angiotensin-converting enzyme inhibitor enalapril on the expression of the ET-1, TNF-alpha, PDGF-B, TGF-beta, and bFGF genes in 24-week-old rat glomeruli after streptozotocin injection. |
| 259 | 8195682 | Enalapril also attenuated the increases in ET-1 mRNA levels observed in the glomeruli of diabetic rats (0.5-fold compared with untreated diabetic rats at 24 weeks [p < 0.01]) but had no effect on increased mRNA levels of TNF-alpha, PDGF-B, TGF-beta, and bFGF. |
| 260 | 8195682 | We have previously reported that the mRNA levels of endothelin (ET-1), tumor necrosis factor-alpha), (TNF-alpha), platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF-beta), and basic fibroblast growth factor (bFGF) all increased with age in diabetic rat glomeruli. |
| 261 | 8195682 | We have now assessed the effect of the angiotensin-converting enzyme inhibitor enalapril on the expression of the ET-1, TNF-alpha, PDGF-B, TGF-beta, and bFGF genes in 24-week-old rat glomeruli after streptozotocin injection. |
| 262 | 8195682 | Enalapril also attenuated the increases in ET-1 mRNA levels observed in the glomeruli of diabetic rats (0.5-fold compared with untreated diabetic rats at 24 weeks [p < 0.01]) but had no effect on increased mRNA levels of TNF-alpha, PDGF-B, TGF-beta, and bFGF. |
| 263 | 8195682 | We have previously reported that the mRNA levels of endothelin (ET-1), tumor necrosis factor-alpha), (TNF-alpha), platelet-derived growth factor (PDGF)-B chain, transforming growth factor (TGF-beta), and basic fibroblast growth factor (bFGF) all increased with age in diabetic rat glomeruli. |
| 264 | 8195682 | We have now assessed the effect of the angiotensin-converting enzyme inhibitor enalapril on the expression of the ET-1, TNF-alpha, PDGF-B, TGF-beta, and bFGF genes in 24-week-old rat glomeruli after streptozotocin injection. |
| 265 | 8195682 | Enalapril also attenuated the increases in ET-1 mRNA levels observed in the glomeruli of diabetic rats (0.5-fold compared with untreated diabetic rats at 24 weeks [p < 0.01]) but had no effect on increased mRNA levels of TNF-alpha, PDGF-B, TGF-beta, and bFGF. |
| 266 | 8405711 | Transforming growth factor-beta 1 enhances glomerular collagen synthesis in diabetic rats. |
| 267 | 8405711 | In vitro glomerular collagen synthesis and its response to various concentrations of transforming growth factor-beta 1 were studied in normal and diabetic rats. |
| 268 | 8405711 | TGF-beta 1 increased collagen synthesis in normal glomeruli in a dose-dependent manner up to 5 ng/ml. |
| 269 | 8405711 | Basal collagen synthesis was increased in diabetic glomeruli, but addition of TGF-beta 1 had no effect. |
| 270 | 8405711 | Antibody to TGF-beta 1 prevented this increase in collagen synthesis. |
| 271 | 8405711 | This study clearly indicates a regulatory role of TGF-beta 1 in renal glomerular collagen synthesis in the normal rat, and suggests a possible causal role for enhanced collagen synthesis in the diabetic rat. |
| 272 | 8405711 | Transforming growth factor-beta 1 enhances glomerular collagen synthesis in diabetic rats. |
| 273 | 8405711 | In vitro glomerular collagen synthesis and its response to various concentrations of transforming growth factor-beta 1 were studied in normal and diabetic rats. |
| 274 | 8405711 | TGF-beta 1 increased collagen synthesis in normal glomeruli in a dose-dependent manner up to 5 ng/ml. |
| 275 | 8405711 | Basal collagen synthesis was increased in diabetic glomeruli, but addition of TGF-beta 1 had no effect. |
| 276 | 8405711 | Antibody to TGF-beta 1 prevented this increase in collagen synthesis. |
| 277 | 8405711 | This study clearly indicates a regulatory role of TGF-beta 1 in renal glomerular collagen synthesis in the normal rat, and suggests a possible causal role for enhanced collagen synthesis in the diabetic rat. |
| 278 | 8405711 | Transforming growth factor-beta 1 enhances glomerular collagen synthesis in diabetic rats. |
| 279 | 8405711 | In vitro glomerular collagen synthesis and its response to various concentrations of transforming growth factor-beta 1 were studied in normal and diabetic rats. |
| 280 | 8405711 | TGF-beta 1 increased collagen synthesis in normal glomeruli in a dose-dependent manner up to 5 ng/ml. |
| 281 | 8405711 | Basal collagen synthesis was increased in diabetic glomeruli, but addition of TGF-beta 1 had no effect. |
| 282 | 8405711 | Antibody to TGF-beta 1 prevented this increase in collagen synthesis. |
| 283 | 8405711 | This study clearly indicates a regulatory role of TGF-beta 1 in renal glomerular collagen synthesis in the normal rat, and suggests a possible causal role for enhanced collagen synthesis in the diabetic rat. |
| 284 | 8405711 | Transforming growth factor-beta 1 enhances glomerular collagen synthesis in diabetic rats. |
| 285 | 8405711 | In vitro glomerular collagen synthesis and its response to various concentrations of transforming growth factor-beta 1 were studied in normal and diabetic rats. |
| 286 | 8405711 | TGF-beta 1 increased collagen synthesis in normal glomeruli in a dose-dependent manner up to 5 ng/ml. |
| 287 | 8405711 | Basal collagen synthesis was increased in diabetic glomeruli, but addition of TGF-beta 1 had no effect. |
| 288 | 8405711 | Antibody to TGF-beta 1 prevented this increase in collagen synthesis. |
| 289 | 8405711 | This study clearly indicates a regulatory role of TGF-beta 1 in renal glomerular collagen synthesis in the normal rat, and suggests a possible causal role for enhanced collagen synthesis in the diabetic rat. |
| 290 | 8405711 | Transforming growth factor-beta 1 enhances glomerular collagen synthesis in diabetic rats. |
| 291 | 8405711 | In vitro glomerular collagen synthesis and its response to various concentrations of transforming growth factor-beta 1 were studied in normal and diabetic rats. |
| 292 | 8405711 | TGF-beta 1 increased collagen synthesis in normal glomeruli in a dose-dependent manner up to 5 ng/ml. |
| 293 | 8405711 | Basal collagen synthesis was increased in diabetic glomeruli, but addition of TGF-beta 1 had no effect. |
| 294 | 8405711 | Antibody to TGF-beta 1 prevented this increase in collagen synthesis. |
| 295 | 8405711 | This study clearly indicates a regulatory role of TGF-beta 1 in renal glomerular collagen synthesis in the normal rat, and suggests a possible causal role for enhanced collagen synthesis in the diabetic rat. |
| 296 | 8405711 | Transforming growth factor-beta 1 enhances glomerular collagen synthesis in diabetic rats. |
| 297 | 8405711 | In vitro glomerular collagen synthesis and its response to various concentrations of transforming growth factor-beta 1 were studied in normal and diabetic rats. |
| 298 | 8405711 | TGF-beta 1 increased collagen synthesis in normal glomeruli in a dose-dependent manner up to 5 ng/ml. |
| 299 | 8405711 | Basal collagen synthesis was increased in diabetic glomeruli, but addition of TGF-beta 1 had no effect. |
| 300 | 8405711 | Antibody to TGF-beta 1 prevented this increase in collagen synthesis. |
| 301 | 8405711 | This study clearly indicates a regulatory role of TGF-beta 1 in renal glomerular collagen synthesis in the normal rat, and suggests a possible causal role for enhanced collagen synthesis in the diabetic rat. |
| 302 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 303 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 304 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 305 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 306 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 307 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 308 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 309 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 310 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 311 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 312 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 313 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 314 | 8468460 | Nuclear transcription of early activation genes (c-fos, c-jun, and c-myc) as determined by nuclear run-off assays, and steady state mRNA levels and/or protein products of intermediate activation genes (IL-2, IL-2R alpha, IL-2R beta, and transferrin receptor) were not affected by TGF-beta 1. |
| 315 | 8468460 | However, TGF-beta 1 inhibited the IL-2-dependent proliferation of Con A lymphoblasts by -50%. |
| 316 | 8468460 | TGF-beta 1 also inhibited the IL-2-dependent phosphorylation of the retinoblastoma susceptibility gene product, which plays an important role in cell cycle progression. |
| 317 | 8468460 | These results suggest that TGF-beta 1 inhibits T cell proliferation by down-regulating predominantly IL-2-mediated proliferative signals. |
| 318 | 8476260 | Angiotensin converting enzyme transforms angiotensin I into angiotensin II and breaks down bradykinin into inactive products. |
| 319 | 8476260 | Endothelium-derived growth inhibitors include heparin (sulfates) and transforming growth factor beta 1, while basic fibroblast growth factors and platelet-derived growth factor and possibly endothelin promote proliferation. |
| 320 | 8482432 | Synthesis and expression of transforming growth factor beta-1, beta-2, and beta-3 in the endocrine and exocrine pancreas. |
| 321 | 8603776 | Our previous investigations have shown that high glucose concentration increases transforming growth factor (TGF)-beta1 mRNA in mesangial and proximal tubule cells and that treatment with anti-TGF-beta antibody results in prevention of the effects of high glucose on cell growth (e.g., induction of cellular hypertrophy) and the stimulation of collagen biosynthesis. |
| 322 | 8603776 | Diabetic mice given IgG demonstrated total kidney and glomerular hypertrophy, significantly elevated urinary TGF-beta1 protein, and increased mRNAs encoding TGF-beta1, type II TGF-beta receptor, alpha1(IV) collagen, and fibronectin. |
| 323 | 8623195 | Transgenic mice whose pancreata express transforming growth factor-beta (TGF-beta) directed by an insulin promoter (Ins-TGF-beta mice) were used to assess the effect of local TGF-beta1 on allograft rejection and on autoimmune diabetes occurring as a cross-reaction to viral antigens. |
| 324 | 8651051 | The neovascularization is decreased by the synergistic effect between the neovascular factors and suppressors such an VEGF, fibroblast growth factor (FGF), and transforming growth factor-beta (TGF-beta). |
| 325 | 8667617 | We have studied mice that are transgenic for an active form of TGF-beta 1 under the control of murine albumin promoter and enhancer DNA sequences. |
| 326 | 8671656 | Partially purified MLR-IA inhibits IL-2 production in a primary allo-MLR, and decreases IFN-gamma production during secondary allo-MLR and Con A activation, whereas it enhances IL-4 production in both primary and secondary Con A activation. |
| 327 | 8671656 | MLR-IA is not neutralized by combination of antibodies specific for transforming growth factor-beta, IL-10, tumor necrosis factor-alpha/beta or IFN-gamma, suggestive of a novel activity. |
| 328 | 8671656 | Our work suggests that a potentially novel immunoregulatory activity, capable of inhibiting T lymphocyte proliferation and IFN-gamma production, and stimulating IL-4 production, may regulate development of autoimmune diabetes in NOD mice. |
| 329 | 8676810 | Impaired renal proteolytic activity caused by such factors as high protein intake, metabolic acidosis, angiotensin II and transforming growth factor-beta 1 in vivo and in vitro may result in decreased protein degradation and subsequent induction of cellular hypertrophy, even in the absence of increased protein synthesis. |
| 330 | 8717444 | Regulation of endothelial IGFBP-3 synthesis and secretion by IGF-I and TGF-beta. |
| 331 | 8717444 | We have examined the regulation of endothelial IGFBP-3 production by IGF-I and TGF-beta, two growth factors thought to play a major roles in the complications of diabetes mellitus. |
| 332 | 8717444 | Our results using both Northern analysis and the fluorescent competitive PCR method indicate that: (1) IGFBP-3 mRNA is increased 2- to 10-fold by IGF-I and maximally reduced to 20% of control by TGF-beta; (2) the changes in mRNA levels correlate with the levels of IGFBP-3 protein secreted into the media by these cells; (3) the induction of IGFBP-3 mRNA and protein by IGF-I analogs was directly related to their ability to bind to the type I IGF receptor, reflecting an IGF-I receptor-mediated process; and (4) steady state IGFBP-3 mRNA levels did not change significantly after a 6 h incubation with actinomycin D in the presence or absence of the growth factors suggesting that the observed IGF-I/TGF-beta effects occur at the level of gene transcription rather than mRNA stability. |
| 333 | 8717444 | Regulation of endothelial IGFBP-3 synthesis and secretion by IGF-I and TGF-beta. |
| 334 | 8717444 | We have examined the regulation of endothelial IGFBP-3 production by IGF-I and TGF-beta, two growth factors thought to play a major roles in the complications of diabetes mellitus. |
| 335 | 8717444 | Our results using both Northern analysis and the fluorescent competitive PCR method indicate that: (1) IGFBP-3 mRNA is increased 2- to 10-fold by IGF-I and maximally reduced to 20% of control by TGF-beta; (2) the changes in mRNA levels correlate with the levels of IGFBP-3 protein secreted into the media by these cells; (3) the induction of IGFBP-3 mRNA and protein by IGF-I analogs was directly related to their ability to bind to the type I IGF receptor, reflecting an IGF-I receptor-mediated process; and (4) steady state IGFBP-3 mRNA levels did not change significantly after a 6 h incubation with actinomycin D in the presence or absence of the growth factors suggesting that the observed IGF-I/TGF-beta effects occur at the level of gene transcription rather than mRNA stability. |
| 336 | 8717444 | Regulation of endothelial IGFBP-3 synthesis and secretion by IGF-I and TGF-beta. |
| 337 | 8717444 | We have examined the regulation of endothelial IGFBP-3 production by IGF-I and TGF-beta, two growth factors thought to play a major roles in the complications of diabetes mellitus. |
| 338 | 8717444 | Our results using both Northern analysis and the fluorescent competitive PCR method indicate that: (1) IGFBP-3 mRNA is increased 2- to 10-fold by IGF-I and maximally reduced to 20% of control by TGF-beta; (2) the changes in mRNA levels correlate with the levels of IGFBP-3 protein secreted into the media by these cells; (3) the induction of IGFBP-3 mRNA and protein by IGF-I analogs was directly related to their ability to bind to the type I IGF receptor, reflecting an IGF-I receptor-mediated process; and (4) steady state IGFBP-3 mRNA levels did not change significantly after a 6 h incubation with actinomycin D in the presence or absence of the growth factors suggesting that the observed IGF-I/TGF-beta effects occur at the level of gene transcription rather than mRNA stability. |
| 339 | 8725283 | Here we have analyzed and compared the effects of transforming growth factor beta 1 (TGF beta 1), TGF alpha, and whey acidic protein (WAP), the Notch-related cell fate protein Int3, and p53 and pRb on mammary development. |
| 340 | 8744057 | The use of neutralizing antibodies to demonstrate the role of transforming growth factor-beta and Amadori-glycated albumin as mediators of experimental diabetic kidney disease. |
| 341 | 8746789 | Recombinant human transforming growth factor beta does not inhibit the effects of interleukin-1 beta on pancreatic islet cells. |
| 342 | 8746789 | The macrophage-derived cytokine, interleukin-1 beta (IL-1 beta), has been implicated to play an important role in the autoimmune beta cell lesion of insulin-dependent diabetes mellitus (IDDM) because of its inhibition of insulin secretion, direct cytotoxicity, and alteration of islet cell antigen expression. |
| 343 | 8746789 | Because transforming growth factor beta (TGF-beta) has been reported to inhibit IL-1 receptor expression in several lymphoid and progenitor cell lines, to induce IL-1 receptor antagonist protein (IRAP) production in human peripheral blood monocytes, and to antagonize several effects of inflammatory cytokines and because oral tolerance may be mediated in part by TGF-beta released by regulatory T lymphocytes, we investigated whether TGF-beta counteracted the effects of IL-1 beta on islet cells. |
| 344 | 8746789 | Islets isolated from Sprague-Dawley rats were cultured with or without recombinant human IL-1 beta and TGF-beta. |
| 345 | 8746789 | Accumulated insulin secretion, cytokine-induced cytotoxicity, and islet cell expression of glutamic acid decarboxylase 65 (GAD-65) and heat-shock protein 70 (HSP-70) were measured in this study. |
| 346 | 8746789 | We found that (1) IL-1 beta at 50 and 100 pg/ml inhibited insulin secretion by 41.9 +/- 14.8 and 52.6 +/- 3.5% and induced cytotoxicity by 46.5 +/- 17.3 and 54.1 +/- 6.1%, respectively. |
| 347 | 8746789 | IL-1 beta at 1000 pg/ml significantly increased HSP-70 expression and decreased GAD-65 expression. (2) TGF-beta at 0.1, 1, 10, and 40 ng/ml had no significant effect on insulin secretion and did not induce cytotoxicity, TGF-beta at 40 ng/ml had no effect on the expression of either HSP-70 or GAD-65. (3) In combination, TGF-beta at 1, 10, and 40 ng/ml did not antagonize the IL-1 beta (50 and 100 pg/ml)-induced inhibition of insulin secretion or cytotoxicity; TGF-beta (40 ng/ml) did not block the effects of IL-1 beta (1000 pg/ml) on HSP-70 or GAD-65 expression. |
| 348 | 8746789 | In conclusion, recombinant human TGF-beta does not counteract these effects of recombinant human IL-1 beta on rat pancreatic islet cells. |
| 349 | 8746789 | Recombinant human transforming growth factor beta does not inhibit the effects of interleukin-1 beta on pancreatic islet cells. |
| 350 | 8746789 | The macrophage-derived cytokine, interleukin-1 beta (IL-1 beta), has been implicated to play an important role in the autoimmune beta cell lesion of insulin-dependent diabetes mellitus (IDDM) because of its inhibition of insulin secretion, direct cytotoxicity, and alteration of islet cell antigen expression. |
| 351 | 8746789 | Because transforming growth factor beta (TGF-beta) has been reported to inhibit IL-1 receptor expression in several lymphoid and progenitor cell lines, to induce IL-1 receptor antagonist protein (IRAP) production in human peripheral blood monocytes, and to antagonize several effects of inflammatory cytokines and because oral tolerance may be mediated in part by TGF-beta released by regulatory T lymphocytes, we investigated whether TGF-beta counteracted the effects of IL-1 beta on islet cells. |
| 352 | 8746789 | Islets isolated from Sprague-Dawley rats were cultured with or without recombinant human IL-1 beta and TGF-beta. |
| 353 | 8746789 | Accumulated insulin secretion, cytokine-induced cytotoxicity, and islet cell expression of glutamic acid decarboxylase 65 (GAD-65) and heat-shock protein 70 (HSP-70) were measured in this study. |
| 354 | 8746789 | We found that (1) IL-1 beta at 50 and 100 pg/ml inhibited insulin secretion by 41.9 +/- 14.8 and 52.6 +/- 3.5% and induced cytotoxicity by 46.5 +/- 17.3 and 54.1 +/- 6.1%, respectively. |
| 355 | 8746789 | IL-1 beta at 1000 pg/ml significantly increased HSP-70 expression and decreased GAD-65 expression. (2) TGF-beta at 0.1, 1, 10, and 40 ng/ml had no significant effect on insulin secretion and did not induce cytotoxicity, TGF-beta at 40 ng/ml had no effect on the expression of either HSP-70 or GAD-65. (3) In combination, TGF-beta at 1, 10, and 40 ng/ml did not antagonize the IL-1 beta (50 and 100 pg/ml)-induced inhibition of insulin secretion or cytotoxicity; TGF-beta (40 ng/ml) did not block the effects of IL-1 beta (1000 pg/ml) on HSP-70 or GAD-65 expression. |
| 356 | 8746789 | In conclusion, recombinant human TGF-beta does not counteract these effects of recombinant human IL-1 beta on rat pancreatic islet cells. |
| 357 | 8746789 | Recombinant human transforming growth factor beta does not inhibit the effects of interleukin-1 beta on pancreatic islet cells. |
| 358 | 8746789 | The macrophage-derived cytokine, interleukin-1 beta (IL-1 beta), has been implicated to play an important role in the autoimmune beta cell lesion of insulin-dependent diabetes mellitus (IDDM) because of its inhibition of insulin secretion, direct cytotoxicity, and alteration of islet cell antigen expression. |
| 359 | 8746789 | Because transforming growth factor beta (TGF-beta) has been reported to inhibit IL-1 receptor expression in several lymphoid and progenitor cell lines, to induce IL-1 receptor antagonist protein (IRAP) production in human peripheral blood monocytes, and to antagonize several effects of inflammatory cytokines and because oral tolerance may be mediated in part by TGF-beta released by regulatory T lymphocytes, we investigated whether TGF-beta counteracted the effects of IL-1 beta on islet cells. |
| 360 | 8746789 | Islets isolated from Sprague-Dawley rats were cultured with or without recombinant human IL-1 beta and TGF-beta. |
| 361 | 8746789 | Accumulated insulin secretion, cytokine-induced cytotoxicity, and islet cell expression of glutamic acid decarboxylase 65 (GAD-65) and heat-shock protein 70 (HSP-70) were measured in this study. |
| 362 | 8746789 | We found that (1) IL-1 beta at 50 and 100 pg/ml inhibited insulin secretion by 41.9 +/- 14.8 and 52.6 +/- 3.5% and induced cytotoxicity by 46.5 +/- 17.3 and 54.1 +/- 6.1%, respectively. |
| 363 | 8746789 | IL-1 beta at 1000 pg/ml significantly increased HSP-70 expression and decreased GAD-65 expression. (2) TGF-beta at 0.1, 1, 10, and 40 ng/ml had no significant effect on insulin secretion and did not induce cytotoxicity, TGF-beta at 40 ng/ml had no effect on the expression of either HSP-70 or GAD-65. (3) In combination, TGF-beta at 1, 10, and 40 ng/ml did not antagonize the IL-1 beta (50 and 100 pg/ml)-induced inhibition of insulin secretion or cytotoxicity; TGF-beta (40 ng/ml) did not block the effects of IL-1 beta (1000 pg/ml) on HSP-70 or GAD-65 expression. |
| 364 | 8746789 | In conclusion, recombinant human TGF-beta does not counteract these effects of recombinant human IL-1 beta on rat pancreatic islet cells. |
| 365 | 8746789 | Recombinant human transforming growth factor beta does not inhibit the effects of interleukin-1 beta on pancreatic islet cells. |
| 366 | 8746789 | The macrophage-derived cytokine, interleukin-1 beta (IL-1 beta), has been implicated to play an important role in the autoimmune beta cell lesion of insulin-dependent diabetes mellitus (IDDM) because of its inhibition of insulin secretion, direct cytotoxicity, and alteration of islet cell antigen expression. |
| 367 | 8746789 | Because transforming growth factor beta (TGF-beta) has been reported to inhibit IL-1 receptor expression in several lymphoid and progenitor cell lines, to induce IL-1 receptor antagonist protein (IRAP) production in human peripheral blood monocytes, and to antagonize several effects of inflammatory cytokines and because oral tolerance may be mediated in part by TGF-beta released by regulatory T lymphocytes, we investigated whether TGF-beta counteracted the effects of IL-1 beta on islet cells. |
| 368 | 8746789 | Islets isolated from Sprague-Dawley rats were cultured with or without recombinant human IL-1 beta and TGF-beta. |
| 369 | 8746789 | Accumulated insulin secretion, cytokine-induced cytotoxicity, and islet cell expression of glutamic acid decarboxylase 65 (GAD-65) and heat-shock protein 70 (HSP-70) were measured in this study. |
| 370 | 8746789 | We found that (1) IL-1 beta at 50 and 100 pg/ml inhibited insulin secretion by 41.9 +/- 14.8 and 52.6 +/- 3.5% and induced cytotoxicity by 46.5 +/- 17.3 and 54.1 +/- 6.1%, respectively. |
| 371 | 8746789 | IL-1 beta at 1000 pg/ml significantly increased HSP-70 expression and decreased GAD-65 expression. (2) TGF-beta at 0.1, 1, 10, and 40 ng/ml had no significant effect on insulin secretion and did not induce cytotoxicity, TGF-beta at 40 ng/ml had no effect on the expression of either HSP-70 or GAD-65. (3) In combination, TGF-beta at 1, 10, and 40 ng/ml did not antagonize the IL-1 beta (50 and 100 pg/ml)-induced inhibition of insulin secretion or cytotoxicity; TGF-beta (40 ng/ml) did not block the effects of IL-1 beta (1000 pg/ml) on HSP-70 or GAD-65 expression. |
| 372 | 8746789 | In conclusion, recombinant human TGF-beta does not counteract these effects of recombinant human IL-1 beta on rat pancreatic islet cells. |
| 373 | 8746789 | Recombinant human transforming growth factor beta does not inhibit the effects of interleukin-1 beta on pancreatic islet cells. |
| 374 | 8746789 | The macrophage-derived cytokine, interleukin-1 beta (IL-1 beta), has been implicated to play an important role in the autoimmune beta cell lesion of insulin-dependent diabetes mellitus (IDDM) because of its inhibition of insulin secretion, direct cytotoxicity, and alteration of islet cell antigen expression. |
| 375 | 8746789 | Because transforming growth factor beta (TGF-beta) has been reported to inhibit IL-1 receptor expression in several lymphoid and progenitor cell lines, to induce IL-1 receptor antagonist protein (IRAP) production in human peripheral blood monocytes, and to antagonize several effects of inflammatory cytokines and because oral tolerance may be mediated in part by TGF-beta released by regulatory T lymphocytes, we investigated whether TGF-beta counteracted the effects of IL-1 beta on islet cells. |
| 376 | 8746789 | Islets isolated from Sprague-Dawley rats were cultured with or without recombinant human IL-1 beta and TGF-beta. |
| 377 | 8746789 | Accumulated insulin secretion, cytokine-induced cytotoxicity, and islet cell expression of glutamic acid decarboxylase 65 (GAD-65) and heat-shock protein 70 (HSP-70) were measured in this study. |
| 378 | 8746789 | We found that (1) IL-1 beta at 50 and 100 pg/ml inhibited insulin secretion by 41.9 +/- 14.8 and 52.6 +/- 3.5% and induced cytotoxicity by 46.5 +/- 17.3 and 54.1 +/- 6.1%, respectively. |
| 379 | 8746789 | IL-1 beta at 1000 pg/ml significantly increased HSP-70 expression and decreased GAD-65 expression. (2) TGF-beta at 0.1, 1, 10, and 40 ng/ml had no significant effect on insulin secretion and did not induce cytotoxicity, TGF-beta at 40 ng/ml had no effect on the expression of either HSP-70 or GAD-65. (3) In combination, TGF-beta at 1, 10, and 40 ng/ml did not antagonize the IL-1 beta (50 and 100 pg/ml)-induced inhibition of insulin secretion or cytotoxicity; TGF-beta (40 ng/ml) did not block the effects of IL-1 beta (1000 pg/ml) on HSP-70 or GAD-65 expression. |
| 380 | 8746789 | In conclusion, recombinant human TGF-beta does not counteract these effects of recombinant human IL-1 beta on rat pancreatic islet cells. |
| 381 | 8760171 | We also examined whether certain VSMC growth factors, such as angiotensin II, platelet-derived growth factor, and transforming growth factor-beta, could also regulate the formation of 8-epi-PGF2 alpha. |
| 382 | 8760354 | Insulin-dependent diabetes mellitus (IDDM) is an autoimmune disease in which cytokines are thought to play an important role in beta-cell destruction and immune regulation. |
| 383 | 8760354 | A major target of beta-cell autoimmunity in IDDM is the enzyme glutamate decarboxylase (GAD). |
| 384 | 8760354 | Accordingly we cultured rat islets in the presence and absence of cytokines, and measured synthesis of both isoforms of GAD, GAD65 and GAD67, by [35S]methionine incorporation and immunoprecipitation with a rabbit antiserum that recognizes both GAD65 and GAD67. |
| 385 | 8760354 | Incubation of islets with interleukin (IL)-1 beta (1 ng/ml, 24 h), tumour necrosis factor alpha (TNF-alpha; 200 units/ml, 24 h) or interferon gamma (IFN-gamma; 500 units/ml, 72 h) significantly decreased the synthesis of both GAD65 and GAD67, but reduced neither total protein synthesis nor insulin accumulation in the medium or content. |
| 386 | 8760354 | Incubation of islets for 24 h in IFN-alpha (1000 units/ml), TNF-beta (50 ng/ml), IL 2 (1000 units/ml), IL-4 (100 ng/ml), IL-6 (10 ng/ml), IL-10 (20 ng/ml), IL-12 (10 ng/ml) or transforming growth factor beta 2 (TGF-beta 2; 5 ng/ml) did not significantly alter GAD65 or GAD67 synthesis. |
| 387 | 8760354 | Inhibition of GAD65 and GAD67 protein synthesis by IL-1 beta, TNF-alpha or IFN-gamma was reversed by co-incubation with the nitric oxide synthase inhibitor, NG-monomethyl arginine (NMMA). |
| 388 | 8760354 | Expression of both GAD65 and GAD67 mRNA, measured by RNase protection assay, was also decreased by IL-1 beta and completely restored to baseline levels by NMMA. |
| 389 | 8760354 | Thus the synthesis of both isoforms of islet GAD is selectively decreased in the presence of IL-1 beta, TNF-alpha or IFN-gamma by a NO-mediated mechanism, probably at the level of cytokine gene transcription. |
| 390 | 8760354 | As GAD autoimmunity has been previously shown to have a pathogenic role in an animal model of IDDM, its inhibition by cytokines might limit the immune response, thereby regulating the rate of beta-cell destruction in IDDM. |
| 391 | 8769952 | Transforming growth factor-beta and insulin-like growth factor-I in relation to diabetes-induced impairment of wound healing. |
| 392 | 8769952 | This study examined the effects of streptozotocin (STZ)-induced diabetes on the healing process using three wound models: (i) a linear skin incision (tensile strength), (ii) subcutaneously implanted polyvinyl alcohol sponge PVAs (collagen deposition), and (iii) stainless steel mesh chamber (TGF-beta, IGF-I and its binding proteins, extracellular matrix remodeling enzymes). |
| 393 | 8769952 | Diabetes of graded metabolic severity induced by variable doses of STZ (25 mg-200 mg/kg) showed stepwise reduction in wound tensile strength and PVAs collagen deposition. |
| 394 | 8769952 | A single dose of TGF-beta (2 micrograms) in a collagen vehicle partially reversed the diabetes-related decrease in the tensile strength of standardized incisions. |
| 395 | 8769952 | Transforming growth factor-beta and insulin-like growth factor-I in relation to diabetes-induced impairment of wound healing. |
| 396 | 8769952 | This study examined the effects of streptozotocin (STZ)-induced diabetes on the healing process using three wound models: (i) a linear skin incision (tensile strength), (ii) subcutaneously implanted polyvinyl alcohol sponge PVAs (collagen deposition), and (iii) stainless steel mesh chamber (TGF-beta, IGF-I and its binding proteins, extracellular matrix remodeling enzymes). |
| 397 | 8769952 | Diabetes of graded metabolic severity induced by variable doses of STZ (25 mg-200 mg/kg) showed stepwise reduction in wound tensile strength and PVAs collagen deposition. |
| 398 | 8769952 | A single dose of TGF-beta (2 micrograms) in a collagen vehicle partially reversed the diabetes-related decrease in the tensile strength of standardized incisions. |
| 399 | 8769952 | Transforming growth factor-beta and insulin-like growth factor-I in relation to diabetes-induced impairment of wound healing. |
| 400 | 8769952 | This study examined the effects of streptozotocin (STZ)-induced diabetes on the healing process using three wound models: (i) a linear skin incision (tensile strength), (ii) subcutaneously implanted polyvinyl alcohol sponge PVAs (collagen deposition), and (iii) stainless steel mesh chamber (TGF-beta, IGF-I and its binding proteins, extracellular matrix remodeling enzymes). |
| 401 | 8769952 | Diabetes of graded metabolic severity induced by variable doses of STZ (25 mg-200 mg/kg) showed stepwise reduction in wound tensile strength and PVAs collagen deposition. |
| 402 | 8769952 | A single dose of TGF-beta (2 micrograms) in a collagen vehicle partially reversed the diabetes-related decrease in the tensile strength of standardized incisions. |
| 403 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 404 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 405 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 406 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 407 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 408 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 409 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 410 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 411 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 412 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 413 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 414 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 415 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 416 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 417 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 418 | 8811326 | Elevated glucose levels stimulate transforming growth factor-beta 1 (TGF-beta 1), suppress interleukin IL-2, IL-6 and IL-10 production and DNA synthesis in peripheral blood mononuclear cells. |
| 419 | 8811326 | In this study we have analyzed the effects of elevated glucose concentration on both DNA synthesis and the production of transforming growth factor-beta 1 (TGF-beta 1) and the interleukins (IL) IL-2, IL-6 and IL-10 in stimulated peripheral blood mononuclear cells (PBMC) obtained from normal individuals. |
| 420 | 8811326 | Production of the cytokines IL-2, IL-6 and IL-10 was suppressed by elevated glucose concentration dose- and time-dependently. |
| 421 | 8811326 | In contrast to the time-dependent decreased effect of glucose-induced TGF-beta 1 production the effects of elevated glucose levels on IL-2, IL-6 and IL-10 production increased with time indicating that TGF-beta 1 production is preceding the reduced IL production. |
| 422 | 8811326 | Our results indicate that high glucose-induced TGF-beta 1 production may suppress immune response by inhibiting the endogenous production of IL-2, IL-6 and IL-10. |
| 423 | 8816968 | Insulin-dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse results from effector T cell-mediated autoimmune processes directed against pancreatic beta cells. |
| 424 | 8816968 | The clone was found to produce substantial amounts of transforming growth factor beta (TGF-beta), IL-10, and IFN-gamma, but not IL-2 or IL-4, indicating that this T cell clone is not a member of either the classic Th1 or Th2 cell type. |
| 425 | 8816968 | On the basis of these observations, we suggest that a new type of CD4+ suppressor T cell, NY4.2, by secreting TGF-beta, can prevent effector T cell-mediated beta cell destruction. |
| 426 | 8816968 | Insulin-dependent diabetes mellitus (IDDM) in the non-obese diabetic (NOD) mouse results from effector T cell-mediated autoimmune processes directed against pancreatic beta cells. |
| 427 | 8816968 | The clone was found to produce substantial amounts of transforming growth factor beta (TGF-beta), IL-10, and IFN-gamma, but not IL-2 or IL-4, indicating that this T cell clone is not a member of either the classic Th1 or Th2 cell type. |
| 428 | 8816968 | On the basis of these observations, we suggest that a new type of CD4+ suppressor T cell, NY4.2, by secreting TGF-beta, can prevent effector T cell-mediated beta cell destruction. |
| 429 | 8817101 | Increased activity of the insulin-like growth factor system in mesangial cells cultured in high glucose conditions. |
| 430 | 8817101 | Transforming growth factor (TGF)-beta has been demonstrated to be upregulated both in vivo and in vitro, whereas studies on the activity of the renal insulin-like growth factor (IGF) system in experimental diabetes have provided conflicting results. |
| 431 | 8817101 | We investigated the effects of prolonged exposure (4 weeks) of cultured human and rat mesangial cells to high (30 mmol/l) glucose vs iso-osmolar mannitol or normal (5.5 mmol/l) glucose levels on: 1) the autocrine/paracrine activity of the IGF system (as assessed by measuring IGF-I and II, IGF-I and II receptors, and IGF binding proteins); and, in parallel, on 2) TGF-beta 1 gene expression; 3) matrix production; and 4) cell proliferation. |
| 432 | 8817101 | High glucose levels progressively increased the medium content of IGF-I and the mRNA levels for IGF-I and IGF-II, increased IGF-I and IGF-II binding and IGF-I receptor gene expression, and reduced IGF binding protein production. |
| 433 | 8823297 | Here we report that oral treatment with insulin prevents virus-induced insulin-dependent diabetes mellitus (IDDM) in a transgenic (tg) mouse model. |
| 434 | 8823297 | Oral treatment with 1 mg of insulin twice per week for 2 mo starting either 1 wk before or 10 d after initiating LCMV infection prevents IDDM in > 50% of the tg mice (observation time 8 mo). |
| 435 | 8823297 | Thus, insulin therapy is effective in preventing progression to overt IDDM in prediabetic tg mice with ongoing islet infiltration. |
| 436 | 8823297 | However, less beta cells are destroyed in insulin-treated mice, upregulation of MHC class I and II molecules does not occur, and antiviral (self) cytotoxic T lymphocytes are not found in the islets, events present in tg mice developing IDDM. |
| 437 | 8823297 | The majority of lymphocytes in the islets of insulin-treated tg mice without IDDM produces IL-4, IL-10, and TGF-beta. |
| 438 | 8840279 | The non-transgenic (non-TG) diabetic mouse glomeruli had an increase in mRNA coding for alpha 1IV collagen, laminin B1, TGF-beta 1, 72 kDa collagenase, and TIMP-3. |
| 439 | 8840279 | However, the 72 kDa gelatinase, TIMP-3, and TGF-beta 1 mRNAs were elevated in the diabetic dwarfs. |
| 440 | 8840279 | The increase of 72 kDa gelatinase, TIMP-3 and TGF-beta 1 mRNAs, independent of GH, suggested that these changes induced by hyperglycemia were not sufficient for the induction of glomerulosclerosis. |
| 441 | 8840279 | The non-transgenic (non-TG) diabetic mouse glomeruli had an increase in mRNA coding for alpha 1IV collagen, laminin B1, TGF-beta 1, 72 kDa collagenase, and TIMP-3. |
| 442 | 8840279 | However, the 72 kDa gelatinase, TIMP-3, and TGF-beta 1 mRNAs were elevated in the diabetic dwarfs. |
| 443 | 8840279 | The increase of 72 kDa gelatinase, TIMP-3 and TGF-beta 1 mRNAs, independent of GH, suggested that these changes induced by hyperglycemia were not sufficient for the induction of glomerulosclerosis. |
| 444 | 8840279 | The non-transgenic (non-TG) diabetic mouse glomeruli had an increase in mRNA coding for alpha 1IV collagen, laminin B1, TGF-beta 1, 72 kDa collagenase, and TIMP-3. |
| 445 | 8840279 | However, the 72 kDa gelatinase, TIMP-3, and TGF-beta 1 mRNAs were elevated in the diabetic dwarfs. |
| 446 | 8840279 | The increase of 72 kDa gelatinase, TIMP-3 and TGF-beta 1 mRNAs, independent of GH, suggested that these changes induced by hyperglycemia were not sufficient for the induction of glomerulosclerosis. |
| 447 | 8883039 | Monthly urinary albumin excretion, glomerular filtration rate, glomerular volume, renal histology and immunohistochemical reaction for type-I collagen were also studied. |
| 448 | 8883039 | The results showed progressively higher glomerular immunohistochemical TGF-beta 1 staining in rats with a diabetes duration of 24 and 40 weeks which was correlated with albuminuria (r = 0.905, p < 0.01) and was temporally associated with the appearance of glomerular deposition of total and type-I collagen. |
| 449 | 8893451 | A major difference was seen between transplanted kidneys, which exhibited clearly positive TGF-beta and LTBP1 (latent TGF-beta binding protein) immunoreactivities, and the non-transplanted kidneys. |
| 450 | 8893451 | Thus, transplantation was the most important predictor for expression of TGF-beta s and LTBP1, and the largest expression increase in the allografts occurred in the interstitium, followed by the glomeruli and blood vessels. |
| 451 | 8893451 | A major difference was seen between transplanted kidneys, which exhibited clearly positive TGF-beta and LTBP1 (latent TGF-beta binding protein) immunoreactivities, and the non-transplanted kidneys. |
| 452 | 8893451 | Thus, transplantation was the most important predictor for expression of TGF-beta s and LTBP1, and the largest expression increase in the allografts occurred in the interstitium, followed by the glomeruli and blood vessels. |
| 453 | 8905209 | Their activation leads to an increased release of cytokines and growth factors including PDGF, interleukins, TNF-alpha, and TGF-beta, all of which may act concomitantly in the disease process. |
| 454 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 455 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 456 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 457 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 458 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 459 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 460 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 461 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 462 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 463 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 464 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 465 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 466 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 467 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 468 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 469 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 470 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 471 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 472 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 473 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 474 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 475 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 476 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 477 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 478 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 479 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 480 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 481 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 482 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 483 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 484 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 485 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 486 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 487 | 8913531 | Effects of transforming growth factor beta, tumor necrosis factor alpha and interferon gamma on pancreatic islet beta-cell responsiveness to transforming growth factor alpha. |
| 488 | 8913531 | The insulin-producing pancreatic islet beta-cell, characterized by low proliferative potential, is normally not responsive to the polypeptide epidermal growth factor (EGF) or its homolog transforming growth factor alpha (TGF-alpha). |
| 489 | 8913531 | Since EGF receptors in other tissues can be up-regulated by other growth factors and by cytokines, we have in this paper investigated whether such a beta-cell responsiveness to TGF-alpha, or EGF, can be conferred by co-culture with interferon gamma (IFN-gamma), tumor necrosis factor alpha (TNF-alpha) or transforming growth factor beta (TGF-beta) in various combinations. |
| 490 | 8913531 | It was found that neither of these TGF-alpha concentrations affected beta-cell mitogenesis, insulin content or insulin secretion. |
| 491 | 8913531 | However, IFN-gamma (1000 U/ml) evoked a modest stimulation of beta-cell replication, while suppressing insulin secretion and leaving the islet insulin content unaltered. |
| 492 | 8913531 | TNF-alpha (1000 U/ml), on the other hand, affected none of these parameters either alone or in any combination with TGF-alpha or IFN-gamma. |
| 493 | 8913531 | However, when TNF-alpha or IFN-gamma, either alone or in combination, were combined with the cytokine interleukin-1 beta, this resulted in islet disintegration, whereas the latter cytokine alone did not exert any gross necrotic changes evident by light microscopy. |
| 494 | 8913531 | TGF-beta (500 pM) stimulated insulin secretion but did not influence islet insulin content or beta-cell mitogenesis either alone or in combination with TGF-alpha (200 pM or 20 nM). |
| 495 | 8913531 | In no instance could any mitogenic or secretory response to low or high concentrations of TGF-alpha be conferred by IFN-gamma. |
| 496 | 8913531 | TNF-alpha or TGF-beta whether used alone or in combinations. |
| 497 | 8913531 | Hence, responsiveness to TGF-alpha or EGF in the beta-cell obviously cannot be achieved by any of these peptides. |
| 498 | 8928843 | High glucose-induced TGF-beta 1 regulates mesangial production of heparan sulfate proteoglycan. |
| 499 | 8960825 | At 70 days of age mononuclear infiltration of islets had begun and was associated with upregulation of interferon gamma (IFN gamma) and iNOS, but downregulation of interleukin-10 and transforming growth factor beta mRNA (p < 0.001). |
| 500 | 8960825 | Oral lipopolysaccharide (LPS) from E. coli and OM-89, an endotoxin free extract containing immunostimulatory glycolipopeptides and heat shock protein (hsp) 65, both downregulated IFN gamma mRNA while only OM-89 in addition suppressed iNOS mRNA and enhanced Th2 cytokine gene expression (p < 0.001). |
| 501 | 8971094 | As TGF-beta inhibited local HGF production in endothelial cell and VSMC, increased TGF-beta induced by high D-glucose may suppress local HGF production. |
| 502 | 8971094 | This study demonstrated that high D-glucose induced endothelial cell death, stimulated VSMC growth, and decreased local HGF production through the stimulation of TGF-beta production both in endothelial cell and VSMC. |
| 503 | 8971094 | As TGF-beta inhibited local HGF production in endothelial cell and VSMC, increased TGF-beta induced by high D-glucose may suppress local HGF production. |
| 504 | 8971094 | This study demonstrated that high D-glucose induced endothelial cell death, stimulated VSMC growth, and decreased local HGF production through the stimulation of TGF-beta production both in endothelial cell and VSMC. |
| 505 | 8971657 | No changes were observed in mRNA expression for platelet-derived growth factor-AA, platelet-derived growth factor-BB, insulin-like growth factor and transforming growth factor-beta 1. |
| 506 | 8981938 | Particle-mediated gene transfer with transforming growth factor-beta1 cDNAs enhances wound repair in rat skin. |
| 507 | 8997162 | The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells. |
| 508 | 8997162 | In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we evaluated the effects of a high concentration of extracellular glucose(25 mM; 450 mg/dl) on [3H]thymidine uptake, hypertrophy, and [3H]proline incorporation into a collagenase-sensitive protein, induced by angiotensin II(Ang II) or transforming growth factor(TGF)-beta, in cultured rat mesangial cells. |
| 509 | 8997162 | The exposure to a high glucose concentration for 7 days significantly inhibited Ang II(10(-6) M)-induced [3H]thymidine uptake, compared to normal glucose concentration (5 mM)(M +/- SD., 1050 +/- 100 cpm/well vs 550 +/- 97, p < 0.05), and markedly prevented the inhibition of [3H]thymidine uptake by TGF-beta(1 ng/ml)(132 +/- 10 vs 340 +/- 67, p < 0.05). |
| 510 | 8997162 | On flow cytometric analysis of cell size, the mean cell size was significantly greater for the cells exposed to high glucose or treated with Ang II or TGF-beta, compared to that for the untreated cells. |
| 511 | 8997162 | But the addition of Ang II or TGF-beta to the cells exposed to high glucose did not show further enlargement in size. |
| 512 | 8997162 | The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. |
| 513 | 8997162 | The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). |
| 514 | 8997162 | In conclusion, although the signaling pathway for DNA synthesis by Ang II or TGF-beta are influenced, possibly mediated by PKC-independent mechanism(s), the pathway inducing hypertrophy or collagen synthesis by both agents appears to be unchanged under the high extracellular glucose concentration in cultured rat mesangial cells. |
| 515 | 8997162 | The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells. |
| 516 | 8997162 | In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we evaluated the effects of a high concentration of extracellular glucose(25 mM; 450 mg/dl) on [3H]thymidine uptake, hypertrophy, and [3H]proline incorporation into a collagenase-sensitive protein, induced by angiotensin II(Ang II) or transforming growth factor(TGF)-beta, in cultured rat mesangial cells. |
| 517 | 8997162 | The exposure to a high glucose concentration for 7 days significantly inhibited Ang II(10(-6) M)-induced [3H]thymidine uptake, compared to normal glucose concentration (5 mM)(M +/- SD., 1050 +/- 100 cpm/well vs 550 +/- 97, p < 0.05), and markedly prevented the inhibition of [3H]thymidine uptake by TGF-beta(1 ng/ml)(132 +/- 10 vs 340 +/- 67, p < 0.05). |
| 518 | 8997162 | On flow cytometric analysis of cell size, the mean cell size was significantly greater for the cells exposed to high glucose or treated with Ang II or TGF-beta, compared to that for the untreated cells. |
| 519 | 8997162 | But the addition of Ang II or TGF-beta to the cells exposed to high glucose did not show further enlargement in size. |
| 520 | 8997162 | The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. |
| 521 | 8997162 | The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). |
| 522 | 8997162 | In conclusion, although the signaling pathway for DNA synthesis by Ang II or TGF-beta are influenced, possibly mediated by PKC-independent mechanism(s), the pathway inducing hypertrophy or collagen synthesis by both agents appears to be unchanged under the high extracellular glucose concentration in cultured rat mesangial cells. |
| 523 | 8997162 | The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells. |
| 524 | 8997162 | In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we evaluated the effects of a high concentration of extracellular glucose(25 mM; 450 mg/dl) on [3H]thymidine uptake, hypertrophy, and [3H]proline incorporation into a collagenase-sensitive protein, induced by angiotensin II(Ang II) or transforming growth factor(TGF)-beta, in cultured rat mesangial cells. |
| 525 | 8997162 | The exposure to a high glucose concentration for 7 days significantly inhibited Ang II(10(-6) M)-induced [3H]thymidine uptake, compared to normal glucose concentration (5 mM)(M +/- SD., 1050 +/- 100 cpm/well vs 550 +/- 97, p < 0.05), and markedly prevented the inhibition of [3H]thymidine uptake by TGF-beta(1 ng/ml)(132 +/- 10 vs 340 +/- 67, p < 0.05). |
| 526 | 8997162 | On flow cytometric analysis of cell size, the mean cell size was significantly greater for the cells exposed to high glucose or treated with Ang II or TGF-beta, compared to that for the untreated cells. |
| 527 | 8997162 | But the addition of Ang II or TGF-beta to the cells exposed to high glucose did not show further enlargement in size. |
| 528 | 8997162 | The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. |
| 529 | 8997162 | The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). |
| 530 | 8997162 | In conclusion, although the signaling pathway for DNA synthesis by Ang II or TGF-beta are influenced, possibly mediated by PKC-independent mechanism(s), the pathway inducing hypertrophy or collagen synthesis by both agents appears to be unchanged under the high extracellular glucose concentration in cultured rat mesangial cells. |
| 531 | 8997162 | The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells. |
| 532 | 8997162 | In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we evaluated the effects of a high concentration of extracellular glucose(25 mM; 450 mg/dl) on [3H]thymidine uptake, hypertrophy, and [3H]proline incorporation into a collagenase-sensitive protein, induced by angiotensin II(Ang II) or transforming growth factor(TGF)-beta, in cultured rat mesangial cells. |
| 533 | 8997162 | The exposure to a high glucose concentration for 7 days significantly inhibited Ang II(10(-6) M)-induced [3H]thymidine uptake, compared to normal glucose concentration (5 mM)(M +/- SD., 1050 +/- 100 cpm/well vs 550 +/- 97, p < 0.05), and markedly prevented the inhibition of [3H]thymidine uptake by TGF-beta(1 ng/ml)(132 +/- 10 vs 340 +/- 67, p < 0.05). |
| 534 | 8997162 | On flow cytometric analysis of cell size, the mean cell size was significantly greater for the cells exposed to high glucose or treated with Ang II or TGF-beta, compared to that for the untreated cells. |
| 535 | 8997162 | But the addition of Ang II or TGF-beta to the cells exposed to high glucose did not show further enlargement in size. |
| 536 | 8997162 | The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. |
| 537 | 8997162 | The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). |
| 538 | 8997162 | In conclusion, although the signaling pathway for DNA synthesis by Ang II or TGF-beta are influenced, possibly mediated by PKC-independent mechanism(s), the pathway inducing hypertrophy or collagen synthesis by both agents appears to be unchanged under the high extracellular glucose concentration in cultured rat mesangial cells. |
| 539 | 8997162 | The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells. |
| 540 | 8997162 | In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we evaluated the effects of a high concentration of extracellular glucose(25 mM; 450 mg/dl) on [3H]thymidine uptake, hypertrophy, and [3H]proline incorporation into a collagenase-sensitive protein, induced by angiotensin II(Ang II) or transforming growth factor(TGF)-beta, in cultured rat mesangial cells. |
| 541 | 8997162 | The exposure to a high glucose concentration for 7 days significantly inhibited Ang II(10(-6) M)-induced [3H]thymidine uptake, compared to normal glucose concentration (5 mM)(M +/- SD., 1050 +/- 100 cpm/well vs 550 +/- 97, p < 0.05), and markedly prevented the inhibition of [3H]thymidine uptake by TGF-beta(1 ng/ml)(132 +/- 10 vs 340 +/- 67, p < 0.05). |
| 542 | 8997162 | On flow cytometric analysis of cell size, the mean cell size was significantly greater for the cells exposed to high glucose or treated with Ang II or TGF-beta, compared to that for the untreated cells. |
| 543 | 8997162 | But the addition of Ang II or TGF-beta to the cells exposed to high glucose did not show further enlargement in size. |
| 544 | 8997162 | The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. |
| 545 | 8997162 | The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). |
| 546 | 8997162 | In conclusion, although the signaling pathway for DNA synthesis by Ang II or TGF-beta are influenced, possibly mediated by PKC-independent mechanism(s), the pathway inducing hypertrophy or collagen synthesis by both agents appears to be unchanged under the high extracellular glucose concentration in cultured rat mesangial cells. |
| 547 | 8997162 | The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells. |
| 548 | 8997162 | In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we evaluated the effects of a high concentration of extracellular glucose(25 mM; 450 mg/dl) on [3H]thymidine uptake, hypertrophy, and [3H]proline incorporation into a collagenase-sensitive protein, induced by angiotensin II(Ang II) or transforming growth factor(TGF)-beta, in cultured rat mesangial cells. |
| 549 | 8997162 | The exposure to a high glucose concentration for 7 days significantly inhibited Ang II(10(-6) M)-induced [3H]thymidine uptake, compared to normal glucose concentration (5 mM)(M +/- SD., 1050 +/- 100 cpm/well vs 550 +/- 97, p < 0.05), and markedly prevented the inhibition of [3H]thymidine uptake by TGF-beta(1 ng/ml)(132 +/- 10 vs 340 +/- 67, p < 0.05). |
| 550 | 8997162 | On flow cytometric analysis of cell size, the mean cell size was significantly greater for the cells exposed to high glucose or treated with Ang II or TGF-beta, compared to that for the untreated cells. |
| 551 | 8997162 | But the addition of Ang II or TGF-beta to the cells exposed to high glucose did not show further enlargement in size. |
| 552 | 8997162 | The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. |
| 553 | 8997162 | The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). |
| 554 | 8997162 | In conclusion, although the signaling pathway for DNA synthesis by Ang II or TGF-beta are influenced, possibly mediated by PKC-independent mechanism(s), the pathway inducing hypertrophy or collagen synthesis by both agents appears to be unchanged under the high extracellular glucose concentration in cultured rat mesangial cells. |
| 555 | 8997162 | The effects of high glucose concentration on angiotensin II- or transforming growth factor-beta-induced DNA synthesis, hypertrophy and collagen synthesis in cultured rat mesangial cells. |
| 556 | 8997162 | In order to investigate whether the intracellular signaling pathways inducing proliferation, hypertrophy and matrix synthesis of mesangial cells are altered in a diabetic environment, we evaluated the effects of a high concentration of extracellular glucose(25 mM; 450 mg/dl) on [3H]thymidine uptake, hypertrophy, and [3H]proline incorporation into a collagenase-sensitive protein, induced by angiotensin II(Ang II) or transforming growth factor(TGF)-beta, in cultured rat mesangial cells. |
| 557 | 8997162 | The exposure to a high glucose concentration for 7 days significantly inhibited Ang II(10(-6) M)-induced [3H]thymidine uptake, compared to normal glucose concentration (5 mM)(M +/- SD., 1050 +/- 100 cpm/well vs 550 +/- 97, p < 0.05), and markedly prevented the inhibition of [3H]thymidine uptake by TGF-beta(1 ng/ml)(132 +/- 10 vs 340 +/- 67, p < 0.05). |
| 558 | 8997162 | On flow cytometric analysis of cell size, the mean cell size was significantly greater for the cells exposed to high glucose or treated with Ang II or TGF-beta, compared to that for the untreated cells. |
| 559 | 8997162 | But the addition of Ang II or TGF-beta to the cells exposed to high glucose did not show further enlargement in size. |
| 560 | 8997162 | The exposure to high glucose and the treatment with Ang II or TGF-beta significantly increased collagen synthesis, measured by [3H]proline incorporation. |
| 561 | 8997162 | The Ang II -or TGF-beta-induced increase of [3H]proline incorporation did not show changes under high glucose culture condition, compared to normal glucose concentration(Ang II, 27880 +/- 3560 cpm vs 26978 +/- 2284, TGF-beta, 26559 +/- 3700 vs 25800 +/- 1660, p > 0.05). |
| 562 | 8997162 | In conclusion, although the signaling pathway for DNA synthesis by Ang II or TGF-beta are influenced, possibly mediated by PKC-independent mechanism(s), the pathway inducing hypertrophy or collagen synthesis by both agents appears to be unchanged under the high extracellular glucose concentration in cultured rat mesangial cells. |
| 563 | 9002545 | There may also exist additive effects of angiotensin II and high glucose on signal-transduction pathways, such as activation of protein kinase C, although the contractile response to angiotensin II may be blunted by high glucose in mesangial cells. |
| 564 | 9002545 | An important downstream mediator of the effects of both angiotensin II and high glucose is the activation of transforming growth factor-beta that can mediate at least some of the hypertrophic and profibrotic effects of either angiotensin II or high glucose in the diabetic kidney. |
| 565 | 9032105 | Expression of transforming growth factor-beta and type IV collagen in early streptozotocin-induced diabetes. |
| 566 | 9032105 | Using in situ hybridization and immunohistochemistry, we determined the expression of TGF-beta and type IV collagen mRNAs and proteins in glomeruli and interstitium of diabetic rats 3, 7, and 14 days after streptozotocin (STZ) administration. |
| 567 | 9032105 | A concomitant increase in TGF-beta and type IV collagen proteins was also observed at each time point. |
| 568 | 9032105 | Insulin treatment substantially inhibited the increased expression of TGF-beta and collagen type IV mRNAs and proteins. |
| 569 | 9032105 | Inhibition of TGF-beta and type IV collagen expression by insulin treatment suggests that they may be useful structural markers for determining the efficacy of therapeutic intervention during early diabetic nephropathy. |
| 570 | 9032105 | Expression of transforming growth factor-beta and type IV collagen in early streptozotocin-induced diabetes. |
| 571 | 9032105 | Using in situ hybridization and immunohistochemistry, we determined the expression of TGF-beta and type IV collagen mRNAs and proteins in glomeruli and interstitium of diabetic rats 3, 7, and 14 days after streptozotocin (STZ) administration. |
| 572 | 9032105 | A concomitant increase in TGF-beta and type IV collagen proteins was also observed at each time point. |
| 573 | 9032105 | Insulin treatment substantially inhibited the increased expression of TGF-beta and collagen type IV mRNAs and proteins. |
| 574 | 9032105 | Inhibition of TGF-beta and type IV collagen expression by insulin treatment suggests that they may be useful structural markers for determining the efficacy of therapeutic intervention during early diabetic nephropathy. |
| 575 | 9032105 | Expression of transforming growth factor-beta and type IV collagen in early streptozotocin-induced diabetes. |
| 576 | 9032105 | Using in situ hybridization and immunohistochemistry, we determined the expression of TGF-beta and type IV collagen mRNAs and proteins in glomeruli and interstitium of diabetic rats 3, 7, and 14 days after streptozotocin (STZ) administration. |
| 577 | 9032105 | A concomitant increase in TGF-beta and type IV collagen proteins was also observed at each time point. |
| 578 | 9032105 | Insulin treatment substantially inhibited the increased expression of TGF-beta and collagen type IV mRNAs and proteins. |
| 579 | 9032105 | Inhibition of TGF-beta and type IV collagen expression by insulin treatment suggests that they may be useful structural markers for determining the efficacy of therapeutic intervention during early diabetic nephropathy. |
| 580 | 9032105 | Expression of transforming growth factor-beta and type IV collagen in early streptozotocin-induced diabetes. |
| 581 | 9032105 | Using in situ hybridization and immunohistochemistry, we determined the expression of TGF-beta and type IV collagen mRNAs and proteins in glomeruli and interstitium of diabetic rats 3, 7, and 14 days after streptozotocin (STZ) administration. |
| 582 | 9032105 | A concomitant increase in TGF-beta and type IV collagen proteins was also observed at each time point. |
| 583 | 9032105 | Insulin treatment substantially inhibited the increased expression of TGF-beta and collagen type IV mRNAs and proteins. |
| 584 | 9032105 | Inhibition of TGF-beta and type IV collagen expression by insulin treatment suggests that they may be useful structural markers for determining the efficacy of therapeutic intervention during early diabetic nephropathy. |
| 585 | 9032105 | Expression of transforming growth factor-beta and type IV collagen in early streptozotocin-induced diabetes. |
| 586 | 9032105 | Using in situ hybridization and immunohistochemistry, we determined the expression of TGF-beta and type IV collagen mRNAs and proteins in glomeruli and interstitium of diabetic rats 3, 7, and 14 days after streptozotocin (STZ) administration. |
| 587 | 9032105 | A concomitant increase in TGF-beta and type IV collagen proteins was also observed at each time point. |
| 588 | 9032105 | Insulin treatment substantially inhibited the increased expression of TGF-beta and collagen type IV mRNAs and proteins. |
| 589 | 9032105 | Inhibition of TGF-beta and type IV collagen expression by insulin treatment suggests that they may be useful structural markers for determining the efficacy of therapeutic intervention during early diabetic nephropathy. |
| 590 | 9034240 | TGF-beta1 triggers oxidative modifications and enhances apoptosis in HIT cells through accumulation of reactive oxygen species by suppression of catalase and glutathione peroxidase. |
| 591 | 9034240 | Transforming growth factor-beta1 (TGF-beta1) is a multifunctional polypeptide that is related to the progression of chronic pancreatitis. |
| 592 | 9034240 | TGF-beta1 suppressed mRNA expression as well as reduced the activities of catalase and GPx. |
| 593 | 9034240 | TGF-beta1 triggers oxidative modifications and enhances apoptosis in HIT cells through accumulation of reactive oxygen species by suppression of catalase and glutathione peroxidase. |
| 594 | 9034240 | Transforming growth factor-beta1 (TGF-beta1) is a multifunctional polypeptide that is related to the progression of chronic pancreatitis. |
| 595 | 9034240 | TGF-beta1 suppressed mRNA expression as well as reduced the activities of catalase and GPx. |
| 596 | 9034240 | TGF-beta1 triggers oxidative modifications and enhances apoptosis in HIT cells through accumulation of reactive oxygen species by suppression of catalase and glutathione peroxidase. |
| 597 | 9034240 | Transforming growth factor-beta1 (TGF-beta1) is a multifunctional polypeptide that is related to the progression of chronic pancreatitis. |
| 598 | 9034240 | TGF-beta1 suppressed mRNA expression as well as reduced the activities of catalase and GPx. |
| 599 | 9046967 | Low doses of oral antigen induce antigen-specific regulatory T-cells in the gut, which act by releasing inhibitory cytokines such as transforming growth factor-beta, interleukin-4, and interleukin-10 at the target organ. |
| 600 | 9046967 | A double-blind, placebo-controlled, phase III multi-center trial of oral myelin in 515 relapsing-remitting multiple sclerosis patients is in progress, as are phase II clinical trials investigating the oral administration of type II collagen in rheumatoid arthritis, S-antigen in uveitis, and insulin in type I diabetes. |
| 601 | 9052888 | To characterize the molecular mechanism of cardiac and renal complications in non-insulin-dependent diabetes mellitus (NIDDM), we examined the gene expression of Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new animal model for human NIDDM, at the ages of 14 weeks (prediabetic stage), 30 weeks (NIDDM stage), and 54 weeks (IDDM stage). |
| 602 | 9052888 | In 14-week-old OLETF rats, cardiac mRNAs for transforming growth factor-beta1 (TGF-beta1) and extracellular matrix, including collagen types I, III, and IV and laminin, were significantly increased compared with control rats (Long-Evans Tokushima Otsuka rats). |
| 603 | 9052888 | Cardiac beta-myosin heavy chain (MHC) mRNA of OLETF was increased at 30 and 54 weeks of age, whereas alpha-MHC mRNA of OLETF was inversely decreased at 54 weeks. |
| 604 | 9062360 | By Northern analysis, TGF-beta1 gene expression was increased 100-150% (P < 0.01) and alpha1 (IV) collagen gene expression was similarly elevated to 30-110% compared to controls (P < 0.05). |
| 605 | 9062360 | Treatment of diabetic rats with aminoguanidine resulted in significant amelioration of the described pathological changes including overexpression of TGF-beta1 and alpha1 (IV) collagen. |
| 606 | 9062360 | By Northern analysis, TGF-beta1 gene expression was increased 100-150% (P < 0.01) and alpha1 (IV) collagen gene expression was similarly elevated to 30-110% compared to controls (P < 0.05). |
| 607 | 9062360 | Treatment of diabetic rats with aminoguanidine resulted in significant amelioration of the described pathological changes including overexpression of TGF-beta1 and alpha1 (IV) collagen. |
| 608 | 9067916 | Epidermal growth factor (EGF), platelet-derived growth factor (PDGF), transforming growth factor (TGF) beta 1, TGF-beta 2 and TGF-beta 3, and tumor necrosis factor (TNF)-alpha and TNF-beta candidate genes were selected for analysis due to their putative roles in diabetic renal disease and chronic glomerulonephritis. |
| 609 | 9067916 | The interleukin-1 receptor antagonist gene (IL1RN) was also genotyped due to its reported association with diabetic nephropathy. |
| 610 | 9075798 | Diet-induced effects on pancreatic cytokine levels were measured at 70 days using reverse transcriptase-polymerase chain reaction analysis of gamma-interferon (IFN-gamma), interleukin-10 (IL-10), and transforming growth factor-beta (TGF-beta). |
| 611 | 9075798 | By 70 days, when mononuclear cells were visible in the islets of most NIH-fed, but not HC-fed rats, the more pronounced inflammatory process in NIH-fed rats was associated with a Th1 cytokine pattern (high IFN-gamma and low IL-10 and TGF-beta), whereas the pancreases of HC-fed rats showed fewer infiltrating cells, low levels of IFN-gamma, and high levels of TGF-beta, typical of a Th2 cytokine pattern. |
| 612 | 9075798 | Diet-induced effects on pancreatic cytokine levels were measured at 70 days using reverse transcriptase-polymerase chain reaction analysis of gamma-interferon (IFN-gamma), interleukin-10 (IL-10), and transforming growth factor-beta (TGF-beta). |
| 613 | 9075798 | By 70 days, when mononuclear cells were visible in the islets of most NIH-fed, but not HC-fed rats, the more pronounced inflammatory process in NIH-fed rats was associated with a Th1 cytokine pattern (high IFN-gamma and low IL-10 and TGF-beta), whereas the pancreases of HC-fed rats showed fewer infiltrating cells, low levels of IFN-gamma, and high levels of TGF-beta, typical of a Th2 cytokine pattern. |
| 614 | 9075810 | Nitric oxide inhibition of transforming growth factor-beta and collagen synthesis in mesangial cells. |
| 615 | 9075810 | Culture of mesangial cells (MCs) in 5.6 vs. 30.0 mmol/l glucose for 3 weeks induced a sustained increase in protein kinase C (PKC) activity, transforming growth factor (TGF)-beta1 mRNA, bioactive TGF-beta, and collagen synthesis. |
| 616 | 9075810 | Nitric oxide (NO), generated exogenously by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure of MC to interleukin-1beta (IL-1beta), suppressed bioactive TGF-beta in MCs cultured in 5.6 or 30.0 mmol/l glucose and suppressed or abolished increases in TGF-beta1 mRNA and collagen synthesis induced by high concentrations of glucose or phorbol 12,13-dibutyrate without altering values obtained with normal glucose concentrations. |
| 617 | 9075810 | The ability of SNAP and IL-1beta to suppress TGF-beta and collagen synthesis was not mediated by cGMP, since the cGMP analog, 8-Br-PET-cGMP, did not mimic NO action and an antagonist of cGMP-dependent protein kinase, Rp-8-pCPT-cGMPs, did not prevent the inhibitory actions of SNAP. |
| 618 | 9075810 | N-omega-L-arginine methyl ester (NMMA) increased TGF-beta in glomerular capillary endothelial cells (GCECs) and stimulated collagen synthesis by MC in a co-culture with GCECs. |
| 619 | 9075810 | Captopril inhibited TGF-beta and collagen synthesis and increased cGMP in co-cultures of GCECs and MCs. |
| 620 | 9075810 | Nitric oxide inhibition of transforming growth factor-beta and collagen synthesis in mesangial cells. |
| 621 | 9075810 | Culture of mesangial cells (MCs) in 5.6 vs. 30.0 mmol/l glucose for 3 weeks induced a sustained increase in protein kinase C (PKC) activity, transforming growth factor (TGF)-beta1 mRNA, bioactive TGF-beta, and collagen synthesis. |
| 622 | 9075810 | Nitric oxide (NO), generated exogenously by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure of MC to interleukin-1beta (IL-1beta), suppressed bioactive TGF-beta in MCs cultured in 5.6 or 30.0 mmol/l glucose and suppressed or abolished increases in TGF-beta1 mRNA and collagen synthesis induced by high concentrations of glucose or phorbol 12,13-dibutyrate without altering values obtained with normal glucose concentrations. |
| 623 | 9075810 | The ability of SNAP and IL-1beta to suppress TGF-beta and collagen synthesis was not mediated by cGMP, since the cGMP analog, 8-Br-PET-cGMP, did not mimic NO action and an antagonist of cGMP-dependent protein kinase, Rp-8-pCPT-cGMPs, did not prevent the inhibitory actions of SNAP. |
| 624 | 9075810 | N-omega-L-arginine methyl ester (NMMA) increased TGF-beta in glomerular capillary endothelial cells (GCECs) and stimulated collagen synthesis by MC in a co-culture with GCECs. |
| 625 | 9075810 | Captopril inhibited TGF-beta and collagen synthesis and increased cGMP in co-cultures of GCECs and MCs. |
| 626 | 9075810 | Nitric oxide inhibition of transforming growth factor-beta and collagen synthesis in mesangial cells. |
| 627 | 9075810 | Culture of mesangial cells (MCs) in 5.6 vs. 30.0 mmol/l glucose for 3 weeks induced a sustained increase in protein kinase C (PKC) activity, transforming growth factor (TGF)-beta1 mRNA, bioactive TGF-beta, and collagen synthesis. |
| 628 | 9075810 | Nitric oxide (NO), generated exogenously by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure of MC to interleukin-1beta (IL-1beta), suppressed bioactive TGF-beta in MCs cultured in 5.6 or 30.0 mmol/l glucose and suppressed or abolished increases in TGF-beta1 mRNA and collagen synthesis induced by high concentrations of glucose or phorbol 12,13-dibutyrate without altering values obtained with normal glucose concentrations. |
| 629 | 9075810 | The ability of SNAP and IL-1beta to suppress TGF-beta and collagen synthesis was not mediated by cGMP, since the cGMP analog, 8-Br-PET-cGMP, did not mimic NO action and an antagonist of cGMP-dependent protein kinase, Rp-8-pCPT-cGMPs, did not prevent the inhibitory actions of SNAP. |
| 630 | 9075810 | N-omega-L-arginine methyl ester (NMMA) increased TGF-beta in glomerular capillary endothelial cells (GCECs) and stimulated collagen synthesis by MC in a co-culture with GCECs. |
| 631 | 9075810 | Captopril inhibited TGF-beta and collagen synthesis and increased cGMP in co-cultures of GCECs and MCs. |
| 632 | 9075810 | Nitric oxide inhibition of transforming growth factor-beta and collagen synthesis in mesangial cells. |
| 633 | 9075810 | Culture of mesangial cells (MCs) in 5.6 vs. 30.0 mmol/l glucose for 3 weeks induced a sustained increase in protein kinase C (PKC) activity, transforming growth factor (TGF)-beta1 mRNA, bioactive TGF-beta, and collagen synthesis. |
| 634 | 9075810 | Nitric oxide (NO), generated exogenously by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure of MC to interleukin-1beta (IL-1beta), suppressed bioactive TGF-beta in MCs cultured in 5.6 or 30.0 mmol/l glucose and suppressed or abolished increases in TGF-beta1 mRNA and collagen synthesis induced by high concentrations of glucose or phorbol 12,13-dibutyrate without altering values obtained with normal glucose concentrations. |
| 635 | 9075810 | The ability of SNAP and IL-1beta to suppress TGF-beta and collagen synthesis was not mediated by cGMP, since the cGMP analog, 8-Br-PET-cGMP, did not mimic NO action and an antagonist of cGMP-dependent protein kinase, Rp-8-pCPT-cGMPs, did not prevent the inhibitory actions of SNAP. |
| 636 | 9075810 | N-omega-L-arginine methyl ester (NMMA) increased TGF-beta in glomerular capillary endothelial cells (GCECs) and stimulated collagen synthesis by MC in a co-culture with GCECs. |
| 637 | 9075810 | Captopril inhibited TGF-beta and collagen synthesis and increased cGMP in co-cultures of GCECs and MCs. |
| 638 | 9075810 | Nitric oxide inhibition of transforming growth factor-beta and collagen synthesis in mesangial cells. |
| 639 | 9075810 | Culture of mesangial cells (MCs) in 5.6 vs. 30.0 mmol/l glucose for 3 weeks induced a sustained increase in protein kinase C (PKC) activity, transforming growth factor (TGF)-beta1 mRNA, bioactive TGF-beta, and collagen synthesis. |
| 640 | 9075810 | Nitric oxide (NO), generated exogenously by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure of MC to interleukin-1beta (IL-1beta), suppressed bioactive TGF-beta in MCs cultured in 5.6 or 30.0 mmol/l glucose and suppressed or abolished increases in TGF-beta1 mRNA and collagen synthesis induced by high concentrations of glucose or phorbol 12,13-dibutyrate without altering values obtained with normal glucose concentrations. |
| 641 | 9075810 | The ability of SNAP and IL-1beta to suppress TGF-beta and collagen synthesis was not mediated by cGMP, since the cGMP analog, 8-Br-PET-cGMP, did not mimic NO action and an antagonist of cGMP-dependent protein kinase, Rp-8-pCPT-cGMPs, did not prevent the inhibitory actions of SNAP. |
| 642 | 9075810 | N-omega-L-arginine methyl ester (NMMA) increased TGF-beta in glomerular capillary endothelial cells (GCECs) and stimulated collagen synthesis by MC in a co-culture with GCECs. |
| 643 | 9075810 | Captopril inhibited TGF-beta and collagen synthesis and increased cGMP in co-cultures of GCECs and MCs. |
| 644 | 9075810 | Nitric oxide inhibition of transforming growth factor-beta and collagen synthesis in mesangial cells. |
| 645 | 9075810 | Culture of mesangial cells (MCs) in 5.6 vs. 30.0 mmol/l glucose for 3 weeks induced a sustained increase in protein kinase C (PKC) activity, transforming growth factor (TGF)-beta1 mRNA, bioactive TGF-beta, and collagen synthesis. |
| 646 | 9075810 | Nitric oxide (NO), generated exogenously by the NO donor S-nitroso-N-acetyl, D,L-penicillamine (SNAP) or endogenously after the exposure of MC to interleukin-1beta (IL-1beta), suppressed bioactive TGF-beta in MCs cultured in 5.6 or 30.0 mmol/l glucose and suppressed or abolished increases in TGF-beta1 mRNA and collagen synthesis induced by high concentrations of glucose or phorbol 12,13-dibutyrate without altering values obtained with normal glucose concentrations. |
| 647 | 9075810 | The ability of SNAP and IL-1beta to suppress TGF-beta and collagen synthesis was not mediated by cGMP, since the cGMP analog, 8-Br-PET-cGMP, did not mimic NO action and an antagonist of cGMP-dependent protein kinase, Rp-8-pCPT-cGMPs, did not prevent the inhibitory actions of SNAP. |
| 648 | 9075810 | N-omega-L-arginine methyl ester (NMMA) increased TGF-beta in glomerular capillary endothelial cells (GCECs) and stimulated collagen synthesis by MC in a co-culture with GCECs. |
| 649 | 9075810 | Captopril inhibited TGF-beta and collagen synthesis and increased cGMP in co-cultures of GCECs and MCs. |
| 650 | 9081122 | Transforming growth factor beta 1 inhibits the proliferative effect of insulin on human infragenicular vascular smooth muscle cells. |
| 651 | 9111509 | Platelet-derived growth factor (PDGF)-B mRNA was high at 2 to 3 months (7.4-fold) and 6 to 9 months (9.5-fold) and was associated with an increased [3H]-thymidine-labeling index and glomerular cell number. |
| 652 | 9111509 | In slow progressors (bGH-m11 mice), the mRNA levels at 2 to 3 months were approximately one half that of rapid progressors (alpha 1(IV) collagen, 3.4-fold; laminin B1 1.9-fold; tenascin, 3-fold; TGF-beta 1, 2.2-fold). |
| 653 | 9111509 | At 6 to 9 months, alpha 1(IV) collagen, TGF-beta 1, and PDGF-B mRNA levels doubled, whereas tenascin and laminin B1 levels remained stable. |
| 654 | 9111509 | At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. |
| 655 | 9111509 | In slow progressors, alpha 1(IV) collagen and TGF-beta 1 mRNA levels continued to increase at a slow rate, but tenascin and laminin mRNA levels were only further increased at 12 to 18 months. |
| 656 | 9111509 | Platelet-derived growth factor (PDGF)-B mRNA was high at 2 to 3 months (7.4-fold) and 6 to 9 months (9.5-fold) and was associated with an increased [3H]-thymidine-labeling index and glomerular cell number. |
| 657 | 9111509 | In slow progressors (bGH-m11 mice), the mRNA levels at 2 to 3 months were approximately one half that of rapid progressors (alpha 1(IV) collagen, 3.4-fold; laminin B1 1.9-fold; tenascin, 3-fold; TGF-beta 1, 2.2-fold). |
| 658 | 9111509 | At 6 to 9 months, alpha 1(IV) collagen, TGF-beta 1, and PDGF-B mRNA levels doubled, whereas tenascin and laminin B1 levels remained stable. |
| 659 | 9111509 | At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. |
| 660 | 9111509 | In slow progressors, alpha 1(IV) collagen and TGF-beta 1 mRNA levels continued to increase at a slow rate, but tenascin and laminin mRNA levels were only further increased at 12 to 18 months. |
| 661 | 9111509 | Platelet-derived growth factor (PDGF)-B mRNA was high at 2 to 3 months (7.4-fold) and 6 to 9 months (9.5-fold) and was associated with an increased [3H]-thymidine-labeling index and glomerular cell number. |
| 662 | 9111509 | In slow progressors (bGH-m11 mice), the mRNA levels at 2 to 3 months were approximately one half that of rapid progressors (alpha 1(IV) collagen, 3.4-fold; laminin B1 1.9-fold; tenascin, 3-fold; TGF-beta 1, 2.2-fold). |
| 663 | 9111509 | At 6 to 9 months, alpha 1(IV) collagen, TGF-beta 1, and PDGF-B mRNA levels doubled, whereas tenascin and laminin B1 levels remained stable. |
| 664 | 9111509 | At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. |
| 665 | 9111509 | In slow progressors, alpha 1(IV) collagen and TGF-beta 1 mRNA levels continued to increase at a slow rate, but tenascin and laminin mRNA levels were only further increased at 12 to 18 months. |
| 666 | 9111509 | Platelet-derived growth factor (PDGF)-B mRNA was high at 2 to 3 months (7.4-fold) and 6 to 9 months (9.5-fold) and was associated with an increased [3H]-thymidine-labeling index and glomerular cell number. |
| 667 | 9111509 | In slow progressors (bGH-m11 mice), the mRNA levels at 2 to 3 months were approximately one half that of rapid progressors (alpha 1(IV) collagen, 3.4-fold; laminin B1 1.9-fold; tenascin, 3-fold; TGF-beta 1, 2.2-fold). |
| 668 | 9111509 | At 6 to 9 months, alpha 1(IV) collagen, TGF-beta 1, and PDGF-B mRNA levels doubled, whereas tenascin and laminin B1 levels remained stable. |
| 669 | 9111509 | At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. |
| 670 | 9111509 | In slow progressors, alpha 1(IV) collagen and TGF-beta 1 mRNA levels continued to increase at a slow rate, but tenascin and laminin mRNA levels were only further increased at 12 to 18 months. |
| 671 | 9112014 | Smooth muscle cells in arteries of diabetic rats and rabbits have unique properties including the overexpression of platelet-derived growth factor (PDGF) beta-receptor compared with controls. |
| 672 | 9112014 | Cultured aortic smooth muscle cells of diabetic rats expressed TGF-beta type II receptor about 8.7 times that of controls at the protein level and 5.7 times at the mRNA level, whereas the expression of the type I receptor did not differ between the two types of smooth muscle cells. |
| 673 | 9112014 | Furthermore, protein expression of fibronectin, and mRNA and protein of TGF-beta type II receptor were increased in the diabetic aorta compared with the control aorta in vivo, implying the importance of the TGF-beta-fibronectin pathway for the unique biology of smooth muscle cells in the diabetic artery. |
| 674 | 9112014 | Smooth muscle cells in arteries of diabetic rats and rabbits have unique properties including the overexpression of platelet-derived growth factor (PDGF) beta-receptor compared with controls. |
| 675 | 9112014 | Cultured aortic smooth muscle cells of diabetic rats expressed TGF-beta type II receptor about 8.7 times that of controls at the protein level and 5.7 times at the mRNA level, whereas the expression of the type I receptor did not differ between the two types of smooth muscle cells. |
| 676 | 9112014 | Furthermore, protein expression of fibronectin, and mRNA and protein of TGF-beta type II receptor were increased in the diabetic aorta compared with the control aorta in vivo, implying the importance of the TGF-beta-fibronectin pathway for the unique biology of smooth muscle cells in the diabetic artery. |
| 677 | 9133552 | Regulation of glomerular epithelial cell production of fibronectin and transforming growth factor-beta by high glucose, not by angiotensin II. |
| 678 | 9133552 | Factors involved with increased accumulation of ECM proteins are high glucose, angiotensin II (ANG II), and transforming growth factor (TGF)-beta. |
| 679 | 9133552 | Therefore, we investigated the effects of high glucose and ANG II on fibronectin and TGF-beta production by human GVECs in vitro. |
| 680 | 9133552 | We found that ANG II had no effect on the production of fibronectin and TGF-beta by GVECs. |
| 681 | 9133552 | Regulation of glomerular epithelial cell production of fibronectin and transforming growth factor-beta by high glucose, not by angiotensin II. |
| 682 | 9133552 | Factors involved with increased accumulation of ECM proteins are high glucose, angiotensin II (ANG II), and transforming growth factor (TGF)-beta. |
| 683 | 9133552 | Therefore, we investigated the effects of high glucose and ANG II on fibronectin and TGF-beta production by human GVECs in vitro. |
| 684 | 9133552 | We found that ANG II had no effect on the production of fibronectin and TGF-beta by GVECs. |
| 685 | 9133552 | Regulation of glomerular epithelial cell production of fibronectin and transforming growth factor-beta by high glucose, not by angiotensin II. |
| 686 | 9133552 | Factors involved with increased accumulation of ECM proteins are high glucose, angiotensin II (ANG II), and transforming growth factor (TGF)-beta. |
| 687 | 9133552 | Therefore, we investigated the effects of high glucose and ANG II on fibronectin and TGF-beta production by human GVECs in vitro. |
| 688 | 9133552 | We found that ANG II had no effect on the production of fibronectin and TGF-beta by GVECs. |
| 689 | 9133555 | Increased renal production of transforming growth factor-beta1 in patients with type II diabetes. |
| 690 | 9133556 | Plasminogen activator inhibitor type 1 (PAI-1) contributes to the pathogenesis of atherothrombosis. |
| 691 | 9133556 | Its plasma level is strongly correlated with parameters that define the insulin resistance syndrome, in particular with BMI and visceral accumulation of body fat, suggesting that PAI-1 may be an adipose tissue-derived circulating peptide. |
| 692 | 9133556 | PAI-1 protein detected by immunolocalization was present at the stromal and adipocyte levels. |
| 693 | 9133556 | Transforming growth factor-beta1 significantly increased PAI-1 antigen production by the adipocyte fraction, whereas tumor necrosis factor-alpha did not have any effect. |
| 694 | 9133556 | Interestingly, after 5 h of incubation, omental tissue explants produced significantly more PAI-1 antigen than did subcutaneous tissue from the same individual, whereas similar production of leptin by the two territories was observed. |
| 695 | 9137900 | Interest has focused on basic fibroblast growth factor (bFGF), insulin-like growth factor-1 (IGF-1), platelet-derived growth factor (PDGF), transforming growth factor beta (TGF beta) and more recently vascular endothelial cell growth factor (VEGF). |
| 696 | 9137900 | Histologic studies have demonstrated the presence of growth factor proteins and receptors and/or their mRNA, mainly VEGF, PDGF, and bFGF, in preretinal membranes of patients with proliferative diabetic retinopathy. |
| 697 | 9137900 | Elevated intravitreal levels of IGF-1 and VEGF correlating with neovascular activity have been found in some patients. |
| 698 | 9137900 | Inhibition of IGF-1 by somatostatin analogs has produced unsatisfactory results. |
| 699 | 9139274 | [Increased urinary excretion of transforming growth factor beta and interleukin-6 in patients with diabetic nephropathy]. |
| 700 | 9139274 | The purpose of the study was to assess TGF-beta and IL-6 urinary excretion (measured with EIA) in 12 IDDM patients (7 F, 5 M, age 20-49 yrs, mean = 33.08) with albuminuria or microalbuminuria. |
| 701 | 9139274 | The data indicate that IL-6 and TGF-beta could be involved in the development of diabetic nephropathy. |
| 702 | 9139274 | [Increased urinary excretion of transforming growth factor beta and interleukin-6 in patients with diabetic nephropathy]. |
| 703 | 9139274 | The purpose of the study was to assess TGF-beta and IL-6 urinary excretion (measured with EIA) in 12 IDDM patients (7 F, 5 M, age 20-49 yrs, mean = 33.08) with albuminuria or microalbuminuria. |
| 704 | 9139274 | The data indicate that IL-6 and TGF-beta could be involved in the development of diabetic nephropathy. |
| 705 | 9139274 | [Increased urinary excretion of transforming growth factor beta and interleukin-6 in patients with diabetic nephropathy]. |
| 706 | 9139274 | The purpose of the study was to assess TGF-beta and IL-6 urinary excretion (measured with EIA) in 12 IDDM patients (7 F, 5 M, age 20-49 yrs, mean = 33.08) with albuminuria or microalbuminuria. |
| 707 | 9139274 | The data indicate that IL-6 and TGF-beta could be involved in the development of diabetic nephropathy. |
| 708 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 709 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 710 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 711 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 712 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 713 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 714 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 715 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 716 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 717 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 718 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 719 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 720 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 721 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 722 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 723 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 724 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 725 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 726 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 727 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 728 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 729 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 730 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 731 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 732 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 733 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 734 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 735 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 736 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 737 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 738 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 739 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 740 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 741 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 742 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 743 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 744 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 745 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 746 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 747 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 748 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 749 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 750 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 751 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 752 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 753 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 754 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 755 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 756 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 757 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 758 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 759 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 760 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 761 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 762 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 763 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 764 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 765 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 766 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 767 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 768 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 769 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 770 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 771 | 9142647 | Tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta 1 (TGF-beta 1) inhibit the expression and activity of Na+/K(+)-ATPase in FRTL-5 rat thyroid cells. |
| 772 | 9142647 | We recently reported that tumor necrosis factor-alpha (TNF-alpha) induction of the synthesis and secretion of transforming growth factor (TGF)-beta 1 by FRTL-5 cells is a thyroid-stimulating hormone (TSH)-dependent and age-dependent process. |
| 773 | 9142647 | TNF-alpha is only cytotoxic to aged (> 40 passages) FRTL-5 cells grown in TSH-containing medium, whereas TGF-beta induces programmed cell death (apoptosis) in epithelial cells but not in FRTL-5 cells, which otherwise retain many properties of normal thyroid follicular cells. |
| 774 | 9142647 | One prominent effect of TNF-alpha (and TGF-beta 1) on FRTL-5 cell function is suppression of iodide uptake, which is markedly stimulated by TSH. |
| 775 | 9142647 | Na+/K(+)-ATPase activity, which drives iodide uptake by thyroid cells, is inhibited by TNF-alpha and TGF-beta. |
| 776 | 9142647 | The following experiments quantitate the effects of TSH, aging, TNF-alpha, and TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase activity in FRTL-5 cells. |
| 777 | 9142647 | Young (< 20 passages) and aged (> 40 passages) FRTL-5 cells were treated with various doses (0-100 ng/ml) of recombinant human TNF-alpha or TGF-beta 1 for various times (0-3 days) with and without 2 U/liter TSH. |
| 778 | 9142647 | Aged FRTL-5 cells were more sensitive to the inhibitory effects of TNF-alpha, whereas young cells were more sensitive to the suppressive effects of TGF-beta 1 on the expression and activity of Na+/K(+)-ATPase. |
| 779 | 9142647 | We conclude that inhibition of Na+/K(+)-ATPase activity by TNF-alpha and TGF-beta in FRTL-5 cells is differentially affected by aging and that this inhibitory effect can be dissociated from effects on cell viability. |
| 780 | 9148380 | The latter include angiotensin II, thromboxane, platelet-derived growth factor, endothelins, insulin-like growth factor-1, and transforming growth factor-beta. |
| 781 | 9148940 | Cdc42Hs, but not Rac1, inhibits serum-stimulated cell cycle progression at G1/S through a mechanism requiring p38/RK. |
| 782 | 9148940 | Antimitogenic stimuli such as environmental or genotoxic stress, transforming growth factor-beta, and the inflammatory cytokines tumor necrosis factor and interleukin-1 activate two extracellular signal-regulated kinase (ERK)-based signaling pathways: the stress-activated protein kinase (SAPK/JNK) pathway and the p38 pathway. |
| 783 | 9148940 | Activated p38 phosphorylates transcription factors important in the regulation of cell growth and apoptosis, including activating transcription factor 2 (ATF2), Max, cAMP response element-binding protein-homologous protein/growth arrest DNA damage 153 (CHDP/GADD153). |
| 784 | 9148940 | In turn, p38 lies downstream of the Rho family GTPases Cdc42Hs and Rac1, as well as at least three mitogen-activated protein kinase (MAPK)/ERK-kinases (MEKs): MAPK kinases-3, -6, and SAPK/ERK-kinase-1. |
| 785 | 9148940 | Using a quantitative microinjection approach, we show here that Cdc42Hs, but not Rac1 or RhoA, can inhibit cell cycle progression at G1/S through a mechanism requiring activation of p38. |
| 786 | 9148940 | Furthermore, these results suggest that although both Cdc42Hs and Rac1 can activate p38 in situ, the effects of Cdc42Hs and Rac1 on cell cycle progression are, in fact, quite distinct. |
| 787 | 9162605 | Patients with insulin-dependent diabetes mellitus (IDDM) and albuminuria are at high risk for severe micro- and macrovascular complications. |
| 788 | 9162605 | Diabetic vascular complications are characterized by structural alterations of extracellular matrix (ECM) components in glomeruli and large vessel walls, namely, accumulation of collagen IV, collagen VI and fibronectin and relative decrease of heparan sulphate proteoglycan (HSPG). |
| 789 | 9162605 | TGF-beta stimulates production of ECM components such as collagen IV, fibronectin, proteoglycans (decorin and biglycan) without increasing HSPG. |
| 790 | 9162605 | TGF-beta antagonists, such as decorin, betaglycan, and possibly also heparin, might be potential candidates for future therapy to prevent diabetic vascular disease. |
| 791 | 9162605 | Patients with insulin-dependent diabetes mellitus (IDDM) and albuminuria are at high risk for severe micro- and macrovascular complications. |
| 792 | 9162605 | Diabetic vascular complications are characterized by structural alterations of extracellular matrix (ECM) components in glomeruli and large vessel walls, namely, accumulation of collagen IV, collagen VI and fibronectin and relative decrease of heparan sulphate proteoglycan (HSPG). |
| 793 | 9162605 | TGF-beta stimulates production of ECM components such as collagen IV, fibronectin, proteoglycans (decorin and biglycan) without increasing HSPG. |
| 794 | 9162605 | TGF-beta antagonists, such as decorin, betaglycan, and possibly also heparin, might be potential candidates for future therapy to prevent diabetic vascular disease. |
| 795 | 9190883 | Our study examines whether rebamipide could ameliorate the pathophysiology associated with experimental diabetes in vivo, such as microalbuminuria, and to reverse the increased production of transforming growth factor-beta1 and fibronectin in SV-40 transformed murine mesangial cells in culture that were stimulated with high glucose. |
| 796 | 9190883 | Rebamipide 2 mM was as effective as 20 mM of dimethylthiourea, a known hydroxyl radical scavenger, in inhibiting the increase in lipid peroxides, transforming growth factor-beta1, fibronectin mRNAs and proteins induced by incubation of cultured mesangial cells with high glucose. |
| 797 | 9190883 | Our study examines whether rebamipide could ameliorate the pathophysiology associated with experimental diabetes in vivo, such as microalbuminuria, and to reverse the increased production of transforming growth factor-beta1 and fibronectin in SV-40 transformed murine mesangial cells in culture that were stimulated with high glucose. |
| 798 | 9190883 | Rebamipide 2 mM was as effective as 20 mM of dimethylthiourea, a known hydroxyl radical scavenger, in inhibiting the increase in lipid peroxides, transforming growth factor-beta1, fibronectin mRNAs and proteins induced by incubation of cultured mesangial cells with high glucose. |
| 799 | 9193591 | IL-10 and TGF-beta gene transfer for xenogeneic islet transplantation: comparison of effect in concordant vs discordant combination. |
| 800 | 9193593 | IL-10 and TGF-beta gene transfer to rodent islets: effect on xenogeneic islet graft survival in naive and B-cell-deficient mice. |
| 801 | 9198233 | Subsequent RT-PCR and in situ hybridization studies suggest that the increased plasma PAI-1 originates primarily from the adipocyte in response to chronically elevated levels of tumor necrosis factor-alpha (TNF-alpha), insulin, and transforming growth factor-beta (TGF-beta). |
| 802 | 9200656 | Glomerular gene expression for the ECM components fibronectin and collagen IV and for TGF-beta was also increased, whereas glomerular cell proliferation was unaffected by diabetes. |
| 803 | 9202063 | Characterization of protein kinase C beta isoform activation on the gene expression of transforming growth factor-beta, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats. |
| 804 | 9202063 | The addition of PKC beta selective inhibitor (LY333531) to cultured mesangial cells inhibited activated PKC activities by high glucose without lowering DAG levels and LY333531 given orally in diabetic rats specifically inhibited the activation of PKC beta1 isoform without decreasing PKC alpha isoform activation. |
| 805 | 9202063 | Oral feeding of LY333531 prevented the increased mRNA expression of TGF-beta1 and extracellular matrix components such as fibronectin and alpha1(IV) collagen in the glomeruli of diabetic rats in parallel with inhibition of glomerular PKC activity. |
| 806 | 9202063 | Characterization of protein kinase C beta isoform activation on the gene expression of transforming growth factor-beta, extracellular matrix components, and prostanoids in the glomeruli of diabetic rats. |
| 807 | 9202063 | The addition of PKC beta selective inhibitor (LY333531) to cultured mesangial cells inhibited activated PKC activities by high glucose without lowering DAG levels and LY333531 given orally in diabetic rats specifically inhibited the activation of PKC beta1 isoform without decreasing PKC alpha isoform activation. |
| 808 | 9202063 | Oral feeding of LY333531 prevented the increased mRNA expression of TGF-beta1 and extracellular matrix components such as fibronectin and alpha1(IV) collagen in the glomeruli of diabetic rats in parallel with inhibition of glomerular PKC activity. |
| 809 | 9202228 | Bovine insulin-like growth factor binding protein-3: organization of the chromosomal gene and functional analysis of its promoter. |
| 810 | 9202228 | Insulin-like growth factor binding protein-3 (IGFBP-3), the major IGFBP in the circulation, is synthesized by the vascular endothelium in vivo and has been shown to be an important modulator of the physiological effects of IGF. |
| 811 | 9202228 | IGFBP-3 is regulated by a number of growth factors/cytokines to which the vascular endothelium is exposed, including IGF-I stimulation and TGF-beta1 inhibition of IGFBP-3 in cultured endothelial cells. |
| 812 | 9202228 | Results of the transfection studies indicated that 1) nearly 80% of the maximal basal promoter activity was retained within the first 130 bp of the 5' flanking sequence; 2) this region responded to IGF-I, despite lacking the TTF-1/TTF-2 (thyroid specific transcription factors) binding elements that are required for IGF-I stimulation of thyroglobulin synthesis. |
| 813 | 9202228 | These binding elements have also been suggested to be involved in IGF-I regulation of IGFBP-3 transcription, thus, implying the existence of novel cis-acting elements that mediate the IGF-I stimulation of bovine endothelial cell IGFBP-3 mRNA synthesis; 3) deletion of the GC rich sequence element resulted in a 60% reduction in basal promoter activity as well as loss of the IGF-1 stimulatory effect; 4) the TGF-beta1 mediated inhibition of IGFBP-3 transcription required sequence element(s) beyond 1.5 kb of its promoter. |
| 814 | 9202228 | Bovine insulin-like growth factor binding protein-3: organization of the chromosomal gene and functional analysis of its promoter. |
| 815 | 9202228 | Insulin-like growth factor binding protein-3 (IGFBP-3), the major IGFBP in the circulation, is synthesized by the vascular endothelium in vivo and has been shown to be an important modulator of the physiological effects of IGF. |
| 816 | 9202228 | IGFBP-3 is regulated by a number of growth factors/cytokines to which the vascular endothelium is exposed, including IGF-I stimulation and TGF-beta1 inhibition of IGFBP-3 in cultured endothelial cells. |
| 817 | 9202228 | Results of the transfection studies indicated that 1) nearly 80% of the maximal basal promoter activity was retained within the first 130 bp of the 5' flanking sequence; 2) this region responded to IGF-I, despite lacking the TTF-1/TTF-2 (thyroid specific transcription factors) binding elements that are required for IGF-I stimulation of thyroglobulin synthesis. |
| 818 | 9202228 | These binding elements have also been suggested to be involved in IGF-I regulation of IGFBP-3 transcription, thus, implying the existence of novel cis-acting elements that mediate the IGF-I stimulation of bovine endothelial cell IGFBP-3 mRNA synthesis; 3) deletion of the GC rich sequence element resulted in a 60% reduction in basal promoter activity as well as loss of the IGF-1 stimulatory effect; 4) the TGF-beta1 mediated inhibition of IGFBP-3 transcription required sequence element(s) beyond 1.5 kb of its promoter. |
| 819 | 9218758 | Molecular role of TGF-beta, secreted from a new type of CD4+ suppressor T cell, NY4.2, in the prevention of autoimmune IDDM in NOD mice. |
| 820 | 9218758 | A new type of CD4+ T cell clone (NY4.2) isolated from pancreatic islet-infiltrated lymphocytes of acutely diabetic non-obese diabetic (NOD) mice prevents the development of insulin-dependent diabetes mellitus (IDDM) in NOD mice, as well as the recurrence of autoimmune diabetes in syngeneic islet-transplanted NOD mice. |
| 821 | 9218758 | This investigation was initiated to determine the molecular role TGF-beta plays in the prevention of autoimmune IDDM by determining its effect on IL-2-induced signal transduction in Con A-activated NOD mouse splenocytes and HT-2 cells. |
| 822 | 9218758 | Second, we determined whether TGF-beta inhibits the activation of Janus kinases (JAKs), as well as signal transducers and activators of transcription (STAT) proteins, involved in an IL-2-induced signalling pathway that normally leads to the proliferation of T cells. |
| 823 | 9218758 | We found that TGF-beta inhibited tyrosine phosphorylation of JAK1, JAK3, STAT3 and STAT5 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 824 | 9218758 | Third, we examined whether TGF-beta inhibits the cooperation between STAT proteins and mitogen-activated protein kinase (MAPK), especially extracellular signal-regulated kinase 2 (ERK2). |
| 825 | 9218758 | We found that TGF-beta inhibited the association of STAT3 and STAT5 with ERK2 in Con A blasts from NOD splenocytes and HT-2 cells. |
| 826 | 9218758 | On the basis of these observations, we conclude that TGF-beta may interfere with signal transduction via inhibition of the IL-2-induced JAK/STAT pathway and inhibition of the association of STAT proteins with ERK2 in T cells from NOD splenocytes, resulting in the inhibition of IL-2-dependent T cell proliferation. |
| 827 | 9218758 | TGF-beta-mediated suppression of T cell activation may be responsible for the prevention of effector T cell-mediated autoimmune IDDM in NOD mice by TGF-beta-producing CD4+ suppressor T cells. |
| 828 | 9237797 | When those cells were cultured and restimulated in vitro with the B-chain of insulin, we also observed a decrease in IFN-gamma expression and an increase in IL-4, TGF-beta and IL-10 expression. |
| 829 | 9258275 | Antioxidant inhibition of protein kinase C-signaled increases in transforming growth factor-beta in mesangial cells. |
| 830 | 9258275 | Protein kinase C (PKC)-signaled increases in transforming growth factor beta (TGF beta) have been implicated in the stimulation of matrix protein synthesis induced by high concentrations of glucose, thromboxane, angiotension II (AII), and other stimuli in cultured glomerular mesangial cells. |
| 831 | 9258275 | Antioxidant inhibition of protein kinase C-signaled increases in transforming growth factor-beta in mesangial cells. |
| 832 | 9258275 | Protein kinase C (PKC)-signaled increases in transforming growth factor beta (TGF beta) have been implicated in the stimulation of matrix protein synthesis induced by high concentrations of glucose, thromboxane, angiotension II (AII), and other stimuli in cultured glomerular mesangial cells. |
| 833 | 9259354 | The suppressive effect of high glucose on NO production by mesangial cells was not modified by inhibition of protein kinase C (H-7), the addition of antioxidants (vitamin E or superoxide dismutase), or a pan-specific anti-transforming growth factor-beta antibody. |
| 834 | 9276088 | In addition, when cultures of mature primary rat osteoblasts were plated onto an in vitro AGE-modified collagen substrate, they showed altered cell functions, in terms of alkaline phosphatase (ALP) activity, osteocalcin secretion, and nodule formation (J Bone Miner Res 11:931-937; 1996). |
| 835 | 9276088 | Growth of UMR 201-10B cells on a type I collagen substrate significantly inhibited cell growth and retinoic acid (RA)-induced upregulation of ALP activity, compared to cells on plastic. |
| 836 | 9276088 | Unmodified collagen stimulated production of osteopontin mRNA, which was reduced by AGE modification to levels attained in cells on plastic. |
| 837 | 9276088 | Growth on control collagen inhibited TGF-beta type II receptor binding in 10B cells, while this inhibition was reduced by AGE modification. |
| 838 | 9276088 | These data further suggest that collagen-mediated events in these cells may be at least in part mediated by regulation of the TGF-beta receptor expression. |
| 839 | 9276088 | In addition, when cultures of mature primary rat osteoblasts were plated onto an in vitro AGE-modified collagen substrate, they showed altered cell functions, in terms of alkaline phosphatase (ALP) activity, osteocalcin secretion, and nodule formation (J Bone Miner Res 11:931-937; 1996). |
| 840 | 9276088 | Growth of UMR 201-10B cells on a type I collagen substrate significantly inhibited cell growth and retinoic acid (RA)-induced upregulation of ALP activity, compared to cells on plastic. |
| 841 | 9276088 | Unmodified collagen stimulated production of osteopontin mRNA, which was reduced by AGE modification to levels attained in cells on plastic. |
| 842 | 9276088 | Growth on control collagen inhibited TGF-beta type II receptor binding in 10B cells, while this inhibition was reduced by AGE modification. |
| 843 | 9276088 | These data further suggest that collagen-mediated events in these cells may be at least in part mediated by regulation of the TGF-beta receptor expression. |
| 844 | 9285495 | Insulin-like growth factor I (IGF-I), IGF-II, IGF binding protein 2 (IGFBP-2), and IGFBP-3 were elevated 3- to 13-fold in nondiabetic retinal ischemia and 1.5- to 3-fold in PDR, indicating that the changes were not restricted to diabetes. |
| 845 | 9285495 | Thus, influx of serum proteins due to microvascular disturbances and hypoxia is proposed as a possible cause for vitreous alterations of IGF-I and of active TGF-beta. |
| 846 | 9294832 | In this study, the effects of treatment of streptozotocin diabetic rats for 2 mo with vitamin C (10 g/kg body wt/d) or dietary vitamin E (200 mg/kg body wt/d) in the drinking water on urinary albumin excretion, glomerular transforming growth factor (TGF)-beta content, and glomerular size were examined. |
| 847 | 9294832 | By contrast, treatment with vitamin E had no effect on albumin clearance despite reductions in glomerular size and TGF-beta. |
| 848 | 9356040 | These effects could be exerted via an AGE-receptor-mediated upregulation of growth factors, such as the IGFs and transforming growth factor-beta (TGF-beta). |
| 849 | 9356040 | We tested this hypothesis in human and rat mesangial cells grown on nonglycated or native bovine serum albumin (BSA), glycated BSA with AGE formation (BSA-AGE), or glycated BSA in which AGE formation was prevented by the use of aminoguanidine (BSA-AM), in the presence or absence of an antibody, alpha-p60, directed against the p60/OST protein named AGE-receptor 1 (AGE-R1), or normal control (pre-immune) serum. |
| 850 | 9356040 | The mRNA and/or protein levels of IGF-I, IGF-II, IGF receptors, IGF binding proteins (IGFBPs), TGF-beta1 and the ECM components fibronectin, laminin, and collagen IV were measured, together with cell proliferation. |
| 851 | 9356040 | Both human and rat mesangial cells grown on BSA-AGE showed increased IGF-I and total and bioactive TGF-beta medium levels and enhanced IGF-I, IGF-II, and TGF-beta1 gene expression, compared with cells grown on BSA, whereas total IGFBP and IGFBP-3 medium content, IGF receptor density and affinity, and IGF-I receptor transcripts were unchanged. |
| 852 | 9356040 | Co-incubation of BSA-AGE with anti-AGE-R1, but not with pre-immune serum, prevented AGE-induced increases in IGF-I, TGF-beta1, and ECM production or gene expression; anti-AGE-R1 also reduced growth factor and matrix synthesis in cells grown on BSA. |
| 853 | 9356040 | These results demonstrate that mesangial IGF and TGF-beta1 synthesis is upregulated by AGE-modified proteins through an AGE-receptor-mediated mechanism. |
| 854 | 9356040 | These effects could be exerted via an AGE-receptor-mediated upregulation of growth factors, such as the IGFs and transforming growth factor-beta (TGF-beta). |
| 855 | 9356040 | We tested this hypothesis in human and rat mesangial cells grown on nonglycated or native bovine serum albumin (BSA), glycated BSA with AGE formation (BSA-AGE), or glycated BSA in which AGE formation was prevented by the use of aminoguanidine (BSA-AM), in the presence or absence of an antibody, alpha-p60, directed against the p60/OST protein named AGE-receptor 1 (AGE-R1), or normal control (pre-immune) serum. |
| 856 | 9356040 | The mRNA and/or protein levels of IGF-I, IGF-II, IGF receptors, IGF binding proteins (IGFBPs), TGF-beta1 and the ECM components fibronectin, laminin, and collagen IV were measured, together with cell proliferation. |
| 857 | 9356040 | Both human and rat mesangial cells grown on BSA-AGE showed increased IGF-I and total and bioactive TGF-beta medium levels and enhanced IGF-I, IGF-II, and TGF-beta1 gene expression, compared with cells grown on BSA, whereas total IGFBP and IGFBP-3 medium content, IGF receptor density and affinity, and IGF-I receptor transcripts were unchanged. |
| 858 | 9356040 | Co-incubation of BSA-AGE with anti-AGE-R1, but not with pre-immune serum, prevented AGE-induced increases in IGF-I, TGF-beta1, and ECM production or gene expression; anti-AGE-R1 also reduced growth factor and matrix synthesis in cells grown on BSA. |
| 859 | 9356040 | These results demonstrate that mesangial IGF and TGF-beta1 synthesis is upregulated by AGE-modified proteins through an AGE-receptor-mediated mechanism. |
| 860 | 9356040 | These effects could be exerted via an AGE-receptor-mediated upregulation of growth factors, such as the IGFs and transforming growth factor-beta (TGF-beta). |
| 861 | 9356040 | We tested this hypothesis in human and rat mesangial cells grown on nonglycated or native bovine serum albumin (BSA), glycated BSA with AGE formation (BSA-AGE), or glycated BSA in which AGE formation was prevented by the use of aminoguanidine (BSA-AM), in the presence or absence of an antibody, alpha-p60, directed against the p60/OST protein named AGE-receptor 1 (AGE-R1), or normal control (pre-immune) serum. |
| 862 | 9356040 | The mRNA and/or protein levels of IGF-I, IGF-II, IGF receptors, IGF binding proteins (IGFBPs), TGF-beta1 and the ECM components fibronectin, laminin, and collagen IV were measured, together with cell proliferation. |
| 863 | 9356040 | Both human and rat mesangial cells grown on BSA-AGE showed increased IGF-I and total and bioactive TGF-beta medium levels and enhanced IGF-I, IGF-II, and TGF-beta1 gene expression, compared with cells grown on BSA, whereas total IGFBP and IGFBP-3 medium content, IGF receptor density and affinity, and IGF-I receptor transcripts were unchanged. |
| 864 | 9356040 | Co-incubation of BSA-AGE with anti-AGE-R1, but not with pre-immune serum, prevented AGE-induced increases in IGF-I, TGF-beta1, and ECM production or gene expression; anti-AGE-R1 also reduced growth factor and matrix synthesis in cells grown on BSA. |
| 865 | 9356040 | These results demonstrate that mesangial IGF and TGF-beta1 synthesis is upregulated by AGE-modified proteins through an AGE-receptor-mediated mechanism. |
| 866 | 9356040 | These effects could be exerted via an AGE-receptor-mediated upregulation of growth factors, such as the IGFs and transforming growth factor-beta (TGF-beta). |
| 867 | 9356040 | We tested this hypothesis in human and rat mesangial cells grown on nonglycated or native bovine serum albumin (BSA), glycated BSA with AGE formation (BSA-AGE), or glycated BSA in which AGE formation was prevented by the use of aminoguanidine (BSA-AM), in the presence or absence of an antibody, alpha-p60, directed against the p60/OST protein named AGE-receptor 1 (AGE-R1), or normal control (pre-immune) serum. |
| 868 | 9356040 | The mRNA and/or protein levels of IGF-I, IGF-II, IGF receptors, IGF binding proteins (IGFBPs), TGF-beta1 and the ECM components fibronectin, laminin, and collagen IV were measured, together with cell proliferation. |
| 869 | 9356040 | Both human and rat mesangial cells grown on BSA-AGE showed increased IGF-I and total and bioactive TGF-beta medium levels and enhanced IGF-I, IGF-II, and TGF-beta1 gene expression, compared with cells grown on BSA, whereas total IGFBP and IGFBP-3 medium content, IGF receptor density and affinity, and IGF-I receptor transcripts were unchanged. |
| 870 | 9356040 | Co-incubation of BSA-AGE with anti-AGE-R1, but not with pre-immune serum, prevented AGE-induced increases in IGF-I, TGF-beta1, and ECM production or gene expression; anti-AGE-R1 also reduced growth factor and matrix synthesis in cells grown on BSA. |
| 871 | 9356040 | These results demonstrate that mesangial IGF and TGF-beta1 synthesis is upregulated by AGE-modified proteins through an AGE-receptor-mediated mechanism. |
| 872 | 9356040 | These effects could be exerted via an AGE-receptor-mediated upregulation of growth factors, such as the IGFs and transforming growth factor-beta (TGF-beta). |
| 873 | 9356040 | We tested this hypothesis in human and rat mesangial cells grown on nonglycated or native bovine serum albumin (BSA), glycated BSA with AGE formation (BSA-AGE), or glycated BSA in which AGE formation was prevented by the use of aminoguanidine (BSA-AM), in the presence or absence of an antibody, alpha-p60, directed against the p60/OST protein named AGE-receptor 1 (AGE-R1), or normal control (pre-immune) serum. |
| 874 | 9356040 | The mRNA and/or protein levels of IGF-I, IGF-II, IGF receptors, IGF binding proteins (IGFBPs), TGF-beta1 and the ECM components fibronectin, laminin, and collagen IV were measured, together with cell proliferation. |
| 875 | 9356040 | Both human and rat mesangial cells grown on BSA-AGE showed increased IGF-I and total and bioactive TGF-beta medium levels and enhanced IGF-I, IGF-II, and TGF-beta1 gene expression, compared with cells grown on BSA, whereas total IGFBP and IGFBP-3 medium content, IGF receptor density and affinity, and IGF-I receptor transcripts were unchanged. |
| 876 | 9356040 | Co-incubation of BSA-AGE with anti-AGE-R1, but not with pre-immune serum, prevented AGE-induced increases in IGF-I, TGF-beta1, and ECM production or gene expression; anti-AGE-R1 also reduced growth factor and matrix synthesis in cells grown on BSA. |
| 877 | 9356040 | These results demonstrate that mesangial IGF and TGF-beta1 synthesis is upregulated by AGE-modified proteins through an AGE-receptor-mediated mechanism. |
| 878 | 9369255 | Using Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new model of human non-insulin-dependent diabetes mellitus (NIDDM), we examined the role of local angiotensin II in cardiovascular and renal complications of NIDDM. |
| 879 | 9369255 | OLETF rats were orally given cilazapril (an angiotensin-converting enzyme inhibitor, 1 or 10 mg/kg), E4177 (an angiotensin AT1 receptor antagonist, 10 mg/kg), or vehicle for 26 or 40 weeks (from the age of 20 to 46 or 60 weeks). |
| 880 | 9369255 | However, both drugs significantly and similarly prevented coronary microvascular remodeling (the increase in wall thickening and perivascular fibrosis in coronary arterioles and small coronary arteries) in OLETF rats, and they were associated with the suppression of cardiac transforming growth factor-beta1 expression. |
| 881 | 9369255 | These results, taken together with the fact that OLETF rats show normal plasma renin levels, support that the AT1 receptor is involved in the pathogenesis of cardiac and renal complications in NIDDM. |
| 882 | 9407457 | Urinary excretion of TGF-beta 1, PDGF-BB and fibronectin in insulin-dependent diabetes mellitus patients. |
| 883 | 9407457 | We studied the urinary excretion of transforming growth factor-beta 1 (TGF-beta 1), platelet-derived growth factor-BB (PDGF) and fibronectin (FN) in 104 patients (52 normoalbuminuric, 24 microalbuminuric, and 28 with overt diabetic nephropathy) with insulin-dependent diabetes mellitus (IDDM) of a long duration and in 30 non-diabetic controls. |
| 884 | 9407457 | IDDM patients had higher urinary excretion of TGF-beta 1, PDGF and FN compared to controls. |
| 885 | 9407457 | Urinary excretion of TGF-beta 1 and PDGF was elevated in all IDDM subgroups, while FN excretion was significantly increased only in patients with macroalbuminuria. |
| 886 | 9407457 | Urinary excretion of TGF-beta 1 and FN did not differ between normoalbuminuric IDDM patients with long duration of diabetes, a group at low risk of ever developing diabetic nephropathy, and IDDM patients with incipient or overt diabetic nephropathy. |
| 887 | 9407457 | In conclusion, although longitudinal follow-up studies are needed to further clarify the issue, our results in long-standing IDDM do not support a hypothesis of urinary excretion of TGF-beta 1, PDGF or FN to predict development of diabetic nephropathy. |
| 888 | 9407457 | Urinary excretion of TGF-beta 1, PDGF-BB and fibronectin in insulin-dependent diabetes mellitus patients. |
| 889 | 9407457 | We studied the urinary excretion of transforming growth factor-beta 1 (TGF-beta 1), platelet-derived growth factor-BB (PDGF) and fibronectin (FN) in 104 patients (52 normoalbuminuric, 24 microalbuminuric, and 28 with overt diabetic nephropathy) with insulin-dependent diabetes mellitus (IDDM) of a long duration and in 30 non-diabetic controls. |
| 890 | 9407457 | IDDM patients had higher urinary excretion of TGF-beta 1, PDGF and FN compared to controls. |
| 891 | 9407457 | Urinary excretion of TGF-beta 1 and PDGF was elevated in all IDDM subgroups, while FN excretion was significantly increased only in patients with macroalbuminuria. |
| 892 | 9407457 | Urinary excretion of TGF-beta 1 and FN did not differ between normoalbuminuric IDDM patients with long duration of diabetes, a group at low risk of ever developing diabetic nephropathy, and IDDM patients with incipient or overt diabetic nephropathy. |
| 893 | 9407457 | In conclusion, although longitudinal follow-up studies are needed to further clarify the issue, our results in long-standing IDDM do not support a hypothesis of urinary excretion of TGF-beta 1, PDGF or FN to predict development of diabetic nephropathy. |
| 894 | 9407457 | Urinary excretion of TGF-beta 1, PDGF-BB and fibronectin in insulin-dependent diabetes mellitus patients. |
| 895 | 9407457 | We studied the urinary excretion of transforming growth factor-beta 1 (TGF-beta 1), platelet-derived growth factor-BB (PDGF) and fibronectin (FN) in 104 patients (52 normoalbuminuric, 24 microalbuminuric, and 28 with overt diabetic nephropathy) with insulin-dependent diabetes mellitus (IDDM) of a long duration and in 30 non-diabetic controls. |
| 896 | 9407457 | IDDM patients had higher urinary excretion of TGF-beta 1, PDGF and FN compared to controls. |
| 897 | 9407457 | Urinary excretion of TGF-beta 1 and PDGF was elevated in all IDDM subgroups, while FN excretion was significantly increased only in patients with macroalbuminuria. |
| 898 | 9407457 | Urinary excretion of TGF-beta 1 and FN did not differ between normoalbuminuric IDDM patients with long duration of diabetes, a group at low risk of ever developing diabetic nephropathy, and IDDM patients with incipient or overt diabetic nephropathy. |
| 899 | 9407457 | In conclusion, although longitudinal follow-up studies are needed to further clarify the issue, our results in long-standing IDDM do not support a hypothesis of urinary excretion of TGF-beta 1, PDGF or FN to predict development of diabetic nephropathy. |
| 900 | 9407457 | Urinary excretion of TGF-beta 1, PDGF-BB and fibronectin in insulin-dependent diabetes mellitus patients. |
| 901 | 9407457 | We studied the urinary excretion of transforming growth factor-beta 1 (TGF-beta 1), platelet-derived growth factor-BB (PDGF) and fibronectin (FN) in 104 patients (52 normoalbuminuric, 24 microalbuminuric, and 28 with overt diabetic nephropathy) with insulin-dependent diabetes mellitus (IDDM) of a long duration and in 30 non-diabetic controls. |
| 902 | 9407457 | IDDM patients had higher urinary excretion of TGF-beta 1, PDGF and FN compared to controls. |
| 903 | 9407457 | Urinary excretion of TGF-beta 1 and PDGF was elevated in all IDDM subgroups, while FN excretion was significantly increased only in patients with macroalbuminuria. |
| 904 | 9407457 | Urinary excretion of TGF-beta 1 and FN did not differ between normoalbuminuric IDDM patients with long duration of diabetes, a group at low risk of ever developing diabetic nephropathy, and IDDM patients with incipient or overt diabetic nephropathy. |
| 905 | 9407457 | In conclusion, although longitudinal follow-up studies are needed to further clarify the issue, our results in long-standing IDDM do not support a hypothesis of urinary excretion of TGF-beta 1, PDGF or FN to predict development of diabetic nephropathy. |
| 906 | 9407457 | Urinary excretion of TGF-beta 1, PDGF-BB and fibronectin in insulin-dependent diabetes mellitus patients. |
| 907 | 9407457 | We studied the urinary excretion of transforming growth factor-beta 1 (TGF-beta 1), platelet-derived growth factor-BB (PDGF) and fibronectin (FN) in 104 patients (52 normoalbuminuric, 24 microalbuminuric, and 28 with overt diabetic nephropathy) with insulin-dependent diabetes mellitus (IDDM) of a long duration and in 30 non-diabetic controls. |
| 908 | 9407457 | IDDM patients had higher urinary excretion of TGF-beta 1, PDGF and FN compared to controls. |
| 909 | 9407457 | Urinary excretion of TGF-beta 1 and PDGF was elevated in all IDDM subgroups, while FN excretion was significantly increased only in patients with macroalbuminuria. |
| 910 | 9407457 | Urinary excretion of TGF-beta 1 and FN did not differ between normoalbuminuric IDDM patients with long duration of diabetes, a group at low risk of ever developing diabetic nephropathy, and IDDM patients with incipient or overt diabetic nephropathy. |
| 911 | 9407457 | In conclusion, although longitudinal follow-up studies are needed to further clarify the issue, our results in long-standing IDDM do not support a hypothesis of urinary excretion of TGF-beta 1, PDGF or FN to predict development of diabetic nephropathy. |
| 912 | 9407457 | Urinary excretion of TGF-beta 1, PDGF-BB and fibronectin in insulin-dependent diabetes mellitus patients. |
| 913 | 9407457 | We studied the urinary excretion of transforming growth factor-beta 1 (TGF-beta 1), platelet-derived growth factor-BB (PDGF) and fibronectin (FN) in 104 patients (52 normoalbuminuric, 24 microalbuminuric, and 28 with overt diabetic nephropathy) with insulin-dependent diabetes mellitus (IDDM) of a long duration and in 30 non-diabetic controls. |
| 914 | 9407457 | IDDM patients had higher urinary excretion of TGF-beta 1, PDGF and FN compared to controls. |
| 915 | 9407457 | Urinary excretion of TGF-beta 1 and PDGF was elevated in all IDDM subgroups, while FN excretion was significantly increased only in patients with macroalbuminuria. |
| 916 | 9407457 | Urinary excretion of TGF-beta 1 and FN did not differ between normoalbuminuric IDDM patients with long duration of diabetes, a group at low risk of ever developing diabetic nephropathy, and IDDM patients with incipient or overt diabetic nephropathy. |
| 917 | 9407457 | In conclusion, although longitudinal follow-up studies are needed to further clarify the issue, our results in long-standing IDDM do not support a hypothesis of urinary excretion of TGF-beta 1, PDGF or FN to predict development of diabetic nephropathy. |
| 918 | 9416429 | Insulin-dependent diabetes mellitus (IDDM) results from the destruction of pancreatic insulin-secreting cells by a T-cell-mediated autoimmune reaction. |
| 919 | 9416429 | However, recent ongoing trials in humans using oral administration of insulin to prevent diabetes are based on a protective mechanism which seems to depend essentially on transforming growth factor-beta. |
| 920 | 9421372 | Protection against autoimmune diabetes with oral insulin is associated with the presence of IL-4 type 2 T-cells in the pancreas and pancreatic lymph nodes. |
| 921 | 9421372 | In the present study, immunohistochemical analysis of the pancreatic glands revealed that injection of T-cells from insulin-fed mice upregulated the number of interleukin (IL)-4-secreting cells within the islets. |
| 922 | 9421372 | Using two strains of NOD mice congenic at the Tbeta, or Thy1, locus, we observed a higher proportion of T-cells from insulin-fed mice in both the spleen (7.73 +/- 0.3 vs. 5.57 +/- 0.2%; P < 0.001) and the pancreatic lymph nodes (10.1 +/- 0.8 vs. 7.2 +/- 0.7%; P < 0.05) of cotransferred mice. |
| 923 | 9421372 | By reverse transcription-polymerase chain reaction (RT-PCR) analysis, mice reconstituted with T-cells from insulin-fed animals had detectable amounts of IL-4 mRNA, specifically in the pancreatic lymph nodes (8 of 9 experimental mice vs. 1 of 9 control mice) and the pancreas (3 of 3 experimental mice vs. 0 of 3 control mice). |
| 924 | 9421372 | Gamma-interferon mRNA was detectable in all cotransferred animals, but IL-10 mRNA and transforming growth factor beta mRNA were undetectable. |
| 925 | 9421372 | We concluded that oral administration of insulin can induce the presence of regulatory T-cells in the pancreas and the corresponding draining lymph nodes, initiate the secretion of IL-4 in this microenvironment sufficiently to suppress the activity of Th1 autoreactive T-cell clones, and ultimately provide protection against autoimmune diabetes. |
| 926 | 9421478 | High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. |
| 927 | 9421478 | We tested if structural analogues of D-glucose may mimic the high glucose effect and found that D-glucosamine was strikingly more potent than D-glucose itself in enhancing the production of TGF-beta protein and subsequent production of the matrix components heparan sulfate proteoglycan and fibronectin in a time- and dose-dependent manner. |
| 928 | 9421478 | Therefore, we suggested that the hexosamine biosynthetic pathway (the key enzyme of which is glutamine:fructose-6-phosphate amidotransferase [GFAT]) contributes to the high glucose-induced TGF-beta1 production. |
| 929 | 9421478 | Inhibition of GFAT by the substrate analogue azaserine or by inhibition of GFAT protein synthesis with antisense oligonucleotide prevented the high glucose-induced increase in cellular glucosamine metabolites and TGF-beta1 expression and bioactivity and subsequent effects on mesangial cell proliferation and matrix production. |
| 930 | 9421478 | Overall, our study indicates that the flux of glucose metabolism through the GFAT catalyzed hexosamine biosynthetic pathway is involved in the glucose-induced mesangial production of TGF-beta leading to increased matrix production. |
| 931 | 9421478 | High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. |
| 932 | 9421478 | We tested if structural analogues of D-glucose may mimic the high glucose effect and found that D-glucosamine was strikingly more potent than D-glucose itself in enhancing the production of TGF-beta protein and subsequent production of the matrix components heparan sulfate proteoglycan and fibronectin in a time- and dose-dependent manner. |
| 933 | 9421478 | Therefore, we suggested that the hexosamine biosynthetic pathway (the key enzyme of which is glutamine:fructose-6-phosphate amidotransferase [GFAT]) contributes to the high glucose-induced TGF-beta1 production. |
| 934 | 9421478 | Inhibition of GFAT by the substrate analogue azaserine or by inhibition of GFAT protein synthesis with antisense oligonucleotide prevented the high glucose-induced increase in cellular glucosamine metabolites and TGF-beta1 expression and bioactivity and subsequent effects on mesangial cell proliferation and matrix production. |
| 935 | 9421478 | Overall, our study indicates that the flux of glucose metabolism through the GFAT catalyzed hexosamine biosynthetic pathway is involved in the glucose-induced mesangial production of TGF-beta leading to increased matrix production. |
| 936 | 9421478 | High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. |
| 937 | 9421478 | We tested if structural analogues of D-glucose may mimic the high glucose effect and found that D-glucosamine was strikingly more potent than D-glucose itself in enhancing the production of TGF-beta protein and subsequent production of the matrix components heparan sulfate proteoglycan and fibronectin in a time- and dose-dependent manner. |
| 938 | 9421478 | Therefore, we suggested that the hexosamine biosynthetic pathway (the key enzyme of which is glutamine:fructose-6-phosphate amidotransferase [GFAT]) contributes to the high glucose-induced TGF-beta1 production. |
| 939 | 9421478 | Inhibition of GFAT by the substrate analogue azaserine or by inhibition of GFAT protein synthesis with antisense oligonucleotide prevented the high glucose-induced increase in cellular glucosamine metabolites and TGF-beta1 expression and bioactivity and subsequent effects on mesangial cell proliferation and matrix production. |
| 940 | 9421478 | Overall, our study indicates that the flux of glucose metabolism through the GFAT catalyzed hexosamine biosynthetic pathway is involved in the glucose-induced mesangial production of TGF-beta leading to increased matrix production. |
| 941 | 9421478 | High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. |
| 942 | 9421478 | We tested if structural analogues of D-glucose may mimic the high glucose effect and found that D-glucosamine was strikingly more potent than D-glucose itself in enhancing the production of TGF-beta protein and subsequent production of the matrix components heparan sulfate proteoglycan and fibronectin in a time- and dose-dependent manner. |
| 943 | 9421478 | Therefore, we suggested that the hexosamine biosynthetic pathway (the key enzyme of which is glutamine:fructose-6-phosphate amidotransferase [GFAT]) contributes to the high glucose-induced TGF-beta1 production. |
| 944 | 9421478 | Inhibition of GFAT by the substrate analogue azaserine or by inhibition of GFAT protein synthesis with antisense oligonucleotide prevented the high glucose-induced increase in cellular glucosamine metabolites and TGF-beta1 expression and bioactivity and subsequent effects on mesangial cell proliferation and matrix production. |
| 945 | 9421478 | Overall, our study indicates that the flux of glucose metabolism through the GFAT catalyzed hexosamine biosynthetic pathway is involved in the glucose-induced mesangial production of TGF-beta leading to increased matrix production. |
| 946 | 9421478 | High glucose-induced transforming growth factor beta1 production is mediated by the hexosamine pathway in porcine glomerular mesangial cells. |
| 947 | 9421478 | We tested if structural analogues of D-glucose may mimic the high glucose effect and found that D-glucosamine was strikingly more potent than D-glucose itself in enhancing the production of TGF-beta protein and subsequent production of the matrix components heparan sulfate proteoglycan and fibronectin in a time- and dose-dependent manner. |
| 948 | 9421478 | Therefore, we suggested that the hexosamine biosynthetic pathway (the key enzyme of which is glutamine:fructose-6-phosphate amidotransferase [GFAT]) contributes to the high glucose-induced TGF-beta1 production. |
| 949 | 9421478 | Inhibition of GFAT by the substrate analogue azaserine or by inhibition of GFAT protein synthesis with antisense oligonucleotide prevented the high glucose-induced increase in cellular glucosamine metabolites and TGF-beta1 expression and bioactivity and subsequent effects on mesangial cell proliferation and matrix production. |
| 950 | 9421478 | Overall, our study indicates that the flux of glucose metabolism through the GFAT catalyzed hexosamine biosynthetic pathway is involved in the glucose-induced mesangial production of TGF-beta leading to increased matrix production. |
| 951 | 9436357 | The TGF-beta family, the activin family, and bone morphogenic proteins belong to the TGF-beta superfamily. |
| 952 | 9436357 | Smad family members (Smad 1, Smad 2, Smad 3 and Smad 4) are expressed in the cultured retinal pigmant epithelial cell line (D407), in which TGF-beta and activin A stimulate the translocation of Smad 2, but not Smad 1 into nuclei, whereas bone morphogenetic protein (BMP) stimulates that of Smad 1, but not Smad 2. |
| 953 | 9436357 | The TGF-beta family, the activin family, and bone morphogenic proteins belong to the TGF-beta superfamily. |
| 954 | 9436357 | Smad family members (Smad 1, Smad 2, Smad 3 and Smad 4) are expressed in the cultured retinal pigmant epithelial cell line (D407), in which TGF-beta and activin A stimulate the translocation of Smad 2, but not Smad 1 into nuclei, whereas bone morphogenetic protein (BMP) stimulates that of Smad 1, but not Smad 2. |
| 955 | 9469500 | Relationships of cell proliferation and expression of integrin subunits and type I collagen in skin fibroblasts with renal lesions in patients with IDDM. |
| 956 | 9469500 | Previous studies have shown that cultured skin fibroblasts (SFs) from insulin-dependent diabetic mellitus (IDDM) patients with diabetic nephropathy (DN) exhibit both increased proliferation and Na+/H+ antiporter activity. |
| 957 | 9469500 | The present study correlated the growth rate and mRNA expression of integrin subunits, extracellular matrix molecules, and transforming growth factor-beta in cultured SFs, with the biopsy determined rate of development of DN lesions ranging from slow to rapid in nine IDDM patients. |
| 958 | 9469500 | Expression of cultured SF alpha3 integrin subunit mRNA levels, as well as type I collagen mRNA (P < 0.05 for both), but not transforming growth factor-beta mRNA levels (Northern blot analysis), were also positively correlated with mesangial expansion score. |
| 959 | 9469500 | Relationships of cell proliferation and expression of integrin subunits and type I collagen in skin fibroblasts with renal lesions in patients with IDDM. |
| 960 | 9469500 | Previous studies have shown that cultured skin fibroblasts (SFs) from insulin-dependent diabetic mellitus (IDDM) patients with diabetic nephropathy (DN) exhibit both increased proliferation and Na+/H+ antiporter activity. |
| 961 | 9469500 | The present study correlated the growth rate and mRNA expression of integrin subunits, extracellular matrix molecules, and transforming growth factor-beta in cultured SFs, with the biopsy determined rate of development of DN lesions ranging from slow to rapid in nine IDDM patients. |
| 962 | 9469500 | Expression of cultured SF alpha3 integrin subunit mRNA levels, as well as type I collagen mRNA (P < 0.05 for both), but not transforming growth factor-beta mRNA levels (Northern blot analysis), were also positively correlated with mesangial expansion score. |
| 963 | 9507208 | Glycated albumin stimulates fibronectin gene expression in glomerular mesangial cells: involvement of the transforming growth factor-beta system. |
| 964 | 9507208 | Albumin modified by Amadori glucose adducts, formed in increased amounts in diabetes, stimulates collagen IV production and gene expression in renal glomerular mesangial cells, and induces mesangial matrix accumulation accompanied by increased mRNA encoding alpha 1 (IV) collagen and fibronectin in diabetic animals. |
| 965 | 9507208 | We postulated that Amadori-modified glycated albumin modulates TGF-beta 1 expression in mesangial cells, and that TGF-beta 1 participates in mediating the glycated albumin-induced increases in mesangial cell matrix production. |
| 966 | 9507208 | To test this hypothesis, we measured mRNA encoding TGF-beta 1, the TGF-beta Type II receptor and fibronectin, a key matrix component of the TGF-beta 1 tissue response, after incubation of mesangial cells with glycated albumin. |
| 967 | 9507208 | Further, they were accompanied by increased translated fibronectin protein, which was prevented with TGF-beta neutralizing antibody, as was the glycated albumin-induced increase in fibronectin mRNA. |
| 968 | 9507208 | The findings indicate that Amadori-modified glycated albumin stimulates mesangial cell TGF-beta 1 gene expression by mechanisms that are operative under normoglycemic conditions. |
| 969 | 9507208 | These data provide the first link between elevated glycated serum albumin concentrations and increased TGF-beta 1 bioactivity in the pathogenesis of mesangial matrix accumulation in diabetes. |
| 970 | 9507208 | Glycated albumin stimulates fibronectin gene expression in glomerular mesangial cells: involvement of the transforming growth factor-beta system. |
| 971 | 9507208 | Albumin modified by Amadori glucose adducts, formed in increased amounts in diabetes, stimulates collagen IV production and gene expression in renal glomerular mesangial cells, and induces mesangial matrix accumulation accompanied by increased mRNA encoding alpha 1 (IV) collagen and fibronectin in diabetic animals. |
| 972 | 9507208 | We postulated that Amadori-modified glycated albumin modulates TGF-beta 1 expression in mesangial cells, and that TGF-beta 1 participates in mediating the glycated albumin-induced increases in mesangial cell matrix production. |
| 973 | 9507208 | To test this hypothesis, we measured mRNA encoding TGF-beta 1, the TGF-beta Type II receptor and fibronectin, a key matrix component of the TGF-beta 1 tissue response, after incubation of mesangial cells with glycated albumin. |
| 974 | 9507208 | Further, they were accompanied by increased translated fibronectin protein, which was prevented with TGF-beta neutralizing antibody, as was the glycated albumin-induced increase in fibronectin mRNA. |
| 975 | 9507208 | The findings indicate that Amadori-modified glycated albumin stimulates mesangial cell TGF-beta 1 gene expression by mechanisms that are operative under normoglycemic conditions. |
| 976 | 9507208 | These data provide the first link between elevated glycated serum albumin concentrations and increased TGF-beta 1 bioactivity in the pathogenesis of mesangial matrix accumulation in diabetes. |
| 977 | 9507208 | Glycated albumin stimulates fibronectin gene expression in glomerular mesangial cells: involvement of the transforming growth factor-beta system. |
| 978 | 9507208 | Albumin modified by Amadori glucose adducts, formed in increased amounts in diabetes, stimulates collagen IV production and gene expression in renal glomerular mesangial cells, and induces mesangial matrix accumulation accompanied by increased mRNA encoding alpha 1 (IV) collagen and fibronectin in diabetic animals. |
| 979 | 9507208 | We postulated that Amadori-modified glycated albumin modulates TGF-beta 1 expression in mesangial cells, and that TGF-beta 1 participates in mediating the glycated albumin-induced increases in mesangial cell matrix production. |
| 980 | 9507208 | To test this hypothesis, we measured mRNA encoding TGF-beta 1, the TGF-beta Type II receptor and fibronectin, a key matrix component of the TGF-beta 1 tissue response, after incubation of mesangial cells with glycated albumin. |
| 981 | 9507208 | Further, they were accompanied by increased translated fibronectin protein, which was prevented with TGF-beta neutralizing antibody, as was the glycated albumin-induced increase in fibronectin mRNA. |
| 982 | 9507208 | The findings indicate that Amadori-modified glycated albumin stimulates mesangial cell TGF-beta 1 gene expression by mechanisms that are operative under normoglycemic conditions. |
| 983 | 9507208 | These data provide the first link between elevated glycated serum albumin concentrations and increased TGF-beta 1 bioactivity in the pathogenesis of mesangial matrix accumulation in diabetes. |
| 984 | 9507208 | Glycated albumin stimulates fibronectin gene expression in glomerular mesangial cells: involvement of the transforming growth factor-beta system. |
| 985 | 9507208 | Albumin modified by Amadori glucose adducts, formed in increased amounts in diabetes, stimulates collagen IV production and gene expression in renal glomerular mesangial cells, and induces mesangial matrix accumulation accompanied by increased mRNA encoding alpha 1 (IV) collagen and fibronectin in diabetic animals. |
| 986 | 9507208 | We postulated that Amadori-modified glycated albumin modulates TGF-beta 1 expression in mesangial cells, and that TGF-beta 1 participates in mediating the glycated albumin-induced increases in mesangial cell matrix production. |
| 987 | 9507208 | To test this hypothesis, we measured mRNA encoding TGF-beta 1, the TGF-beta Type II receptor and fibronectin, a key matrix component of the TGF-beta 1 tissue response, after incubation of mesangial cells with glycated albumin. |
| 988 | 9507208 | Further, they were accompanied by increased translated fibronectin protein, which was prevented with TGF-beta neutralizing antibody, as was the glycated albumin-induced increase in fibronectin mRNA. |
| 989 | 9507208 | The findings indicate that Amadori-modified glycated albumin stimulates mesangial cell TGF-beta 1 gene expression by mechanisms that are operative under normoglycemic conditions. |
| 990 | 9507208 | These data provide the first link between elevated glycated serum albumin concentrations and increased TGF-beta 1 bioactivity in the pathogenesis of mesangial matrix accumulation in diabetes. |
| 991 | 9507208 | Glycated albumin stimulates fibronectin gene expression in glomerular mesangial cells: involvement of the transforming growth factor-beta system. |
| 992 | 9507208 | Albumin modified by Amadori glucose adducts, formed in increased amounts in diabetes, stimulates collagen IV production and gene expression in renal glomerular mesangial cells, and induces mesangial matrix accumulation accompanied by increased mRNA encoding alpha 1 (IV) collagen and fibronectin in diabetic animals. |
| 993 | 9507208 | We postulated that Amadori-modified glycated albumin modulates TGF-beta 1 expression in mesangial cells, and that TGF-beta 1 participates in mediating the glycated albumin-induced increases in mesangial cell matrix production. |
| 994 | 9507208 | To test this hypothesis, we measured mRNA encoding TGF-beta 1, the TGF-beta Type II receptor and fibronectin, a key matrix component of the TGF-beta 1 tissue response, after incubation of mesangial cells with glycated albumin. |
| 995 | 9507208 | Further, they were accompanied by increased translated fibronectin protein, which was prevented with TGF-beta neutralizing antibody, as was the glycated albumin-induced increase in fibronectin mRNA. |
| 996 | 9507208 | The findings indicate that Amadori-modified glycated albumin stimulates mesangial cell TGF-beta 1 gene expression by mechanisms that are operative under normoglycemic conditions. |
| 997 | 9507208 | These data provide the first link between elevated glycated serum albumin concentrations and increased TGF-beta 1 bioactivity in the pathogenesis of mesangial matrix accumulation in diabetes. |
| 998 | 9507208 | Glycated albumin stimulates fibronectin gene expression in glomerular mesangial cells: involvement of the transforming growth factor-beta system. |
| 999 | 9507208 | Albumin modified by Amadori glucose adducts, formed in increased amounts in diabetes, stimulates collagen IV production and gene expression in renal glomerular mesangial cells, and induces mesangial matrix accumulation accompanied by increased mRNA encoding alpha 1 (IV) collagen and fibronectin in diabetic animals. |
| 1000 | 9507208 | We postulated that Amadori-modified glycated albumin modulates TGF-beta 1 expression in mesangial cells, and that TGF-beta 1 participates in mediating the glycated albumin-induced increases in mesangial cell matrix production. |
| 1001 | 9507208 | To test this hypothesis, we measured mRNA encoding TGF-beta 1, the TGF-beta Type II receptor and fibronectin, a key matrix component of the TGF-beta 1 tissue response, after incubation of mesangial cells with glycated albumin. |
| 1002 | 9507208 | Further, they were accompanied by increased translated fibronectin protein, which was prevented with TGF-beta neutralizing antibody, as was the glycated albumin-induced increase in fibronectin mRNA. |
| 1003 | 9507208 | The findings indicate that Amadori-modified glycated albumin stimulates mesangial cell TGF-beta 1 gene expression by mechanisms that are operative under normoglycemic conditions. |
| 1004 | 9507208 | These data provide the first link between elevated glycated serum albumin concentrations and increased TGF-beta 1 bioactivity in the pathogenesis of mesangial matrix accumulation in diabetes. |
| 1005 | 9519748 | Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition. |
| 1006 | 9519748 | Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. |
| 1007 | 9519748 | In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. |
| 1008 | 9519748 | At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). |
| 1009 | 9519748 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. |
| 1010 | 9519748 | Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. |
| 1011 | 9519748 | Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. |
| 1012 | 9519748 | Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition. |
| 1013 | 9519748 | Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. |
| 1014 | 9519748 | In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. |
| 1015 | 9519748 | At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). |
| 1016 | 9519748 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. |
| 1017 | 9519748 | Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. |
| 1018 | 9519748 | Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. |
| 1019 | 9519748 | Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition. |
| 1020 | 9519748 | Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. |
| 1021 | 9519748 | In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. |
| 1022 | 9519748 | At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). |
| 1023 | 9519748 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. |
| 1024 | 9519748 | Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. |
| 1025 | 9519748 | Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. |
| 1026 | 9519748 | Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition. |
| 1027 | 9519748 | Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. |
| 1028 | 9519748 | In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. |
| 1029 | 9519748 | At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). |
| 1030 | 9519748 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. |
| 1031 | 9519748 | Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. |
| 1032 | 9519748 | Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. |
| 1033 | 9519748 | Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition. |
| 1034 | 9519748 | Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. |
| 1035 | 9519748 | In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. |
| 1036 | 9519748 | At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). |
| 1037 | 9519748 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. |
| 1038 | 9519748 | Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. |
| 1039 | 9519748 | Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. |
| 1040 | 9519748 | Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition. |
| 1041 | 9519748 | Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. |
| 1042 | 9519748 | In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. |
| 1043 | 9519748 | At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). |
| 1044 | 9519748 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. |
| 1045 | 9519748 | Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. |
| 1046 | 9519748 | Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. |
| 1047 | 9519748 | Expression of transforming growth factor-beta1 and type IV collagen in the renal tubulointerstitium in experimental diabetes: effects of ACE inhibition. |
| 1048 | 9519748 | Transforming growth factor-beta (TGF-beta) and the renin-angiotensin system (RAS) have both been implicated in the pathogenesis of glomerulosclerosis in diabetic kidney disease. |
| 1049 | 9519748 | In the present study, we investigated tubulointerstitial injury, TGF-beta1 expression, and the effect of blocking the RAS by inhibition of ACE. |
| 1050 | 9519748 | At 6 months, experimental diabetes was associated with tubulointerstitial damage, a 70% increase in expression of TGF-beta1 (P < 0.05 vs. control), and a 120% increase in alpha1 (IV) collagen gene expression (P < 0.01 vs. control). |
| 1051 | 9519748 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and alpha1 (IV) collagen mRNA in renal tubules. |
| 1052 | 9519748 | Administration of the ACE inhibitor ramipril prevented tubulointerstitial injury and the overexpression of TGF-beta1 and alpha1 (IV) collagen mRNA. |
| 1053 | 9519748 | Changes in gene expression were accompanied by parallel changes in immunostaining for TGF-beta1 and type IV collagen. |
| 1054 | 9520423 | The tumor suppressor SMAD4, also known as DPC4, is believed to be an essential factor that mediates TGF-beta signals. |
| 1055 | 9525704 | The factors that mediate increased renal TGF-beta activity involve hyperglycemia per se and the intermediary action of other potent mediators such as angiotensin II, thromboxane, endothelins, and platelet-derived growth factor. |
| 1056 | 9526909 | Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. |
| 1057 | 9526909 | Diabetes alone did not alter the gingival cytokine profile for platelet-derived growth factor B (PDGF-B), interleukin 1-beta (IL-1beta), transforming growth factor-beta (TGF-beta), and tumor necrosis factor-alpha (TNF-alpha). |
| 1058 | 9526909 | Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. |
| 1059 | 9526909 | Thus, diabetes-induced metabolic alterations do not affect gingival cytokine levels per se; however, they do alter the normal host response to periodontitis through blockage of periodontitis-induced increases in PDGF-B and IL-1beta. |
| 1060 | 9550435 | Islet grafts and spleens from TNF-alpha-treated mice at 10 days after islet transplantation contained significantly fewer CD4+ and CD8+ T cells, and significantly decreased mRNA levels of type 1 cytokines (IFN-gamma, IL-2, and TNF-beta) than islet grafts and spleens from control mice. |
| 1061 | 9550435 | Regarding type 2 cytokines, IL-4 mRNA levels were not changed significantly in islet grafts or spleens of TNF-alpha-treated mice, whereas IL-10 mRNA levels were decreased significantly in islet grafts of TNF-alpha-treated mice and not significantly changed in spleens. |
| 1062 | 9550435 | TGF-beta mRNA levels in islet grafts and spleens were similar in TNF-alpha-treated and control mice. |
| 1063 | 9550435 | These results suggest that TNF-alpha partially protects beta cells in syngeneic islet grafts from recurrent autoimmune destruction by reducing CD4+ and CD8+ T cells and down-regulating type 1 cytokines, both systemically and locally in the islet graft. |
| 1064 | 9556350 | While in control BB rats high levels of IFNgamma mRNA were detectable by RT-PCR, insulin treatment almost completely suppressed IFNgamma mRNA levels without concomitant upregulation of counterregulatory IL-10 and TGFbeta gene expression. |
| 1065 | 9556350 | Insulin also suppressed gene expression of inducible nitric oxide synthase. |
| 1066 | 9572571 | A central role for protein kinase C overactivity in diabetic glomerulosclerosis: implications for prevention with antioxidants, fish oil, and ACE inhibitors. |
| 1067 | 9572571 | The primary etiologic factor in diabetic glomerulosclerosis appears to be an overproduction of transforming growth factor-beta by mesangial cells, which in turn reflects a hyperglycemically mediated overactivation of protein kinase C (PKC) throughout the glomerulus. |
| 1068 | 9572571 | Membrane-active antioxidants, fish oil, and angiotensin-converting enzyme inhibitors can act to down-regulate glomerular PKC activity, via a variety of mechanisms that may include activation of diacylglycerol kinase and suppression of phosphatidate phosphohydrolase, support of endothelial nitric oxide and heparan sulfate production, inhibition of thromboxane and angiotensin synthesis/activity, and correction of glomerular hypertension. |
| 1069 | 9576014 | Oral administration of insulin to NOD mice suppresses or delays the onset of diabetes by skewing the response toward CD4+ Th2 cells and TGF-beta producing cells. |
| 1070 | 9576014 | When cytokine profiles were examined, feeding led to a predominance of IL-10 and TGF-beta production. |
| 1071 | 9576014 | Furthermore, feeding SEA in combination with insulin B-chain augmented the level of IL-10 production to insulin. |
| 1072 | 9576014 | T-cell lines established from SEA-fed and -immunized mice secreted IL-4 and IL-10 cytokines whereas the T-cell lines from control-fed mice immunized with SEA secreted predominantly IL-2 and IFN-gamma. |
| 1073 | 9576014 | These results demonstrate that orally administered insulin can induce regulatory T-cells secreting IL-4, IL-10, and TGF-beta and that Th2 responses to oral insulin could be augmented in a synergistic way by feeding SEA and insulin B-chain together. |
| 1074 | 9576014 | Oral administration of insulin to NOD mice suppresses or delays the onset of diabetes by skewing the response toward CD4+ Th2 cells and TGF-beta producing cells. |
| 1075 | 9576014 | When cytokine profiles were examined, feeding led to a predominance of IL-10 and TGF-beta production. |
| 1076 | 9576014 | Furthermore, feeding SEA in combination with insulin B-chain augmented the level of IL-10 production to insulin. |
| 1077 | 9576014 | T-cell lines established from SEA-fed and -immunized mice secreted IL-4 and IL-10 cytokines whereas the T-cell lines from control-fed mice immunized with SEA secreted predominantly IL-2 and IFN-gamma. |
| 1078 | 9576014 | These results demonstrate that orally administered insulin can induce regulatory T-cells secreting IL-4, IL-10, and TGF-beta and that Th2 responses to oral insulin could be augmented in a synergistic way by feeding SEA and insulin B-chain together. |
| 1079 | 9590367 | Urinary measurement of transforming growth factor-beta and type IV collagen as new markers of renal injury: application in diabetic nephropathy. |
| 1080 | 9590367 | Transforming growth factor-beta1 (TGF-11) and retinol binding protein (RBP) were measured with modification of commercially available methods used to assay serum specimens; type 3 collagen (T3C) was measured with a new immunonephelometric assay. |
| 1081 | 9590367 | The clinical utility of measuring a panel of these markers was demonstrated in urine samples from 16 control subjects and from 46 individuals with insulin-dependent diabetes mellitus (IDDM) with various albumin excretion rates (AERs). |
| 1082 | 9590367 | Urinary measurement of transforming growth factor-beta and type IV collagen as new markers of renal injury: application in diabetic nephropathy. |
| 1083 | 9590367 | Transforming growth factor-beta1 (TGF-11) and retinol binding protein (RBP) were measured with modification of commercially available methods used to assay serum specimens; type 3 collagen (T3C) was measured with a new immunonephelometric assay. |
| 1084 | 9590367 | The clinical utility of measuring a panel of these markers was demonstrated in urine samples from 16 control subjects and from 46 individuals with insulin-dependent diabetes mellitus (IDDM) with various albumin excretion rates (AERs). |
| 1085 | 9592624 | A growing body of evidence shows that changes in (1) insulin-like growth factor I regulation, and (2) the transforming growth factor beta loop exist in the kidney in the diabetic hypertrophic kidney and in diabetic glomerulosclerosis. |
| 1086 | 9609460 | Thereafter, the effects of TSP on the activation of transforming growth factor beta (TGF-beta) and fibronectin production were investigated in MCs. |
| 1087 | 9609460 | Treatment of MCs with TSP (final concentrations 1 and 5 microg/ml) for 24 h resulted in an increase (1.3- and 2.1-fold, respectively) in active TGF-beta, which was determined with an enzyme-linked immunosorbent assay using TGF-beta-soluble receptor type II, in the culture media without having any effect on the production of total TGF-beta. |
| 1088 | 9609460 | These results indicate that the TSP production is promoted by a high ambient glucose concentration in human MCs and that TSP, in turn, causes an increase in fibronectin production via activation of TGF-beta. |
| 1089 | 9609460 | Thereafter, the effects of TSP on the activation of transforming growth factor beta (TGF-beta) and fibronectin production were investigated in MCs. |
| 1090 | 9609460 | Treatment of MCs with TSP (final concentrations 1 and 5 microg/ml) for 24 h resulted in an increase (1.3- and 2.1-fold, respectively) in active TGF-beta, which was determined with an enzyme-linked immunosorbent assay using TGF-beta-soluble receptor type II, in the culture media without having any effect on the production of total TGF-beta. |
| 1091 | 9609460 | These results indicate that the TSP production is promoted by a high ambient glucose concentration in human MCs and that TSP, in turn, causes an increase in fibronectin production via activation of TGF-beta. |
| 1092 | 9609460 | Thereafter, the effects of TSP on the activation of transforming growth factor beta (TGF-beta) and fibronectin production were investigated in MCs. |
| 1093 | 9609460 | Treatment of MCs with TSP (final concentrations 1 and 5 microg/ml) for 24 h resulted in an increase (1.3- and 2.1-fold, respectively) in active TGF-beta, which was determined with an enzyme-linked immunosorbent assay using TGF-beta-soluble receptor type II, in the culture media without having any effect on the production of total TGF-beta. |
| 1094 | 9609460 | These results indicate that the TSP production is promoted by a high ambient glucose concentration in human MCs and that TSP, in turn, causes an increase in fibronectin production via activation of TGF-beta. |
| 1095 | 9636194 | These observations raise the possibility that TF and TGF-beta may contribute to the increased cardiovascular disease that accompanies obesity and related non-insulin-dependent diabetes mellitus, and that the adipocyte plays a key role in this process. |
| 1096 | 9639038 | In support of this hypothesis, we found that steady state levels of mRNA encoding the TGF-beta type II receptor were significantly increased in renal cortex from db/db diabetic mice. |
| 1097 | 9639038 | Additionally, the translated TGF-beta type II receptor protein, assessed by immunoblot, also was increased in diabetic kidneys. |
| 1098 | 9639038 | However, in contrast to rodents with insulin-deficient diabetes, steady state levels of mRNA encoding TGF-beta1 in the renal cortex of diabetic db/db mice did not differ from those in cortex from nondiabetic (db/m) littermate controls. |
| 1099 | 9639038 | The findings are consistent with upregulation of TGF-beta type II receptor activity as a consequence of hyperglycemia in the hyperinsulinemic db/db mouse and suggest that hyperinsulinemia inhibits TGF-beta1 production. |
| 1100 | 9639038 | In support of this hypothesis, we found that steady state levels of mRNA encoding the TGF-beta type II receptor were significantly increased in renal cortex from db/db diabetic mice. |
| 1101 | 9639038 | Additionally, the translated TGF-beta type II receptor protein, assessed by immunoblot, also was increased in diabetic kidneys. |
| 1102 | 9639038 | However, in contrast to rodents with insulin-deficient diabetes, steady state levels of mRNA encoding TGF-beta1 in the renal cortex of diabetic db/db mice did not differ from those in cortex from nondiabetic (db/m) littermate controls. |
| 1103 | 9639038 | The findings are consistent with upregulation of TGF-beta type II receptor activity as a consequence of hyperglycemia in the hyperinsulinemic db/db mouse and suggest that hyperinsulinemia inhibits TGF-beta1 production. |
| 1104 | 9639038 | In support of this hypothesis, we found that steady state levels of mRNA encoding the TGF-beta type II receptor were significantly increased in renal cortex from db/db diabetic mice. |
| 1105 | 9639038 | Additionally, the translated TGF-beta type II receptor protein, assessed by immunoblot, also was increased in diabetic kidneys. |
| 1106 | 9639038 | However, in contrast to rodents with insulin-deficient diabetes, steady state levels of mRNA encoding TGF-beta1 in the renal cortex of diabetic db/db mice did not differ from those in cortex from nondiabetic (db/m) littermate controls. |
| 1107 | 9639038 | The findings are consistent with upregulation of TGF-beta type II receptor activity as a consequence of hyperglycemia in the hyperinsulinemic db/db mouse and suggest that hyperinsulinemia inhibits TGF-beta1 production. |
| 1108 | 9639038 | In support of this hypothesis, we found that steady state levels of mRNA encoding the TGF-beta type II receptor were significantly increased in renal cortex from db/db diabetic mice. |
| 1109 | 9639038 | Additionally, the translated TGF-beta type II receptor protein, assessed by immunoblot, also was increased in diabetic kidneys. |
| 1110 | 9639038 | However, in contrast to rodents with insulin-deficient diabetes, steady state levels of mRNA encoding TGF-beta1 in the renal cortex of diabetic db/db mice did not differ from those in cortex from nondiabetic (db/m) littermate controls. |
| 1111 | 9639038 | The findings are consistent with upregulation of TGF-beta type II receptor activity as a consequence of hyperglycemia in the hyperinsulinemic db/db mouse and suggest that hyperinsulinemia inhibits TGF-beta1 production. |
| 1112 | 9667075 | Therefore, we examined the effect of IGF-I, EGF, TGF-beta and RANTES on NO production by RMC maintained in normal (5.6 mM) or high glucose (33.3 mM) for 48 h. |
| 1113 | 9667075 | In normal glucose media, IGF-I, EGF, and RANTES had no effect on nitrite accumulation while TGF-beta inhibited NO synthesis. |
| 1114 | 9667075 | In high glucose conditions, IGF-I and EGF significantly enhanced NO production. |
| 1115 | 9667075 | The effects of RANTES and TGF-beta were unchanged by an elevated glucose concentration. |
| 1116 | 9667075 | EGF-induced stimulation of NO production in high glucose media was associated with parallel alterations in iNOS gene and protein expression. |
| 1117 | 9667075 | The modest enhancement in nitrite accumulation provoked by IGF-I in high glucose conditions was not accompanied by demonstrable increases in iNOS mRNA abundance or protein content. |
| 1118 | 9667075 | Therefore, we examined the effect of IGF-I, EGF, TGF-beta and RANTES on NO production by RMC maintained in normal (5.6 mM) or high glucose (33.3 mM) for 48 h. |
| 1119 | 9667075 | In normal glucose media, IGF-I, EGF, and RANTES had no effect on nitrite accumulation while TGF-beta inhibited NO synthesis. |
| 1120 | 9667075 | In high glucose conditions, IGF-I and EGF significantly enhanced NO production. |
| 1121 | 9667075 | The effects of RANTES and TGF-beta were unchanged by an elevated glucose concentration. |
| 1122 | 9667075 | EGF-induced stimulation of NO production in high glucose media was associated with parallel alterations in iNOS gene and protein expression. |
| 1123 | 9667075 | The modest enhancement in nitrite accumulation provoked by IGF-I in high glucose conditions was not accompanied by demonstrable increases in iNOS mRNA abundance or protein content. |
| 1124 | 9667075 | Therefore, we examined the effect of IGF-I, EGF, TGF-beta and RANTES on NO production by RMC maintained in normal (5.6 mM) or high glucose (33.3 mM) for 48 h. |
| 1125 | 9667075 | In normal glucose media, IGF-I, EGF, and RANTES had no effect on nitrite accumulation while TGF-beta inhibited NO synthesis. |
| 1126 | 9667075 | In high glucose conditions, IGF-I and EGF significantly enhanced NO production. |
| 1127 | 9667075 | The effects of RANTES and TGF-beta were unchanged by an elevated glucose concentration. |
| 1128 | 9667075 | EGF-induced stimulation of NO production in high glucose media was associated with parallel alterations in iNOS gene and protein expression. |
| 1129 | 9667075 | The modest enhancement in nitrite accumulation provoked by IGF-I in high glucose conditions was not accompanied by demonstrable increases in iNOS mRNA abundance or protein content. |
| 1130 | 9686920 | The following antibodies were used for this immunohistochemical study: monoclonal antibodies against the heparan sulphate side chain (JM403) and core protein (JM72) of the glomerular heparan sulphate proteoglycan; polyclonal antibodies against the core protein (B31); polyclonal antibodies against collagen types I, III, and IV, fibronectin, and laminin; and monoclonal antibodies against the noncollagenous domain of alpha1(collagen IV) and alpha3(collagen IV), against transforming growth factor beta(2G7), and against advanced glycosylation end products (4G9). |
| 1131 | 9686920 | Increased intensity of staining was found for collagen type I and advanced glycosylation end products in patients with diabetic nephropathy. |
| 1132 | 9689088 | SMAD2, which is a tumor suppressor involved in colorectal and lung cancer, has been shown to induce dorsal mesoderm in Xenopus laevis in response to transforming growth factor beta and activins. |
| 1133 | 9691086 | Paracrine effect of transforming growth factor-beta1 (TGF-beta1) on autoimmune insulitis and diabetes was studied by transgenic production of the active form of porcine TGF-beta1 (pTGF-beta1) in pancreatic islet (islet) alpha cells in nonobese diabetic (NOD) mice under the control of rat glucagon promoter (RGP) (NOD-RGP-TGF-beta1). |
| 1134 | 9691086 | Based on these, it is concluded that autoimmune diabetes in NOD mice is not a systemic disease and it can be completely prevented by the paracrine TGF-beta1 in the islet compartment through protection against CD4(+) and CD8(+) effector lymphocytes. |
| 1135 | 9691086 | Paracrine effect of transforming growth factor-beta1 (TGF-beta1) on autoimmune insulitis and diabetes was studied by transgenic production of the active form of porcine TGF-beta1 (pTGF-beta1) in pancreatic islet (islet) alpha cells in nonobese diabetic (NOD) mice under the control of rat glucagon promoter (RGP) (NOD-RGP-TGF-beta1). |
| 1136 | 9691086 | Based on these, it is concluded that autoimmune diabetes in NOD mice is not a systemic disease and it can be completely prevented by the paracrine TGF-beta1 in the islet compartment through protection against CD4(+) and CD8(+) effector lymphocytes. |
| 1137 | 9767526 | Transcriptional activation of transforming growth factor-beta1 in mesangial cell culture by high glucose concentration. |
| 1138 | 9792466 | HOC were isolated from healthy adults who underwent selective orthopedic surgery and treated with cytokines released in the bone microenvironment during coupling i.e Interleukin-1beta (IL-1beta), Tumor Necrosis Factor alpha (TNFalpha), Transforming Growth Factor beta1 and 2 (TGFbeta 1 and 2) and Endothelin-1 (ET-1). |
| 1139 | 9792466 | We observed that (1) IL-1beta and TNFalpha induced IL-6 in a dose and time-dependent fashion, (2) TGFbeta 1 and 2 enhanced basal and IL-1beta and TNFalpha induced IL-6 expression, (3) ET-1 elicited a dose-dependent stimulatory effect on IL-6 expression. (4) E2, DHT and DHEA alone and in combination with IL-1beta and TNFalpha elicited no reproducible dose-dependent effect on IL-6 production, whereas Dexa inhibited basal and IL-1beta and TNFalpha induced IL-6 expression dose dependently. |
| 1140 | 9792466 | In conclusion, IL-1beta, TNFalpha, TGFbeta 1 and 2 and ET-1 may participate in the regulation of bone resorption by stimulating IL-6 expression in HOC. |
| 1141 | 9792466 | HOC were isolated from healthy adults who underwent selective orthopedic surgery and treated with cytokines released in the bone microenvironment during coupling i.e Interleukin-1beta (IL-1beta), Tumor Necrosis Factor alpha (TNFalpha), Transforming Growth Factor beta1 and 2 (TGFbeta 1 and 2) and Endothelin-1 (ET-1). |
| 1142 | 9792466 | We observed that (1) IL-1beta and TNFalpha induced IL-6 in a dose and time-dependent fashion, (2) TGFbeta 1 and 2 enhanced basal and IL-1beta and TNFalpha induced IL-6 expression, (3) ET-1 elicited a dose-dependent stimulatory effect on IL-6 expression. (4) E2, DHT and DHEA alone and in combination with IL-1beta and TNFalpha elicited no reproducible dose-dependent effect on IL-6 production, whereas Dexa inhibited basal and IL-1beta and TNFalpha induced IL-6 expression dose dependently. |
| 1143 | 9792466 | In conclusion, IL-1beta, TNFalpha, TGFbeta 1 and 2 and ET-1 may participate in the regulation of bone resorption by stimulating IL-6 expression in HOC. |
| 1144 | 9792466 | HOC were isolated from healthy adults who underwent selective orthopedic surgery and treated with cytokines released in the bone microenvironment during coupling i.e Interleukin-1beta (IL-1beta), Tumor Necrosis Factor alpha (TNFalpha), Transforming Growth Factor beta1 and 2 (TGFbeta 1 and 2) and Endothelin-1 (ET-1). |
| 1145 | 9792466 | We observed that (1) IL-1beta and TNFalpha induced IL-6 in a dose and time-dependent fashion, (2) TGFbeta 1 and 2 enhanced basal and IL-1beta and TNFalpha induced IL-6 expression, (3) ET-1 elicited a dose-dependent stimulatory effect on IL-6 expression. (4) E2, DHT and DHEA alone and in combination with IL-1beta and TNFalpha elicited no reproducible dose-dependent effect on IL-6 production, whereas Dexa inhibited basal and IL-1beta and TNFalpha induced IL-6 expression dose dependently. |
| 1146 | 9792466 | In conclusion, IL-1beta, TNFalpha, TGFbeta 1 and 2 and ET-1 may participate in the regulation of bone resorption by stimulating IL-6 expression in HOC. |
| 1147 | 9805643 | Von Willebrand factor (vWf), a multimeric glycoprotein mainly synthesised by endothelial cells, is involved in platelet adhesion and aggregation and acts as the carrier of coagulation factor VIII in plasma. |
| 1148 | 9805643 | Concomitant with high vWf levels, other possible mechanisms of endothelial damage include reduced synthesis or release of nitric oxide, hyperglycaemic pseudohypoxia and protein kinase-C activation, increased synthesis of proteins bearing advanced glycosylation end-products or transforming growth factor-beta (TGF-beta) activation of coagulation and inhibition of fibrinolysis. |
| 1149 | 9808089 | This study examines lines of all three glomerular cell types derived from female B6SJLF1/J mice, as well as mRNA levels for collagens alpha1(I), alpha1(IV), alpha3 (IV), alpha5 (IV), and alpha1 (VI), laminin, tenascin, matrix metalloproteinase-2 (MMP-2), and MMP-9. |
| 1150 | 9808089 | MMP-2 and MMP-9 enzyme activity was measured by zymography. |
| 1151 | 9808089 | However, they express only low levels of MMP-2 and no detectable MMP-9. |
| 1152 | 9808089 | Stimulation with exogenous transforming growth factor-beta1 leads to a significant increase in collagen I, tissue inhibitors of metalloproteinase-1, and MMP-9 in conditioned media. |
| 1153 | 9815141 | The core protein of the proteoglycan decorin binds and neutralizes transforming growth factor-beta (TGF-beta). |
| 1154 | 9815141 | Activation of TGF-beta is crucial to tissue injury in diabetic nephropathy, but it is not currently known whether decorin plays a role in this disease. |
| 1155 | 9815141 | When mouse mesangial and proximal tubular cells are exposed to TGF-beta1 (1 ng/ml), decorin mRNA is significantly decreased. |
| 1156 | 9815141 | Our findings suggest that the increased decorin expression in the diabetic kidney may counteract the hypertrophic and prosclerotic effects of increased TGF-beta levels and that a negative feedback loop may exist between decorin and TGF-beta. |
| 1157 | 9815141 | The core protein of the proteoglycan decorin binds and neutralizes transforming growth factor-beta (TGF-beta). |
| 1158 | 9815141 | Activation of TGF-beta is crucial to tissue injury in diabetic nephropathy, but it is not currently known whether decorin plays a role in this disease. |
| 1159 | 9815141 | When mouse mesangial and proximal tubular cells are exposed to TGF-beta1 (1 ng/ml), decorin mRNA is significantly decreased. |
| 1160 | 9815141 | Our findings suggest that the increased decorin expression in the diabetic kidney may counteract the hypertrophic and prosclerotic effects of increased TGF-beta levels and that a negative feedback loop may exist between decorin and TGF-beta. |
| 1161 | 9815141 | The core protein of the proteoglycan decorin binds and neutralizes transforming growth factor-beta (TGF-beta). |
| 1162 | 9815141 | Activation of TGF-beta is crucial to tissue injury in diabetic nephropathy, but it is not currently known whether decorin plays a role in this disease. |
| 1163 | 9815141 | When mouse mesangial and proximal tubular cells are exposed to TGF-beta1 (1 ng/ml), decorin mRNA is significantly decreased. |
| 1164 | 9815141 | Our findings suggest that the increased decorin expression in the diabetic kidney may counteract the hypertrophic and prosclerotic effects of increased TGF-beta levels and that a negative feedback loop may exist between decorin and TGF-beta. |
| 1165 | 9815141 | The core protein of the proteoglycan decorin binds and neutralizes transforming growth factor-beta (TGF-beta). |
| 1166 | 9815141 | Activation of TGF-beta is crucial to tissue injury in diabetic nephropathy, but it is not currently known whether decorin plays a role in this disease. |
| 1167 | 9815141 | When mouse mesangial and proximal tubular cells are exposed to TGF-beta1 (1 ng/ml), decorin mRNA is significantly decreased. |
| 1168 | 9815141 | Our findings suggest that the increased decorin expression in the diabetic kidney may counteract the hypertrophic and prosclerotic effects of increased TGF-beta levels and that a negative feedback loop may exist between decorin and TGF-beta. |
| 1169 | 9819366 | Reverse transcription-PCR analysis revealed that local production of IL-12p40 led to the decrease of interferon-gamma and the augmentation of transforming growth factor-beta at the graft site. |
| 1170 | 9845822 | In this study, we measured the urinary TGF-beta1 excretion in 57 patients with non-insulin-dependent diabetes mellitus and in 20 healthy volunteers to examine whether the determination of urinary TGF-beta1 excretion would facilitate the evaluation of the degree of mesangial expansion in patients with diabetic nephropathy. |
| 1171 | 9848784 | TGF-beta1 gene mutations in insulin-dependent diabetes mellitus and diabetic nephropathy. |
| 1172 | 9848784 | PCR assays were established for easy and fast analysis of two transforming growth factor-beta1 (TGF-beta1) gene mutations, a C to T transition at position 76 in exon 5 resulting in a change from threonine to isoleucine in position 263 (Thr263Ile) of the propeptide and a deletion of a C in the intron sequence eight bases prior to exon 5 (713-8delC). |
| 1173 | 9848784 | These mutations were evaluated in insulin-dependent diabetes mellitus (IDDM) patients (n = 137) and control subjects (n = 105) and in IDDM patients with (n = 170) and without (n = 99) nephropathy. |
| 1174 | 9848784 | No association of the two TGF-beta1 sequence variations with IDDM in general was found. |
| 1175 | 9848784 | TGF-beta1 gene mutations in insulin-dependent diabetes mellitus and diabetic nephropathy. |
| 1176 | 9848784 | PCR assays were established for easy and fast analysis of two transforming growth factor-beta1 (TGF-beta1) gene mutations, a C to T transition at position 76 in exon 5 resulting in a change from threonine to isoleucine in position 263 (Thr263Ile) of the propeptide and a deletion of a C in the intron sequence eight bases prior to exon 5 (713-8delC). |
| 1177 | 9848784 | These mutations were evaluated in insulin-dependent diabetes mellitus (IDDM) patients (n = 137) and control subjects (n = 105) and in IDDM patients with (n = 170) and without (n = 99) nephropathy. |
| 1178 | 9848784 | No association of the two TGF-beta1 sequence variations with IDDM in general was found. |
| 1179 | 9848784 | TGF-beta1 gene mutations in insulin-dependent diabetes mellitus and diabetic nephropathy. |
| 1180 | 9848784 | PCR assays were established for easy and fast analysis of two transforming growth factor-beta1 (TGF-beta1) gene mutations, a C to T transition at position 76 in exon 5 resulting in a change from threonine to isoleucine in position 263 (Thr263Ile) of the propeptide and a deletion of a C in the intron sequence eight bases prior to exon 5 (713-8delC). |
| 1181 | 9848784 | These mutations were evaluated in insulin-dependent diabetes mellitus (IDDM) patients (n = 137) and control subjects (n = 105) and in IDDM patients with (n = 170) and without (n = 99) nephropathy. |
| 1182 | 9848784 | No association of the two TGF-beta1 sequence variations with IDDM in general was found. |
| 1183 | 9856360 | Angiotensin converting enzyme inhibition reduces the expression of transforming growth factor-beta1 and type IV collagen in diabetic vasculopathy. |
| 1184 | 9867067 | In a subgroup of animals, RNA was extracted from the mesenteric vasculature for assessment of gene expression of the prosclerotic cytokine, transforming growth factor beta 1 (TGFbeta1), and the matrix protein, type IV collagen. |
| 1185 | 9887080 | Renal type I inositol 1,4,5-trisphosphate receptor is reduced in streptozotocin-induced diabetic rats and mice. |
| 1186 | 9887080 | We have previously demonstrated that the cytokine transforming growth factor-beta1 (TGF-beta1) is increased in early diabetic kidney disease and TGF-beta1 inhibits the expression of the inositol 1,4,5-trisphosphate (IP3)-gated calcium channel, the type I IP3 receptor (IP3R), in mesangial cells. |
| 1187 | 9887080 | Reduction of type I IP3R also occurred in parallel with renal hypertrophy, increased creatinine clearance, and increased renal TGF-beta1 expression in the diabetic rats. |
| 1188 | 9887080 | Two-week-old diabetic mice also had reduced renal type I IP3R protein and mRNA expression in association with renal hypertrophy and increased TGF-beta1 mRNA expression. |
| 1189 | 9887080 | Renal type I inositol 1,4,5-trisphosphate receptor is reduced in streptozotocin-induced diabetic rats and mice. |
| 1190 | 9887080 | We have previously demonstrated that the cytokine transforming growth factor-beta1 (TGF-beta1) is increased in early diabetic kidney disease and TGF-beta1 inhibits the expression of the inositol 1,4,5-trisphosphate (IP3)-gated calcium channel, the type I IP3 receptor (IP3R), in mesangial cells. |
| 1191 | 9887080 | Reduction of type I IP3R also occurred in parallel with renal hypertrophy, increased creatinine clearance, and increased renal TGF-beta1 expression in the diabetic rats. |
| 1192 | 9887080 | Two-week-old diabetic mice also had reduced renal type I IP3R protein and mRNA expression in association with renal hypertrophy and increased TGF-beta1 mRNA expression. |
| 1193 | 9887080 | Renal type I inositol 1,4,5-trisphosphate receptor is reduced in streptozotocin-induced diabetic rats and mice. |
| 1194 | 9887080 | We have previously demonstrated that the cytokine transforming growth factor-beta1 (TGF-beta1) is increased in early diabetic kidney disease and TGF-beta1 inhibits the expression of the inositol 1,4,5-trisphosphate (IP3)-gated calcium channel, the type I IP3 receptor (IP3R), in mesangial cells. |
| 1195 | 9887080 | Reduction of type I IP3R also occurred in parallel with renal hypertrophy, increased creatinine clearance, and increased renal TGF-beta1 expression in the diabetic rats. |
| 1196 | 9887080 | Two-week-old diabetic mice also had reduced renal type I IP3R protein and mRNA expression in association with renal hypertrophy and increased TGF-beta1 mRNA expression. |
| 1197 | 9892241 | Under control of the Ren-1c promoter, locally produced transforming growth factor-beta1 induces accumulation of glomerular extracellular matrix in transgenic mice. |
| 1198 | 9892610 | Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes. |
| 1199 | 9892610 | Previous studies have shown that induction of autoimmune diabetes by adult thymectomy and split dose irradiation of PVG.RT1(u) rats can be prevented by their reconstitution with peripheral CD4(+)CD45RC-TCR-alpha/beta+RT6(+) cells and CD4(+)CD8(-) thymocytes from normal syngeneic donors. |
| 1200 | 9892610 | RT1(u) rats, development of thyroiditis was prevented by the transfer of CD4(+)CD45RC- and CD4(+)CD8(-) thymocytes from normal donors but not by CD4(+)CD45RC+ peripheral T cells. |
| 1201 | 9892610 | We now show that transforming growth factor (TGF)-beta and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats. |
| 1202 | 9892610 | The prevention of both diabetes and thyroiditis by CD4(+)CD45RC- peripheral cells and CD4(+)CD8(-) thymocytes therefore does not support the view that the mechanism of regulation involves a switch from a T helper cell type 1 (Th1) to a Th2-like response, but rather relies upon a specific suppression of the autoimmune responses involving TGF-beta and IL-4. |
| 1203 | 9892610 | Regulatory T cells in the control of autoimmunity: the essential role of transforming growth factor beta and interleukin 4 in the prevention of autoimmune thyroiditis in rats by peripheral CD4(+)CD45RC- cells and CD4(+)CD8(-) thymocytes. |
| 1204 | 9892610 | Previous studies have shown that induction of autoimmune diabetes by adult thymectomy and split dose irradiation of PVG.RT1(u) rats can be prevented by their reconstitution with peripheral CD4(+)CD45RC-TCR-alpha/beta+RT6(+) cells and CD4(+)CD8(-) thymocytes from normal syngeneic donors. |
| 1205 | 9892610 | RT1(u) rats, development of thyroiditis was prevented by the transfer of CD4(+)CD45RC- and CD4(+)CD8(-) thymocytes from normal donors but not by CD4(+)CD45RC+ peripheral T cells. |
| 1206 | 9892610 | We now show that transforming growth factor (TGF)-beta and interleukin (IL)-4 both play essential roles in the mechanism of this protection since administration of monoclonal antibodies that block the biological activity of either of these cytokines abrogates the protective effect of the donor cells in the recipient rats. |
| 1207 | 9892610 | The prevention of both diabetes and thyroiditis by CD4(+)CD45RC- peripheral cells and CD4(+)CD8(-) thymocytes therefore does not support the view that the mechanism of regulation involves a switch from a T helper cell type 1 (Th1) to a Th2-like response, but rather relies upon a specific suppression of the autoimmune responses involving TGF-beta and IL-4. |
| 1208 | 9914941 | Bone contains several growth factors, including bone morphogenetic proteins (BMPs), transforming growth factor beta (TGF-beta), insulin-like growth factors I and II (IGF-I and IGF-II), platelet derived growth factor (PDGF) and basic and acidic fibroblast growth factor (bFGF and aFGF). |
| 1209 | 9930378 | In Sprague-Dawley rats, angiotensin II (Ang II) infusion was associated with increased density of amylin-binding sites as well as elevated blood pressure. |
| 1210 | 9930378 | In a model of IDDM (streptozotocin diabetes), amylin and angiotensinogen IR are both restricted to a subset of brush border epithelial cells close to glomeruli which, in the developing kidney, expressed amylin mRNA. |
| 1211 | 9930378 | Thus in this IDDM model, we hypothesize that amylin mRNA transcription which is normally downregulated in the adult, is upregulated in this subset of these brush border epithelial cells, and that it stimulates the activity of a local RAS by an intracellular mechanism, leading to the biosynthesis of Ang II. |
| 1212 | 9930378 | It remains to be determined that if amylin is playing a role in stimulating local Ang II production at these sites, this provides a mechanism for activation of TGF-beta, ultimately leading to interstitial fibrosis. |
| 1213 | 10026205 | High glucose stimulated expression of transforming growth factor beta1 (TGF-beta1), and addition of TGF-beta1 to mesangial cells triggered CTGF expression. |
| 1214 | 10026205 | CTGF expression induced by high glucose was partially suppressed by anti-TGF-beta1 antibody and by the protein kinase C inhibitor GF 109203X. |
| 1215 | 10026205 | Together, these data suggest that 1) high glucose stimulates mesangial CTGF expression by TGFbeta1-dependent and protein kinase C dependent pathways, and 2) CTGF may be a mediator of TGFbeta1-driven matrix production within a diabetic milieu. |
| 1216 | 10049952 | Development of disease can be prevented by reconstitution of PVG rats shortly after their final irradiation with either peripheral CD4(+)CD45RC- T cells or CD4(+)CD8(-) thymocytes from syngeneic donors. |
| 1217 | 10049952 | Although the activity of both populations is known to depend on the activities of endogenously produced interleukin 4 and transforming growth factor beta, implying a common mechanism, the issue of antigen specificity of the cells involved has not yet been addressed. |
| 1218 | 10049952 | Significantly, in contrast to the peripheral CD4(+) T cells, CD4(+)CD8(-) thymocytes from 131I-treated PVG donors were still able to prevent thyroiditis upon adoptive transfer. |
| 1219 | 10079220 | The transforming growth factor-beta (TGF-beta) signals are mediated by a family of at least nine SMAD proteins, of which SMAD5 is thought to relay signals of the bone morphogenetic protein (BMP) pathway. |
| 1220 | 10098490 | Intact CTGF was increased by cAMP but not by transforming growth factor-beta (TGFbeta). |
| 1221 | 10098490 | CTGF messenger RNA (mRNA) was not changed by cAMP nor TGFbeta. |
| 1222 | 10098490 | In the microvessel cells, TGFbeta increased and cAMP did not change CTGF mRNA levels, with neither TGFbeta nor cAMP increasing CTGF protein. |
| 1223 | 10098490 | The discordance between protein and mRNA levels in large vessel and microvessel endothelial cells was mostly explained by the effects of cAMP and TGFbeta on media proteolytic activity; in large vessel cells, cAMP inhibited degradation of CTGF, whereas in microvessel cells, TGFbeta and cAMP stimulated proteolytic activity against CTGF. |
| 1224 | 10098490 | We conclude that in large vessel endothelial cells, cAMP increased intact CTGF protein by inhibiting degradation of CTGF, whereas TGFbeta stimulated neither CTGF mRNA nor protein; in microvessel cells, TGFbeta increased CTGF mRNA, while both TGFbeta and cAMP stimulated CTGF degradation. |
| 1225 | 10098490 | Intact CTGF was increased by cAMP but not by transforming growth factor-beta (TGFbeta). |
| 1226 | 10098490 | CTGF messenger RNA (mRNA) was not changed by cAMP nor TGFbeta. |
| 1227 | 10098490 | In the microvessel cells, TGFbeta increased and cAMP did not change CTGF mRNA levels, with neither TGFbeta nor cAMP increasing CTGF protein. |
| 1228 | 10098490 | The discordance between protein and mRNA levels in large vessel and microvessel endothelial cells was mostly explained by the effects of cAMP and TGFbeta on media proteolytic activity; in large vessel cells, cAMP inhibited degradation of CTGF, whereas in microvessel cells, TGFbeta and cAMP stimulated proteolytic activity against CTGF. |
| 1229 | 10098490 | We conclude that in large vessel endothelial cells, cAMP increased intact CTGF protein by inhibiting degradation of CTGF, whereas TGFbeta stimulated neither CTGF mRNA nor protein; in microvessel cells, TGFbeta increased CTGF mRNA, while both TGFbeta and cAMP stimulated CTGF degradation. |
| 1230 | 10098490 | Intact CTGF was increased by cAMP but not by transforming growth factor-beta (TGFbeta). |
| 1231 | 10098490 | CTGF messenger RNA (mRNA) was not changed by cAMP nor TGFbeta. |
| 1232 | 10098490 | In the microvessel cells, TGFbeta increased and cAMP did not change CTGF mRNA levels, with neither TGFbeta nor cAMP increasing CTGF protein. |
| 1233 | 10098490 | The discordance between protein and mRNA levels in large vessel and microvessel endothelial cells was mostly explained by the effects of cAMP and TGFbeta on media proteolytic activity; in large vessel cells, cAMP inhibited degradation of CTGF, whereas in microvessel cells, TGFbeta and cAMP stimulated proteolytic activity against CTGF. |
| 1234 | 10098490 | We conclude that in large vessel endothelial cells, cAMP increased intact CTGF protein by inhibiting degradation of CTGF, whereas TGFbeta stimulated neither CTGF mRNA nor protein; in microvessel cells, TGFbeta increased CTGF mRNA, while both TGFbeta and cAMP stimulated CTGF degradation. |
| 1235 | 10098490 | Intact CTGF was increased by cAMP but not by transforming growth factor-beta (TGFbeta). |
| 1236 | 10098490 | CTGF messenger RNA (mRNA) was not changed by cAMP nor TGFbeta. |
| 1237 | 10098490 | In the microvessel cells, TGFbeta increased and cAMP did not change CTGF mRNA levels, with neither TGFbeta nor cAMP increasing CTGF protein. |
| 1238 | 10098490 | The discordance between protein and mRNA levels in large vessel and microvessel endothelial cells was mostly explained by the effects of cAMP and TGFbeta on media proteolytic activity; in large vessel cells, cAMP inhibited degradation of CTGF, whereas in microvessel cells, TGFbeta and cAMP stimulated proteolytic activity against CTGF. |
| 1239 | 10098490 | We conclude that in large vessel endothelial cells, cAMP increased intact CTGF protein by inhibiting degradation of CTGF, whereas TGFbeta stimulated neither CTGF mRNA nor protein; in microvessel cells, TGFbeta increased CTGF mRNA, while both TGFbeta and cAMP stimulated CTGF degradation. |
| 1240 | 10098490 | Intact CTGF was increased by cAMP but not by transforming growth factor-beta (TGFbeta). |
| 1241 | 10098490 | CTGF messenger RNA (mRNA) was not changed by cAMP nor TGFbeta. |
| 1242 | 10098490 | In the microvessel cells, TGFbeta increased and cAMP did not change CTGF mRNA levels, with neither TGFbeta nor cAMP increasing CTGF protein. |
| 1243 | 10098490 | The discordance between protein and mRNA levels in large vessel and microvessel endothelial cells was mostly explained by the effects of cAMP and TGFbeta on media proteolytic activity; in large vessel cells, cAMP inhibited degradation of CTGF, whereas in microvessel cells, TGFbeta and cAMP stimulated proteolytic activity against CTGF. |
| 1244 | 10098490 | We conclude that in large vessel endothelial cells, cAMP increased intact CTGF protein by inhibiting degradation of CTGF, whereas TGFbeta stimulated neither CTGF mRNA nor protein; in microvessel cells, TGFbeta increased CTGF mRNA, while both TGFbeta and cAMP stimulated CTGF degradation. |
| 1245 | 10099841 | PC-conditioned medium (PC-CM) from normal rabbits stimulated in vitro angiogenesis of diabetic ECs more than that of normal ECs. in vitro angiogenesis was also more stimulated in diabetic ECs than in normal ECs by basic fibroblast growth factor (bFGF) or transforming growth factor-beta 1, indicating that diabetic ECs are different from normal ECs in terms of angiogenic potential. |
| 1246 | 10198261 | This behavior was not reproduced treating the hepatocytes with the growth factors EGF, interleukin Ibeta, interleukin-6, and TGF-beta1. |
| 1247 | 10199140 | In the presence of diabetes or persistent hyperglycemia, many cytokines including growth factors such as PDGF, HB-EGF, IL-1 beta and TNF alpha are upregulated in intimal cells of the arterial or aortic wall. |
| 1248 | 10199140 | In addition, diabetes causes abnormal responsibility to HB-EGF, PDGF and TGF-beta in medial smooth muscle cells leading to the elevated activity to their proliferation and migration into the intima. |
| 1249 | 10202998 | While GH effects on glomerular hypertrophy are likely mediated by insulin-like growth factor I (IGF-I), GH effects on glomerular sclerosis are independent of IGF-I. |
| 1250 | 10202998 | Those effects rather require multiple signaling pathways functioning in series, e.g. angiotensin II binding preceding transforming growth factor beta (TGF-beta) release, or pro-inflammatory factor release preceding repair/scarring processes. |
| 1251 | 10203356 | Interaction of angiotensin II and mechanical stretch on vascular endothelial growth factor production by human mesangial cells. |
| 1252 | 10203356 | The antiproteinuric effect of angiotensin-converting enzyme inhibitors underscores the importance of a hemodynamic injury and the renin-angiotensin system in the proteinuria of various glomerular diseases. |
| 1253 | 10203356 | Vascular endothelial growth factor (VEGF), a potent promoter of vascular permeability, is induced in mesangial cells by both mechanical stretch and TGF-beta1. |
| 1254 | 10203356 | This study investigates the effect of TGF-beta blockade, angiotensin II (AngII), and the interaction between AngII and stretch on human mesangial cell VEGF production. |
| 1255 | 10203356 | Exposure to AngII (1 microM) induced a significant increase in VEGF mRNA and protein levels (1.5+/-0.1 and 1.7+/-0.3, respectively, fold increase over control, P<0.05). |
| 1256 | 10203356 | The AngII receptor (AT1) antagonist Losartan (10 microM) prevented AngII-induced, but not stretch-induced, VEGF protein secretion (AngII 1.7+/-0.3, AngII + Losartan 1.0+/-0.1, P<0.05; stretch 2.4+/-0.4, stretch + Losartan 2.6+/-0.5). |
| 1257 | 10203356 | Simultaneous exposure to both AngII and stretch for 12 h had an additive effect on VEGF production (AngII 1.6+/-0.1, stretch 2.6+/-0.27, AngII + stretch 3.1+/-0.35). |
| 1258 | 10203356 | Conversely, preexposure to stretch magnified AngII-induced VEGF protein secretion (unstretched + AngII 1.3+/-0.0, stretched + AngII 1.9+/-0.1, P<0.01) with a parallel 1.5-fold increase in AT1 receptor levels. |
| 1259 | 10203356 | AngII and stretch can both independently induce VEGF production; in addition, mechanical stretch upregulates the AT1 receptor, enhancing the cellular response to AngII. |
| 1260 | 10203356 | Interaction of angiotensin II and mechanical stretch on vascular endothelial growth factor production by human mesangial cells. |
| 1261 | 10203356 | The antiproteinuric effect of angiotensin-converting enzyme inhibitors underscores the importance of a hemodynamic injury and the renin-angiotensin system in the proteinuria of various glomerular diseases. |
| 1262 | 10203356 | Vascular endothelial growth factor (VEGF), a potent promoter of vascular permeability, is induced in mesangial cells by both mechanical stretch and TGF-beta1. |
| 1263 | 10203356 | This study investigates the effect of TGF-beta blockade, angiotensin II (AngII), and the interaction between AngII and stretch on human mesangial cell VEGF production. |
| 1264 | 10203356 | Exposure to AngII (1 microM) induced a significant increase in VEGF mRNA and protein levels (1.5+/-0.1 and 1.7+/-0.3, respectively, fold increase over control, P<0.05). |
| 1265 | 10203356 | The AngII receptor (AT1) antagonist Losartan (10 microM) prevented AngII-induced, but not stretch-induced, VEGF protein secretion (AngII 1.7+/-0.3, AngII + Losartan 1.0+/-0.1, P<0.05; stretch 2.4+/-0.4, stretch + Losartan 2.6+/-0.5). |
| 1266 | 10203356 | Simultaneous exposure to both AngII and stretch for 12 h had an additive effect on VEGF production (AngII 1.6+/-0.1, stretch 2.6+/-0.27, AngII + stretch 3.1+/-0.35). |
| 1267 | 10203356 | Conversely, preexposure to stretch magnified AngII-induced VEGF protein secretion (unstretched + AngII 1.3+/-0.0, stretched + AngII 1.9+/-0.1, P<0.01) with a parallel 1.5-fold increase in AT1 receptor levels. |
| 1268 | 10203356 | AngII and stretch can both independently induce VEGF production; in addition, mechanical stretch upregulates the AT1 receptor, enhancing the cellular response to AngII. |
| 1269 | 10319913 | GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus. |
| 1270 | 10319913 | It is now believed that the GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes have an important role in the development of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 1271 | 10319913 | The protein encoded by daf-2 is 35% identical to the human insulin receptor, daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 can enhance superoxide dismutase (SOD) expression. |
| 1272 | 10319913 | EFAs and their metabolites can alter the cell membrane fluidity and enhance the expression of GLUT-4 and insulin receptors. |
| 1273 | 10319913 | EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. |
| 1274 | 10319913 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 1275 | 10319913 | Based on this evidence, it is proposed that GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin interact with each other in ways which may have relevance to the development or abrogation of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 1276 | 10319913 | GLUT-4, tumor necrosis factor, essential fatty acids and daf-genes and their role in insulin resistance and non-insulin dependent diabetes mellitus. |
| 1277 | 10319913 | It is now believed that the GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes have an important role in the development of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 1278 | 10319913 | The protein encoded by daf-2 is 35% identical to the human insulin receptor, daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 can enhance superoxide dismutase (SOD) expression. |
| 1279 | 10319913 | EFAs and their metabolites can alter the cell membrane fluidity and enhance the expression of GLUT-4 and insulin receptors. |
| 1280 | 10319913 | EFAs can suppress TNF-alpha production and secretion, a mechanism that may have relevance to the role of these fatty acids in the pathogenesis of insulin resistance, obesity and NIDDM. |
| 1281 | 10319913 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 1282 | 10319913 | Based on this evidence, it is proposed that GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin interact with each other in ways which may have relevance to the development or abrogation of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 1283 | 10330050 | Glycated albumin stimulation of PKC-beta activity is linked to increased collagen IV in mesangial cells. |
| 1284 | 10330050 | Albumin modified by Amadori-glucose adducts induces coordinate increases in the expression of extracellular matrix proteins, transforming growth factor (TGF)-beta1, and the TGF-beta type II receptor in glomerular mesangial cells. |
| 1285 | 10330050 | Because activation of protein kinase C (PKC) accompanies the increased mesangial cell expression of matrix proteins and TGF-beta1 induced by high ambient glucose, we postulated that glycated albumin (GA) modulates PKC activity and that PKC participates in mediating the GA-induced stimulation of matrix production. |
| 1286 | 10330050 | The findings indicate that Amadori-modified albumin stimulates mesangial cell PKC activity, and that activation of the PKC-beta isoform is linked to the stimulation of collagen type IV production. |
| 1287 | 10330050 | Glycated albumin stimulation of PKC-beta activity is linked to increased collagen IV in mesangial cells. |
| 1288 | 10330050 | Albumin modified by Amadori-glucose adducts induces coordinate increases in the expression of extracellular matrix proteins, transforming growth factor (TGF)-beta1, and the TGF-beta type II receptor in glomerular mesangial cells. |
| 1289 | 10330050 | Because activation of protein kinase C (PKC) accompanies the increased mesangial cell expression of matrix proteins and TGF-beta1 induced by high ambient glucose, we postulated that glycated albumin (GA) modulates PKC activity and that PKC participates in mediating the GA-induced stimulation of matrix production. |
| 1290 | 10330050 | The findings indicate that Amadori-modified albumin stimulates mesangial cell PKC activity, and that activation of the PKC-beta isoform is linked to the stimulation of collagen type IV production. |
| 1291 | 10330296 | Regulatory Th2-type T cell lines against insulin and GAD peptides derived from orally- and nasally-treated NOD mice suppress diabetes. |
| 1292 | 10330296 | Ourselves and others have previously shown that oral and nasal administration of insulin or glutamic acid decarboxylase (GAD) suppresses development of diabetes in the NOD mouse and that this suppression appears secondary to the generation of regulatory T cells that act by secreting anti-inflammatory cytokines such as IL-4 and TGF-beta. |
| 1293 | 10330296 | In the present study, we analysed cytokine patterns associated with mucosal administration of insulin B-chain, B-chain peptide 10-24 and GAD peptide 524-543 and derived lines and clones from mucosally-treated animals. |
| 1294 | 10330296 | There was significantly less IFN-gamma production in mucosally-treated mice associated with increased production of IL-10 and TGF-beta. |
| 1295 | 10330296 | T cell clones, established from draining lymph nodes of fed or nasally-treated animals, secreted IL-4, IL-10 and TGF-beta whereas those from non-fed mice secreted IL-2 and IFN-gamma. |
| 1296 | 10330296 | Regulatory Th2-type T cell lines against insulin and GAD peptides derived from orally- and nasally-treated NOD mice suppress diabetes. |
| 1297 | 10330296 | Ourselves and others have previously shown that oral and nasal administration of insulin or glutamic acid decarboxylase (GAD) suppresses development of diabetes in the NOD mouse and that this suppression appears secondary to the generation of regulatory T cells that act by secreting anti-inflammatory cytokines such as IL-4 and TGF-beta. |
| 1298 | 10330296 | In the present study, we analysed cytokine patterns associated with mucosal administration of insulin B-chain, B-chain peptide 10-24 and GAD peptide 524-543 and derived lines and clones from mucosally-treated animals. |
| 1299 | 10330296 | There was significantly less IFN-gamma production in mucosally-treated mice associated with increased production of IL-10 and TGF-beta. |
| 1300 | 10330296 | T cell clones, established from draining lymph nodes of fed or nasally-treated animals, secreted IL-4, IL-10 and TGF-beta whereas those from non-fed mice secreted IL-2 and IFN-gamma. |
| 1301 | 10330296 | Regulatory Th2-type T cell lines against insulin and GAD peptides derived from orally- and nasally-treated NOD mice suppress diabetes. |
| 1302 | 10330296 | Ourselves and others have previously shown that oral and nasal administration of insulin or glutamic acid decarboxylase (GAD) suppresses development of diabetes in the NOD mouse and that this suppression appears secondary to the generation of regulatory T cells that act by secreting anti-inflammatory cytokines such as IL-4 and TGF-beta. |
| 1303 | 10330296 | In the present study, we analysed cytokine patterns associated with mucosal administration of insulin B-chain, B-chain peptide 10-24 and GAD peptide 524-543 and derived lines and clones from mucosally-treated animals. |
| 1304 | 10330296 | There was significantly less IFN-gamma production in mucosally-treated mice associated with increased production of IL-10 and TGF-beta. |
| 1305 | 10330296 | T cell clones, established from draining lymph nodes of fed or nasally-treated animals, secreted IL-4, IL-10 and TGF-beta whereas those from non-fed mice secreted IL-2 and IFN-gamma. |
| 1306 | 10333051 | Suppression of transforming growth factor beta and vascular endothelial growth factor in diabetic nephropathy in rats by a novel advanced glycation end product inhibitor, OPB-9195. |
| 1307 | 10359806 | CCR5(+) and CXCR3(+) T cells are increased in multiple sclerosis and their ligands MIP-1alpha and IP-10 are expressed in demyelinating brain lesions. |
| 1308 | 10359806 | Th2 cells; human Th1 clones express CXCR3 and CCR5 and Th2 clones express CCR3 and CCR4. |
| 1309 | 10359806 | We found CXCR3(+) T cells increased in blood of relapsing-remitting MS, and both CCR5(+) and CXCR3(+) T cells increased in progressive MS compared with controls. |
| 1310 | 10359806 | Furthermore, peripheral blood CCR5(+) T cells secreted high levels of IFN-gamma. |
| 1311 | 10359806 | In the brain, the CCR5 ligand, MIP-1alpha, was strongly associated with microglia/macrophages, and the CXCR3 ligand, IP-10, was expressed by astrocytes in MS lesions but not unaffected white matter of control or MS subjects. |
| 1312 | 10359806 | Areas of plaque formation were infiltrated by CCR5-expressing and, to a lesser extent, CXCR3-expressing cells; Interleukin (IL)-18 and IFN-gamma were expressed in demyelinating lesions. |
| 1313 | 10359806 | No leukocyte expression of CCR3, CCR4, or six other chemokines, or anti-inflammatory cytokines IL-5, IL-10, IL-13, and transforming growth factor-beta was observed. |
| 1314 | 10359806 | Furthermore, these results provide a rationale for the use of agents that block CCR5 and/or CXCR3 as a therapeutic approach in the treatment of MS. |
| 1315 | 10374910 | Oral tolerization with ovalbumin (OVA) increased levels of IL-10 and TGF-beta in gut tissue while IFN-gamma mRNA levels remained unchanged in both autoimmune diabetes prone NOD and normal C57BL/6 mice. |
| 1316 | 10382275 | We also show that serum lipids cause a generalized decrease in macrophage cytokine production using interleukin-1 beta (IL-1 beta), tumor necrosis factor alpha (TNF-alpha), platelet-derived growth factor (PDGF), and transforming growth factor beta 1 (TGF-beta 1) as marker cytokines. |
| 1317 | 10382596 | The role of nitric oxide synthase isoforms and arginase in the pathogenesis of diabetic foot ulcers: possible modulatory effects by transforming growth factor beta 1. |
| 1318 | 10404280 | NADPH diaphorase staining was used to identify NOS and immunostaining technique was used to identify nNOS in the penile nerve fibers. |
| 1319 | 10404280 | RT-PCR was used to identify mRNA expression of nNOS, eNOS, iNOS, ER-beta, ER-alpha, NGF, IGF-I, TGF-beta 1, and AR. |
| 1320 | 10404280 | Western blot was used to identify nNOS, IGF-I, NGF, and TFG-beta protein expressions. |
| 1321 | 10404280 | RT-PCR showed down-regulation of nNOS (large form), iNOS and ER-beta mRNA expression, Immunoblot showed down-regulation of nNOS protein expression and nNOS immunostaining showed less positive staining in the dorsal and intracavernous nerves in the diabetic group. |
| 1322 | 10410831 | The authors review the potential roles of some important receptors, such as the insulin receptor, beta 3-adrenergic receptor, leptin receptor and peroxisome proliferator-activated receptor gamma, in the pathogenesis of human type 2 diabetes. |
| 1323 | 10410831 | They emphasize the significance of effective glycemic control by examining the evidence that strongly suggests the association of chronic complications of type 2 diabetes with abnormalities of receptors for the advanced glycation end products, transforming growth factor-beta and platelet-derived growth factor. |
| 1324 | 10432377 | Other factors such as hemodynamic forces, protein glycation products, and several mediators (for example, angiotensin II, endothelin-1, thromboxane, and platelet-derived growth factor) may further amplify the synthesis of TGF-beta and/or the expression of its receptors in the diabetic state. |
| 1325 | 10432377 | The molecular mechanism arresting mesangial cells in the G1 phase of the cell cycle is the induction of cyclin-dependent kinase (CdK) inhibitors such as p27Kip1 and p21, which bind to and inactivate cyclin-CdK complexes responsible for G1-phase exit. |
| 1326 | 10432377 | High-glucose-induced activation of protein kinase C and stimulated TGF-beta expression appear to be essential for stimulated expression of p27Kip1. |
| 1327 | 10432377 | Other factors such as hemodynamic forces, protein glycation products, and several mediators (for example, angiotensin II, endothelin-1, thromboxane, and platelet-derived growth factor) may further amplify the synthesis of TGF-beta and/or the expression of its receptors in the diabetic state. |
| 1328 | 10432377 | The molecular mechanism arresting mesangial cells in the G1 phase of the cell cycle is the induction of cyclin-dependent kinase (CdK) inhibitors such as p27Kip1 and p21, which bind to and inactivate cyclin-CdK complexes responsible for G1-phase exit. |
| 1329 | 10432377 | High-glucose-induced activation of protein kinase C and stimulated TGF-beta expression appear to be essential for stimulated expression of p27Kip1. |
| 1330 | 10461173 | In particular, the growth hormone/insulin-like growth factor system and the transforming growth factor beta system have measurable effects on the development of diabetic kidney disease through a complex intrarenal system. |
| 1331 | 10464178 | Furthermore, NOD mice which spontaneously develop diabetes are susceptible to EAE induction with myelin oligodendrocyte glycoprotein (MOG) 35-55, whereas a MHC congenic strain, III, which also expresses I-A(g7) MHC haplotype does not develop diabetes and is also resistant to EAE induction. |
| 1332 | 10464178 | In the susceptible strains (SJL and NOD) in vitro, there are high levels of IFN-gamma production, whereas the resistant strains (B10.S or III) secreted primarily IL-4/IL-10 and transforming growth factor (TGF)-beta, and had decreased levels of IFN-gamma. |
| 1333 | 10464178 | When brains from susceptible and resistant mice were examined by immunohistochemical methods for cytokine expression, the brains from resistant mice showed fewer infiltrates which predominantly expressed IL-4 and IL-10 and/or TGF-beta. |
| 1334 | 10464178 | Brains from NOD and SJL with EAE showed mainly IL-2 and IFN-gamma positive cells. |
| 1335 | 10471535 | TGF-beta-1 up-regulates cyclin D1 expression in COLO-357 cells, whereas suppression of cyclin D1 levels is associated with down-regulation of the type I TGF-beta receptor. |
| 1336 | 10471535 | Transforming growth factor-beta1 (TGF-beta1) inhibits cell growth in susceptible cells by interacting with a family of protein kinases that control cell cycle progression. |
| 1337 | 10471535 | In the present study, we investigated the effects of TGF-beta1 on cyclin D1 expression and activity in COLO-357 human pancreatic cancer cells. |
| 1338 | 10471535 | TGF-beta1 increased cyclin D1 mRNA and protein levels. |
| 1339 | 10471535 | Despite its stimulatory effects on cyclin D1 levels, TGF-beta1 inhibited cyclin D1-associated kinase activity and the growth of COLO-357 cells. |
| 1340 | 10471535 | Furthermore, suppression of cyclin D1 expression with a cyclin D1 antisense cDNA resulted in loss of TGF-beta1-mediated growth inhibition in association with reduced induction of cyclin D1, p21(C)(ip)(1) and plasminogen activator inhibitor-1 (PAI-1). |
| 1341 | 10471535 | TGF-beta-1 up-regulates cyclin D1 expression in COLO-357 cells, whereas suppression of cyclin D1 levels is associated with down-regulation of the type I TGF-beta receptor. |
| 1342 | 10471535 | Transforming growth factor-beta1 (TGF-beta1) inhibits cell growth in susceptible cells by interacting with a family of protein kinases that control cell cycle progression. |
| 1343 | 10471535 | In the present study, we investigated the effects of TGF-beta1 on cyclin D1 expression and activity in COLO-357 human pancreatic cancer cells. |
| 1344 | 10471535 | TGF-beta1 increased cyclin D1 mRNA and protein levels. |
| 1345 | 10471535 | Despite its stimulatory effects on cyclin D1 levels, TGF-beta1 inhibited cyclin D1-associated kinase activity and the growth of COLO-357 cells. |
| 1346 | 10471535 | Furthermore, suppression of cyclin D1 expression with a cyclin D1 antisense cDNA resulted in loss of TGF-beta1-mediated growth inhibition in association with reduced induction of cyclin D1, p21(C)(ip)(1) and plasminogen activator inhibitor-1 (PAI-1). |
| 1347 | 10471535 | TGF-beta-1 up-regulates cyclin D1 expression in COLO-357 cells, whereas suppression of cyclin D1 levels is associated with down-regulation of the type I TGF-beta receptor. |
| 1348 | 10471535 | Transforming growth factor-beta1 (TGF-beta1) inhibits cell growth in susceptible cells by interacting with a family of protein kinases that control cell cycle progression. |
| 1349 | 10471535 | In the present study, we investigated the effects of TGF-beta1 on cyclin D1 expression and activity in COLO-357 human pancreatic cancer cells. |
| 1350 | 10471535 | TGF-beta1 increased cyclin D1 mRNA and protein levels. |
| 1351 | 10471535 | Despite its stimulatory effects on cyclin D1 levels, TGF-beta1 inhibited cyclin D1-associated kinase activity and the growth of COLO-357 cells. |
| 1352 | 10471535 | Furthermore, suppression of cyclin D1 expression with a cyclin D1 antisense cDNA resulted in loss of TGF-beta1-mediated growth inhibition in association with reduced induction of cyclin D1, p21(C)(ip)(1) and plasminogen activator inhibitor-1 (PAI-1). |
| 1353 | 10471535 | TGF-beta-1 up-regulates cyclin D1 expression in COLO-357 cells, whereas suppression of cyclin D1 levels is associated with down-regulation of the type I TGF-beta receptor. |
| 1354 | 10471535 | Transforming growth factor-beta1 (TGF-beta1) inhibits cell growth in susceptible cells by interacting with a family of protein kinases that control cell cycle progression. |
| 1355 | 10471535 | In the present study, we investigated the effects of TGF-beta1 on cyclin D1 expression and activity in COLO-357 human pancreatic cancer cells. |
| 1356 | 10471535 | TGF-beta1 increased cyclin D1 mRNA and protein levels. |
| 1357 | 10471535 | Despite its stimulatory effects on cyclin D1 levels, TGF-beta1 inhibited cyclin D1-associated kinase activity and the growth of COLO-357 cells. |
| 1358 | 10471535 | Furthermore, suppression of cyclin D1 expression with a cyclin D1 antisense cDNA resulted in loss of TGF-beta1-mediated growth inhibition in association with reduced induction of cyclin D1, p21(C)(ip)(1) and plasminogen activator inhibitor-1 (PAI-1). |
| 1359 | 10471535 | TGF-beta-1 up-regulates cyclin D1 expression in COLO-357 cells, whereas suppression of cyclin D1 levels is associated with down-regulation of the type I TGF-beta receptor. |
| 1360 | 10471535 | Transforming growth factor-beta1 (TGF-beta1) inhibits cell growth in susceptible cells by interacting with a family of protein kinases that control cell cycle progression. |
| 1361 | 10471535 | In the present study, we investigated the effects of TGF-beta1 on cyclin D1 expression and activity in COLO-357 human pancreatic cancer cells. |
| 1362 | 10471535 | TGF-beta1 increased cyclin D1 mRNA and protein levels. |
| 1363 | 10471535 | Despite its stimulatory effects on cyclin D1 levels, TGF-beta1 inhibited cyclin D1-associated kinase activity and the growth of COLO-357 cells. |
| 1364 | 10471535 | Furthermore, suppression of cyclin D1 expression with a cyclin D1 antisense cDNA resulted in loss of TGF-beta1-mediated growth inhibition in association with reduced induction of cyclin D1, p21(C)(ip)(1) and plasminogen activator inhibitor-1 (PAI-1). |
| 1365 | 10480600 | Insulin B-chain reactive CD4+ regulatory T-cells induced by oral insulin treatment protect from type 1 diabetes by blocking the cytokine secretion and pancreatic infiltration of diabetogenic effector T-cells. |
| 1366 | 10480600 | We demonstrate that oral insulin feeding of NOD mice induces the function of insulin B-chain reactive CD4+ regulatory T-cells, which compete with diabetogenic effector T-cells for the recognition of insulin in NOD.Scid recipient mice. |
| 1367 | 10480600 | These effector T-cells become deprived of interleukin (IL)-2 and interferon (IFN)-gamma and are unable to expand and migrate to the pancreas. |
| 1368 | 10480600 | Type 1 diabetes-protective splenic regulatory T-cells secrete relatively little transforming growth factor (TGF)-beta1, suggesting that TGF-beta may not contribute to the inactivation of effector T-cells in NOD.Scid recipients. |
| 1369 | 10484060 | Regulation of transforming growth factor-beta, basic fibroblast growth factor, and vascular endothelial cell growth factor mRNA in peripheral blood leukocytes in patients with diabetic retinopathy. |
| 1370 | 10484060 | In the present study, we examined the effect of glucose concentration on the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta (TGF-beta) mRNA using reverse transcriptase-polymerase chain reaction (RT-betaCR) in normal healthy leukocytes in vitro and in leukocytes from patients with type 1 diabetes mellitus. |
| 1371 | 10484060 | In vitro, the level of TGF-beta mRNA was altered in response to the glucose concentration (maximum at 10 mmol/L), while bFGF mRNA remained relatively constant and VEGF mRNA varied with no clear correlation with the glucose concentration. |
| 1372 | 10484060 | Leukocytes from type 1 patients showed no difference in bFGF or TGF-beta mRNA levels compared with age-matched healthy controls. |
| 1373 | 10484060 | Regulation of transforming growth factor-beta, basic fibroblast growth factor, and vascular endothelial cell growth factor mRNA in peripheral blood leukocytes in patients with diabetic retinopathy. |
| 1374 | 10484060 | In the present study, we examined the effect of glucose concentration on the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta (TGF-beta) mRNA using reverse transcriptase-polymerase chain reaction (RT-betaCR) in normal healthy leukocytes in vitro and in leukocytes from patients with type 1 diabetes mellitus. |
| 1375 | 10484060 | In vitro, the level of TGF-beta mRNA was altered in response to the glucose concentration (maximum at 10 mmol/L), while bFGF mRNA remained relatively constant and VEGF mRNA varied with no clear correlation with the glucose concentration. |
| 1376 | 10484060 | Leukocytes from type 1 patients showed no difference in bFGF or TGF-beta mRNA levels compared with age-matched healthy controls. |
| 1377 | 10484060 | Regulation of transforming growth factor-beta, basic fibroblast growth factor, and vascular endothelial cell growth factor mRNA in peripheral blood leukocytes in patients with diabetic retinopathy. |
| 1378 | 10484060 | In the present study, we examined the effect of glucose concentration on the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta (TGF-beta) mRNA using reverse transcriptase-polymerase chain reaction (RT-betaCR) in normal healthy leukocytes in vitro and in leukocytes from patients with type 1 diabetes mellitus. |
| 1379 | 10484060 | In vitro, the level of TGF-beta mRNA was altered in response to the glucose concentration (maximum at 10 mmol/L), while bFGF mRNA remained relatively constant and VEGF mRNA varied with no clear correlation with the glucose concentration. |
| 1380 | 10484060 | Leukocytes from type 1 patients showed no difference in bFGF or TGF-beta mRNA levels compared with age-matched healthy controls. |
| 1381 | 10484060 | Regulation of transforming growth factor-beta, basic fibroblast growth factor, and vascular endothelial cell growth factor mRNA in peripheral blood leukocytes in patients with diabetic retinopathy. |
| 1382 | 10484060 | In the present study, we examined the effect of glucose concentration on the expression of vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), and transforming growth factor-beta (TGF-beta) mRNA using reverse transcriptase-polymerase chain reaction (RT-betaCR) in normal healthy leukocytes in vitro and in leukocytes from patients with type 1 diabetes mellitus. |
| 1383 | 10484060 | In vitro, the level of TGF-beta mRNA was altered in response to the glucose concentration (maximum at 10 mmol/L), while bFGF mRNA remained relatively constant and VEGF mRNA varied with no clear correlation with the glucose concentration. |
| 1384 | 10484060 | Leukocytes from type 1 patients showed no difference in bFGF or TGF-beta mRNA levels compared with age-matched healthy controls. |
| 1385 | 10498890 | The TGF-beta signaling inhibitor Smad7 enhances tumorigenicity in pancreatic cancer. |
| 1386 | 10498890 | Activated TbetaRI then mediates TGF-beta signals by inducing the phosphorylation of Smad2 and/or Smad3, which separately hetetorodimerize with Smad4 and translocate to the nucleus. |
| 1387 | 10498890 | Phosphorylation of Smad2/Smad3 by activated TbetaRI is inhibited by two newly discovered members of the Smad family, Smad6 and Smad7. |
| 1388 | 10498890 | Stable transfection of COLO-357 human pancreatic cancer cells with a full-length Smad7 construct leads to complete loss of the growth inhibitory response to TGF-beta1, without altering TGF-beta1-mediated induction of PAI-I. |
| 1389 | 10498890 | The TGF-beta signaling inhibitor Smad7 enhances tumorigenicity in pancreatic cancer. |
| 1390 | 10498890 | Activated TbetaRI then mediates TGF-beta signals by inducing the phosphorylation of Smad2 and/or Smad3, which separately hetetorodimerize with Smad4 and translocate to the nucleus. |
| 1391 | 10498890 | Phosphorylation of Smad2/Smad3 by activated TbetaRI is inhibited by two newly discovered members of the Smad family, Smad6 and Smad7. |
| 1392 | 10498890 | Stable transfection of COLO-357 human pancreatic cancer cells with a full-length Smad7 construct leads to complete loss of the growth inhibitory response to TGF-beta1, without altering TGF-beta1-mediated induction of PAI-I. |
| 1393 | 10498890 | The TGF-beta signaling inhibitor Smad7 enhances tumorigenicity in pancreatic cancer. |
| 1394 | 10498890 | Activated TbetaRI then mediates TGF-beta signals by inducing the phosphorylation of Smad2 and/or Smad3, which separately hetetorodimerize with Smad4 and translocate to the nucleus. |
| 1395 | 10498890 | Phosphorylation of Smad2/Smad3 by activated TbetaRI is inhibited by two newly discovered members of the Smad family, Smad6 and Smad7. |
| 1396 | 10498890 | Stable transfection of COLO-357 human pancreatic cancer cells with a full-length Smad7 construct leads to complete loss of the growth inhibitory response to TGF-beta1, without altering TGF-beta1-mediated induction of PAI-I. |
| 1397 | 10512375 | Because angiotensin II (AII) is involved in the pathogenesis of diabetic nephropathy, the present studies were performed to determine if AII mediates glucose-induced 1) inhibition of mesangial collagenase activity, 2) mesangial matrix accumulation, and 3) in-crease in transforming growth factor (TGF)-beta1 secretion in mesangial cells. |
| 1398 | 10512375 | Exposure of mesangial cells to 30 mmol/l glucose (high glucose) vs. 5 mmol/glucose (normal glucose) for 5 days resulted in a significant decrease in collagenase activity (25%) that was normalized by 10(-4) mol/l losartan, a type 1 angiotensin II (AT1) receptor antagonist. |
| 1399 | 10512375 | Also, AII decreased collagenase (MMP-2) levels but stimulated TGF-beta1 secretion in mesangial cells. |
| 1400 | 10512377 | Expression of the genes encoding several matrix proteins, including the laminin gamma1 and beta1 subunits, is increased in glomeruli or renal cortex from diabetic animals or in mesangial cells cultured in high concentrations of glucose. |
| 1401 | 10512377 | Transforming growth factor (TGF)-beta1 and IGF-1 have been implicated as mediators of this response. |
| 1402 | 10512377 | In the present study, we assessed the influence of high glucose concentrations and the roles of TGF-beta1 and IGF-1 in the regulation of laminin C1 gene expression in cultured mesangial cells. |
| 1403 | 10512377 | IGF-1 also increased laminin C1 mRNA abundance in RMC or MES-13 cells, whereas TGF-beta1 was without effect. |
| 1404 | 10512377 | Moreover, neutralizing antibody to TGF-beta or to IGF-1 receptor did not suppress increases in laminin C1 promoter activity induced by culture of stable integrants in high glucose. |
| 1405 | 10512377 | The ability of high glucose concentrations and IGF-1 to increase laminin C1 promoter activity in cultured mesangial cells, and the suppression of glucose actions by the NO donor SNAP, provide potential mechanisms whereby the synthesis of the laminin gamma1 chain may be regulated in the glomerulus in diabetes. |
| 1406 | 10512377 | In this regard, TGF-beta and protein kinase C were not implicated as mediators of the effect of high glucose on laminin C1 promoter activity. |
| 1407 | 10512377 | Expression of the genes encoding several matrix proteins, including the laminin gamma1 and beta1 subunits, is increased in glomeruli or renal cortex from diabetic animals or in mesangial cells cultured in high concentrations of glucose. |
| 1408 | 10512377 | Transforming growth factor (TGF)-beta1 and IGF-1 have been implicated as mediators of this response. |
| 1409 | 10512377 | In the present study, we assessed the influence of high glucose concentrations and the roles of TGF-beta1 and IGF-1 in the regulation of laminin C1 gene expression in cultured mesangial cells. |
| 1410 | 10512377 | IGF-1 also increased laminin C1 mRNA abundance in RMC or MES-13 cells, whereas TGF-beta1 was without effect. |
| 1411 | 10512377 | Moreover, neutralizing antibody to TGF-beta or to IGF-1 receptor did not suppress increases in laminin C1 promoter activity induced by culture of stable integrants in high glucose. |
| 1412 | 10512377 | The ability of high glucose concentrations and IGF-1 to increase laminin C1 promoter activity in cultured mesangial cells, and the suppression of glucose actions by the NO donor SNAP, provide potential mechanisms whereby the synthesis of the laminin gamma1 chain may be regulated in the glomerulus in diabetes. |
| 1413 | 10512377 | In this regard, TGF-beta and protein kinase C were not implicated as mediators of the effect of high glucose on laminin C1 promoter activity. |
| 1414 | 10512377 | Expression of the genes encoding several matrix proteins, including the laminin gamma1 and beta1 subunits, is increased in glomeruli or renal cortex from diabetic animals or in mesangial cells cultured in high concentrations of glucose. |
| 1415 | 10512377 | Transforming growth factor (TGF)-beta1 and IGF-1 have been implicated as mediators of this response. |
| 1416 | 10512377 | In the present study, we assessed the influence of high glucose concentrations and the roles of TGF-beta1 and IGF-1 in the regulation of laminin C1 gene expression in cultured mesangial cells. |
| 1417 | 10512377 | IGF-1 also increased laminin C1 mRNA abundance in RMC or MES-13 cells, whereas TGF-beta1 was without effect. |
| 1418 | 10512377 | Moreover, neutralizing antibody to TGF-beta or to IGF-1 receptor did not suppress increases in laminin C1 promoter activity induced by culture of stable integrants in high glucose. |
| 1419 | 10512377 | The ability of high glucose concentrations and IGF-1 to increase laminin C1 promoter activity in cultured mesangial cells, and the suppression of glucose actions by the NO donor SNAP, provide potential mechanisms whereby the synthesis of the laminin gamma1 chain may be regulated in the glomerulus in diabetes. |
| 1420 | 10512377 | In this regard, TGF-beta and protein kinase C were not implicated as mediators of the effect of high glucose on laminin C1 promoter activity. |
| 1421 | 10512377 | Expression of the genes encoding several matrix proteins, including the laminin gamma1 and beta1 subunits, is increased in glomeruli or renal cortex from diabetic animals or in mesangial cells cultured in high concentrations of glucose. |
| 1422 | 10512377 | Transforming growth factor (TGF)-beta1 and IGF-1 have been implicated as mediators of this response. |
| 1423 | 10512377 | In the present study, we assessed the influence of high glucose concentrations and the roles of TGF-beta1 and IGF-1 in the regulation of laminin C1 gene expression in cultured mesangial cells. |
| 1424 | 10512377 | IGF-1 also increased laminin C1 mRNA abundance in RMC or MES-13 cells, whereas TGF-beta1 was without effect. |
| 1425 | 10512377 | Moreover, neutralizing antibody to TGF-beta or to IGF-1 receptor did not suppress increases in laminin C1 promoter activity induced by culture of stable integrants in high glucose. |
| 1426 | 10512377 | The ability of high glucose concentrations and IGF-1 to increase laminin C1 promoter activity in cultured mesangial cells, and the suppression of glucose actions by the NO donor SNAP, provide potential mechanisms whereby the synthesis of the laminin gamma1 chain may be regulated in the glomerulus in diabetes. |
| 1427 | 10512377 | In this regard, TGF-beta and protein kinase C were not implicated as mediators of the effect of high glucose on laminin C1 promoter activity. |
| 1428 | 10526261 | Depot-specific release of leptin from subcutaneous and omental adipocytes in suspension culture: effect of tumor necrosis factor-alpha and transforming growth factor-beta1. |
| 1429 | 10561136 | Captopril-induced reduction of serum levels of transforming growth factor-beta1 correlates with long-term renoprotection in insulin-dependent diabetic patients. |
| 1430 | 10561136 | Because angiotensin II is known to stimulate the prosclerotic cytokine, transforming growth factor-beta (TGF-beta), we postulated that the renoprotective effect may be due to inhibition of TGF-beta1 production. |
| 1431 | 10561136 | Captopril-induced reduction of serum levels of transforming growth factor-beta1 correlates with long-term renoprotection in insulin-dependent diabetic patients. |
| 1432 | 10561136 | Because angiotensin II is known to stimulate the prosclerotic cytokine, transforming growth factor-beta (TGF-beta), we postulated that the renoprotective effect may be due to inhibition of TGF-beta1 production. |
| 1433 | 10564565 | Immunohistochemical localization showed an increase in transforming growth factor-beta1 in curcumin-treated wounds compared to controls. |
| 1434 | 10564565 | Enhanced transforming growth factor-beta1 mRNA expression in treated wounds was confirmed by in situ hybridization, and laser scan cytometry. |
| 1435 | 10564565 | Immunohistochemical localization showed an increase in transforming growth factor-beta1 in curcumin-treated wounds compared to controls. |
| 1436 | 10564565 | Enhanced transforming growth factor-beta1 mRNA expression in treated wounds was confirmed by in situ hybridization, and laser scan cytometry. |
| 1437 | 10570081 | GLUT1 and TGF-beta: the link between hyperglycaemia and diabetic nephropathy. |
| 1438 | 10570081 | Recent experimental work implicates transforming growth factor-beta (TGF-beta) as an aetiologic mediator of diabetic nephropathy and the ubiquitous glucose transporter GLUT1 as an important permissive factor for the tissue injury caused by hyperglycaemia. |
| 1439 | 10570081 | Treatment of rat mesangial cells with TGF-beta up-regulates GLUT1 mRNA and protein levels and significantly increases glucose uptake. |
| 1440 | 10570081 | Thus, TGF-beta and GLUT1, two proteins that are up-regulated in glomerular mesangial cells in a hyperglycaemic milieu, can influence the expression of one another. |
| 1441 | 10570081 | GLUT1 and TGF-beta: the link between hyperglycaemia and diabetic nephropathy. |
| 1442 | 10570081 | Recent experimental work implicates transforming growth factor-beta (TGF-beta) as an aetiologic mediator of diabetic nephropathy and the ubiquitous glucose transporter GLUT1 as an important permissive factor for the tissue injury caused by hyperglycaemia. |
| 1443 | 10570081 | Treatment of rat mesangial cells with TGF-beta up-regulates GLUT1 mRNA and protein levels and significantly increases glucose uptake. |
| 1444 | 10570081 | Thus, TGF-beta and GLUT1, two proteins that are up-regulated in glomerular mesangial cells in a hyperglycaemic milieu, can influence the expression of one another. |
| 1445 | 10570081 | GLUT1 and TGF-beta: the link between hyperglycaemia and diabetic nephropathy. |
| 1446 | 10570081 | Recent experimental work implicates transforming growth factor-beta (TGF-beta) as an aetiologic mediator of diabetic nephropathy and the ubiquitous glucose transporter GLUT1 as an important permissive factor for the tissue injury caused by hyperglycaemia. |
| 1447 | 10570081 | Treatment of rat mesangial cells with TGF-beta up-regulates GLUT1 mRNA and protein levels and significantly increases glucose uptake. |
| 1448 | 10570081 | Thus, TGF-beta and GLUT1, two proteins that are up-regulated in glomerular mesangial cells in a hyperglycaemic milieu, can influence the expression of one another. |
| 1449 | 10570081 | GLUT1 and TGF-beta: the link between hyperglycaemia and diabetic nephropathy. |
| 1450 | 10570081 | Recent experimental work implicates transforming growth factor-beta (TGF-beta) as an aetiologic mediator of diabetic nephropathy and the ubiquitous glucose transporter GLUT1 as an important permissive factor for the tissue injury caused by hyperglycaemia. |
| 1451 | 10570081 | Treatment of rat mesangial cells with TGF-beta up-regulates GLUT1 mRNA and protein levels and significantly increases glucose uptake. |
| 1452 | 10570081 | Thus, TGF-beta and GLUT1, two proteins that are up-regulated in glomerular mesangial cells in a hyperglycaemic milieu, can influence the expression of one another. |
| 1453 | 10571771 | On exposure to glucose, proximal tubular cells elaborate vasoactive hormones, including angiotensin II and injurious cytokines such as transforming growth factor-beta (TGF-beta), as well as extracellular matrix proteins. |
| 1454 | 10571771 | In turn, angiotensin II may further increase TGF-beta expression in both proximal tubular and interstitial cells, thus amplifying the stimulus to fibrogenesis in the renal tubulointerstitium. |
| 1455 | 10571771 | On exposure to glucose, proximal tubular cells elaborate vasoactive hormones, including angiotensin II and injurious cytokines such as transforming growth factor-beta (TGF-beta), as well as extracellular matrix proteins. |
| 1456 | 10571771 | In turn, angiotensin II may further increase TGF-beta expression in both proximal tubular and interstitial cells, thus amplifying the stimulus to fibrogenesis in the renal tubulointerstitium. |
| 1457 | 10571774 | Role for transforming growth factor-beta1 in alport renal disease progression. |
| 1458 | 10600653 | We also examined the relationship between vitreous concentrations of hHGF and transforming growth factor-beta(2) (TGF-beta(2)), the predominant TGF-beta isoform in the vitreous, in 14 patients with PDR. |
| 1459 | 10600653 | Vitreous hHGF concentrations were directly proportional to vitreous concentrations of latent TGF-beta(2) (r=0. 831; P=0.0002), but inversely proportional to vitreous concentrations of active TGF-beta(2) (r=0.495; P=0.072), which inhibits hHGF production. |
| 1460 | 10600653 | A decreased conversion of latent into active TGF-beta(2) in ocular disorders such as PDR is likely to result in an increased concentration of hHGF in the vitreous. |
| 1461 | 10600653 | We also examined the relationship between vitreous concentrations of hHGF and transforming growth factor-beta(2) (TGF-beta(2)), the predominant TGF-beta isoform in the vitreous, in 14 patients with PDR. |
| 1462 | 10600653 | Vitreous hHGF concentrations were directly proportional to vitreous concentrations of latent TGF-beta(2) (r=0. 831; P=0.0002), but inversely proportional to vitreous concentrations of active TGF-beta(2) (r=0.495; P=0.072), which inhibits hHGF production. |
| 1463 | 10600653 | A decreased conversion of latent into active TGF-beta(2) in ocular disorders such as PDR is likely to result in an increased concentration of hHGF in the vitreous. |
| 1464 | 10600653 | We also examined the relationship between vitreous concentrations of hHGF and transforming growth factor-beta(2) (TGF-beta(2)), the predominant TGF-beta isoform in the vitreous, in 14 patients with PDR. |
| 1465 | 10600653 | Vitreous hHGF concentrations were directly proportional to vitreous concentrations of latent TGF-beta(2) (r=0. 831; P=0.0002), but inversely proportional to vitreous concentrations of active TGF-beta(2) (r=0.495; P=0.072), which inhibits hHGF production. |
| 1466 | 10600653 | A decreased conversion of latent into active TGF-beta(2) in ocular disorders such as PDR is likely to result in an increased concentration of hHGF in the vitreous. |
| 1467 | 10616837 | Connective tissue growth factor (CTGF) is a peptide secreted by cultured endothelial cells and fibroblasts when stimulated by transforming growth factor-beta (TGF-beta), and is overexpressed during fibrotic processes in coronary arteries and in skin. |
| 1468 | 10616837 | Exposure of MC to recombinant human CTGF significantly increased fibronectin and collagen type I production. |
| 1469 | 10616837 | Exposure of MC to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in diabetic glomerulosclerosis, markedly induced the expression of CTGF transcripts, while recombinant human CTGF was able to autoinduce its own expression. |
| 1470 | 10616837 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta-neutralizing antibody blocked this stimulation. |
| 1471 | 10616837 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation and progressive glomerulosclerosis, acting downstream of TGF-beta. |
| 1472 | 10616837 | Connective tissue growth factor (CTGF) is a peptide secreted by cultured endothelial cells and fibroblasts when stimulated by transforming growth factor-beta (TGF-beta), and is overexpressed during fibrotic processes in coronary arteries and in skin. |
| 1473 | 10616837 | Exposure of MC to recombinant human CTGF significantly increased fibronectin and collagen type I production. |
| 1474 | 10616837 | Exposure of MC to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in diabetic glomerulosclerosis, markedly induced the expression of CTGF transcripts, while recombinant human CTGF was able to autoinduce its own expression. |
| 1475 | 10616837 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta-neutralizing antibody blocked this stimulation. |
| 1476 | 10616837 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation and progressive glomerulosclerosis, acting downstream of TGF-beta. |
| 1477 | 10616837 | Connective tissue growth factor (CTGF) is a peptide secreted by cultured endothelial cells and fibroblasts when stimulated by transforming growth factor-beta (TGF-beta), and is overexpressed during fibrotic processes in coronary arteries and in skin. |
| 1478 | 10616837 | Exposure of MC to recombinant human CTGF significantly increased fibronectin and collagen type I production. |
| 1479 | 10616837 | Exposure of MC to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in diabetic glomerulosclerosis, markedly induced the expression of CTGF transcripts, while recombinant human CTGF was able to autoinduce its own expression. |
| 1480 | 10616837 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta-neutralizing antibody blocked this stimulation. |
| 1481 | 10616837 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation and progressive glomerulosclerosis, acting downstream of TGF-beta. |
| 1482 | 10616837 | Connective tissue growth factor (CTGF) is a peptide secreted by cultured endothelial cells and fibroblasts when stimulated by transforming growth factor-beta (TGF-beta), and is overexpressed during fibrotic processes in coronary arteries and in skin. |
| 1483 | 10616837 | Exposure of MC to recombinant human CTGF significantly increased fibronectin and collagen type I production. |
| 1484 | 10616837 | Exposure of MC to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in diabetic glomerulosclerosis, markedly induced the expression of CTGF transcripts, while recombinant human CTGF was able to autoinduce its own expression. |
| 1485 | 10616837 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta-neutralizing antibody blocked this stimulation. |
| 1486 | 10616837 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation and progressive glomerulosclerosis, acting downstream of TGF-beta. |
| 1487 | 10616843 | Lovastatin inhibits transforming growth factor-beta1 expression in diabetic rat glomeruli and cultured rat mesangial cells. |
| 1488 | 10616843 | In untreated diabetic rats, there were significant increases in blood glucose, urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression in the glomeruli compared with normal control rats treated with citrate buffer only. |
| 1489 | 10616843 | Treatment with lovastatin in diabetic rats significantly suppressed the increase in urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression despite high blood glucose levels. |
| 1490 | 10616843 | Lovastatin inhibits transforming growth factor-beta1 expression in diabetic rat glomeruli and cultured rat mesangial cells. |
| 1491 | 10616843 | In untreated diabetic rats, there were significant increases in blood glucose, urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression in the glomeruli compared with normal control rats treated with citrate buffer only. |
| 1492 | 10616843 | Treatment with lovastatin in diabetic rats significantly suppressed the increase in urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression despite high blood glucose levels. |
| 1493 | 10616843 | Lovastatin inhibits transforming growth factor-beta1 expression in diabetic rat glomeruli and cultured rat mesangial cells. |
| 1494 | 10616843 | In untreated diabetic rats, there were significant increases in blood glucose, urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression in the glomeruli compared with normal control rats treated with citrate buffer only. |
| 1495 | 10616843 | Treatment with lovastatin in diabetic rats significantly suppressed the increase in urine albumin excretion, kidney weight, glomerular volume, and TGF-beta1 mRNA expression despite high blood glucose levels. |
| 1496 | 10666411 | Compared with control animals, diabetic animals had significant increases in vessel weight, wall-to-lumen ratio, mast cell infiltration, extracellular matrix deposition, and gene expression of epidermal growth factor (EGF) and transforming growth factor-beta(1). |
| 1497 | 10666411 | Bosentan treatment significantly reduced mesenteric weight, wall-to-lumen ratio, mast cell infiltration, matrix deposition, and EGF mRNA but did not prevent the overexpression of transforming growth factor-beta(1) mRNA in diabetic rats. |
| 1498 | 10666411 | Compared with control animals, diabetic animals had significant increases in vessel weight, wall-to-lumen ratio, mast cell infiltration, extracellular matrix deposition, and gene expression of epidermal growth factor (EGF) and transforming growth factor-beta(1). |
| 1499 | 10666411 | Bosentan treatment significantly reduced mesenteric weight, wall-to-lumen ratio, mast cell infiltration, matrix deposition, and EGF mRNA but did not prevent the overexpression of transforming growth factor-beta(1) mRNA in diabetic rats. |
| 1500 | 10681646 | Analysis of proximal tubular fluid that was collected by nephron micropuncture indicates ultrafiltration of IGF-I, TGF-beta and HGF. |
| 1501 | 10681646 | TGF-beta and HGF cause increased expression and basolateral secretion of MCP-1 in proximal tubular and collecting duct cells. |
| 1502 | 10681646 | Analysis of proximal tubular fluid that was collected by nephron micropuncture indicates ultrafiltration of IGF-I, TGF-beta and HGF. |
| 1503 | 10681646 | TGF-beta and HGF cause increased expression and basolateral secretion of MCP-1 in proximal tubular and collecting duct cells. |
| 1504 | 10698197 | TGF-beta1, TGF-beta2, and receptor mRNA and protein were detected in the control nondiabetic kidney. |
| 1505 | 10698197 | It was found that dramatic and dynamic changes occur in all parts of the renal TGF-beta axis in both models of experimental diabetes, but TGF-beta2 and TGF-betaRII proteins were the predominant responsive element, particularly during the acute phase of disease. |
| 1506 | 10698197 | TGF-beta1, TGF-beta2, and receptor mRNA and protein were detected in the control nondiabetic kidney. |
| 1507 | 10698197 | It was found that dramatic and dynamic changes occur in all parts of the renal TGF-beta axis in both models of experimental diabetes, but TGF-beta2 and TGF-betaRII proteins were the predominant responsive element, particularly during the acute phase of disease. |
| 1508 | 10698958 | We have recently shown that a PKC beta inhibitor ameliorates not only early diabetes-induced glomerular dysfunction such as glomerular hyperfiltration and albuminuria, but also overexpression of glomerular mRNA for transforming growth factor beta1 (TGF-beta1) and extracellular matrix (ECM) proteins in streptozotocin-induced diabetic rats, a model for type 1 diabetes. |
| 1509 | 10698958 | Administration of a PKC beta inhibitor reduced urinary albumin excretion rates and inhibited glomerular PKC activation in diabetic db/db mice. |
| 1510 | 10698958 | Administration of a PKC beta inhibitor also prevented the mesangial expansion observed in diabetic db/db mice, possibly through attenuation of glomerular expression of TGF-beta and ECM proteins such as fibronectin and type IV collagen. |
| 1511 | 10698958 | We have recently shown that a PKC beta inhibitor ameliorates not only early diabetes-induced glomerular dysfunction such as glomerular hyperfiltration and albuminuria, but also overexpression of glomerular mRNA for transforming growth factor beta1 (TGF-beta1) and extracellular matrix (ECM) proteins in streptozotocin-induced diabetic rats, a model for type 1 diabetes. |
| 1512 | 10698958 | Administration of a PKC beta inhibitor reduced urinary albumin excretion rates and inhibited glomerular PKC activation in diabetic db/db mice. |
| 1513 | 10698958 | Administration of a PKC beta inhibitor also prevented the mesangial expansion observed in diabetic db/db mice, possibly through attenuation of glomerular expression of TGF-beta and ECM proteins such as fibronectin and type IV collagen. |
| 1514 | 10714434 | The analysis of in vitro transforming growth factor-beta1 (TGF-beta1) production by peripheral blood in overt and pre-clinical type 1 diabetes mellitus. |
| 1515 | 10714434 | The alterations of TGF-beta1 production are believed to contribute to the development of insulin-dependent diabetes mellitus (IDDM) in animal models as well as in humans. |
| 1516 | 10714434 | The aim of our study was to evaluate in vitro TGF-beta1 production by peripheral blood of newly diagnosed type 1 diabetes patients and subjects in the pre-clinical stage of the disease in comparison to healthy controls and relatives of IDDM patients with low genetic risk for diabetes development. |
| 1517 | 10714434 | In the first degree relatives HLA typing (for DR3, DR4 and DQB1*0602 alleles), measurements of anti-pancreatic antibodies (ICA, GADA, IA-2A, IAA) and intravenous glucose tolerance tests were performed. |
| 1518 | 10714434 | In the group of first degree relatives TGF-beta1 levels were highest in subjects with the presence of two or more pancreatic autoantibodies and/or with impaired insulin release in IVGTT, but lowest in relatives with protective DQB1*0602 alleles (P < 0.01). |
| 1519 | 10714434 | There was also a significant positive correlation between the TGF-beta1 levels and HbA1C in the IDDM subjects and first degree relatives (P < 0.03). |
| 1520 | 10714434 | The analysis of in vitro transforming growth factor-beta1 (TGF-beta1) production by peripheral blood in overt and pre-clinical type 1 diabetes mellitus. |
| 1521 | 10714434 | The alterations of TGF-beta1 production are believed to contribute to the development of insulin-dependent diabetes mellitus (IDDM) in animal models as well as in humans. |
| 1522 | 10714434 | The aim of our study was to evaluate in vitro TGF-beta1 production by peripheral blood of newly diagnosed type 1 diabetes patients and subjects in the pre-clinical stage of the disease in comparison to healthy controls and relatives of IDDM patients with low genetic risk for diabetes development. |
| 1523 | 10714434 | In the first degree relatives HLA typing (for DR3, DR4 and DQB1*0602 alleles), measurements of anti-pancreatic antibodies (ICA, GADA, IA-2A, IAA) and intravenous glucose tolerance tests were performed. |
| 1524 | 10714434 | In the group of first degree relatives TGF-beta1 levels were highest in subjects with the presence of two or more pancreatic autoantibodies and/or with impaired insulin release in IVGTT, but lowest in relatives with protective DQB1*0602 alleles (P < 0.01). |
| 1525 | 10714434 | There was also a significant positive correlation between the TGF-beta1 levels and HbA1C in the IDDM subjects and first degree relatives (P < 0.03). |
| 1526 | 10714434 | The analysis of in vitro transforming growth factor-beta1 (TGF-beta1) production by peripheral blood in overt and pre-clinical type 1 diabetes mellitus. |
| 1527 | 10714434 | The alterations of TGF-beta1 production are believed to contribute to the development of insulin-dependent diabetes mellitus (IDDM) in animal models as well as in humans. |
| 1528 | 10714434 | The aim of our study was to evaluate in vitro TGF-beta1 production by peripheral blood of newly diagnosed type 1 diabetes patients and subjects in the pre-clinical stage of the disease in comparison to healthy controls and relatives of IDDM patients with low genetic risk for diabetes development. |
| 1529 | 10714434 | In the first degree relatives HLA typing (for DR3, DR4 and DQB1*0602 alleles), measurements of anti-pancreatic antibodies (ICA, GADA, IA-2A, IAA) and intravenous glucose tolerance tests were performed. |
| 1530 | 10714434 | In the group of first degree relatives TGF-beta1 levels were highest in subjects with the presence of two or more pancreatic autoantibodies and/or with impaired insulin release in IVGTT, but lowest in relatives with protective DQB1*0602 alleles (P < 0.01). |
| 1531 | 10714434 | There was also a significant positive correlation between the TGF-beta1 levels and HbA1C in the IDDM subjects and first degree relatives (P < 0.03). |
| 1532 | 10714434 | The analysis of in vitro transforming growth factor-beta1 (TGF-beta1) production by peripheral blood in overt and pre-clinical type 1 diabetes mellitus. |
| 1533 | 10714434 | The alterations of TGF-beta1 production are believed to contribute to the development of insulin-dependent diabetes mellitus (IDDM) in animal models as well as in humans. |
| 1534 | 10714434 | The aim of our study was to evaluate in vitro TGF-beta1 production by peripheral blood of newly diagnosed type 1 diabetes patients and subjects in the pre-clinical stage of the disease in comparison to healthy controls and relatives of IDDM patients with low genetic risk for diabetes development. |
| 1535 | 10714434 | In the first degree relatives HLA typing (for DR3, DR4 and DQB1*0602 alleles), measurements of anti-pancreatic antibodies (ICA, GADA, IA-2A, IAA) and intravenous glucose tolerance tests were performed. |
| 1536 | 10714434 | In the group of first degree relatives TGF-beta1 levels were highest in subjects with the presence of two or more pancreatic autoantibodies and/or with impaired insulin release in IVGTT, but lowest in relatives with protective DQB1*0602 alleles (P < 0.01). |
| 1537 | 10714434 | There was also a significant positive correlation between the TGF-beta1 levels and HbA1C in the IDDM subjects and first degree relatives (P < 0.03). |
| 1538 | 10714434 | The analysis of in vitro transforming growth factor-beta1 (TGF-beta1) production by peripheral blood in overt and pre-clinical type 1 diabetes mellitus. |
| 1539 | 10714434 | The alterations of TGF-beta1 production are believed to contribute to the development of insulin-dependent diabetes mellitus (IDDM) in animal models as well as in humans. |
| 1540 | 10714434 | The aim of our study was to evaluate in vitro TGF-beta1 production by peripheral blood of newly diagnosed type 1 diabetes patients and subjects in the pre-clinical stage of the disease in comparison to healthy controls and relatives of IDDM patients with low genetic risk for diabetes development. |
| 1541 | 10714434 | In the first degree relatives HLA typing (for DR3, DR4 and DQB1*0602 alleles), measurements of anti-pancreatic antibodies (ICA, GADA, IA-2A, IAA) and intravenous glucose tolerance tests were performed. |
| 1542 | 10714434 | In the group of first degree relatives TGF-beta1 levels were highest in subjects with the presence of two or more pancreatic autoantibodies and/or with impaired insulin release in IVGTT, but lowest in relatives with protective DQB1*0602 alleles (P < 0.01). |
| 1543 | 10714434 | There was also a significant positive correlation between the TGF-beta1 levels and HbA1C in the IDDM subjects and first degree relatives (P < 0.03). |
| 1544 | 10726914 | Activation of transforming growth factor-beta1 in diabetic kidney disease. |
| 1545 | 10726914 | The aim of this study was to investigate whether circulating transforming growth factor beta 1 (TGF-beta1) and tumor necrosis factor alpha (TNF-alpha) are associated with diabetic kidney disease. |
| 1546 | 10726914 | Serum levels of active and total TGF-beta1 and TNF-alpha were measured in type 2 diabetic patients with nephropathy (n = 23) or without (n = 35) and normoglycemic controls (n = 12). |
| 1547 | 10726914 | Active TGF-beta1 concentrations were correlated with urinary albumin excretion (r = .49, P < .003) and serum creatinine (r= .55, P < .01). |
| 1548 | 10726914 | Activation of transforming growth factor-beta1 in diabetic kidney disease. |
| 1549 | 10726914 | The aim of this study was to investigate whether circulating transforming growth factor beta 1 (TGF-beta1) and tumor necrosis factor alpha (TNF-alpha) are associated with diabetic kidney disease. |
| 1550 | 10726914 | Serum levels of active and total TGF-beta1 and TNF-alpha were measured in type 2 diabetic patients with nephropathy (n = 23) or without (n = 35) and normoglycemic controls (n = 12). |
| 1551 | 10726914 | Active TGF-beta1 concentrations were correlated with urinary albumin excretion (r = .49, P < .003) and serum creatinine (r= .55, P < .01). |
| 1552 | 10726914 | Activation of transforming growth factor-beta1 in diabetic kidney disease. |
| 1553 | 10726914 | The aim of this study was to investigate whether circulating transforming growth factor beta 1 (TGF-beta1) and tumor necrosis factor alpha (TNF-alpha) are associated with diabetic kidney disease. |
| 1554 | 10726914 | Serum levels of active and total TGF-beta1 and TNF-alpha were measured in type 2 diabetic patients with nephropathy (n = 23) or without (n = 35) and normoglycemic controls (n = 12). |
| 1555 | 10726914 | Active TGF-beta1 concentrations were correlated with urinary albumin excretion (r = .49, P < .003) and serum creatinine (r= .55, P < .01). |
| 1556 | 10726914 | Activation of transforming growth factor-beta1 in diabetic kidney disease. |
| 1557 | 10726914 | The aim of this study was to investigate whether circulating transforming growth factor beta 1 (TGF-beta1) and tumor necrosis factor alpha (TNF-alpha) are associated with diabetic kidney disease. |
| 1558 | 10726914 | Serum levels of active and total TGF-beta1 and TNF-alpha were measured in type 2 diabetic patients with nephropathy (n = 23) or without (n = 35) and normoglycemic controls (n = 12). |
| 1559 | 10726914 | Active TGF-beta1 concentrations were correlated with urinary albumin excretion (r = .49, P < .003) and serum creatinine (r= .55, P < .01). |
| 1560 | 10729385 | Medial SMC in OLETF rats expressed more platelet-derived growth factor (PDGF) beta-receptor and fibronectin at the protein level than those from control, Long-Evans Tokushima Otsuka (LETO) rats, not only after but also before the onset of diabetes mellitus. |
| 1561 | 10729385 | In in vitro culture system, fibronectin synthesis was stimulated by transforming growth factor-beta1(TGF-beta1) in SMC from OLETF rats, but not in those from LETO rats, suggesting that SMC from OLETF rats respond to TGF-beta1. |
| 1562 | 10744662 | Regulation by extracellular glucose concentration, cyclic mechanical strain, and transforming growth factor-beta1. |
| 1563 | 10744662 | We used cloning in silico coupled with polymerase chain reaction to demonstrate that IHG-2 is part of the 3'-untranslated region of gremlin, a member of the DAN family of secreted proteins that antagonize the bioactivities of members of the transforming growth factor (TGF)-beta superfamily. |
| 1564 | 10744662 | Mesangial cell gremlin mRNA levels were induced by high glucose, cyclic mechanical strain, and TGF-beta1 in vitro, and gremlin mRNA levels were elevated in the renal cortex of rats with streptozotocin-induced diabetic nephropathy in vivo. gremlin expression was observed in parallel with induction of bone morphogenetic protein-2 (BMP-2), a target for gremlin in models of cell differentiation. |
| 1565 | 10744662 | Regulation by extracellular glucose concentration, cyclic mechanical strain, and transforming growth factor-beta1. |
| 1566 | 10744662 | We used cloning in silico coupled with polymerase chain reaction to demonstrate that IHG-2 is part of the 3'-untranslated region of gremlin, a member of the DAN family of secreted proteins that antagonize the bioactivities of members of the transforming growth factor (TGF)-beta superfamily. |
| 1567 | 10744662 | Mesangial cell gremlin mRNA levels were induced by high glucose, cyclic mechanical strain, and TGF-beta1 in vitro, and gremlin mRNA levels were elevated in the renal cortex of rats with streptozotocin-induced diabetic nephropathy in vivo. gremlin expression was observed in parallel with induction of bone morphogenetic protein-2 (BMP-2), a target for gremlin in models of cell differentiation. |
| 1568 | 10746823 | Transcriptional regulation of transforming growth factor beta1 by glucose: investigation into the role of the hexosamine biosynthesis pathway. |
| 1569 | 10751215 | In experimental diabetic glomerular sclerosis, there is translocation of high-molecular-weight growth factors, namely, hepatocyte growth factor (HGF) and transforming growth factor (TGF)-beta, from plasma into tubular fluid, both of which act on tubular cells through apical membrane receptors. |
| 1570 | 10751215 | In the present studies, the hypothesis is examined that ultrafiltered HGF and TGF-beta induce increased expression of extracellular matrix (ECM) proteins directly in tubular cells, or induce increased expression of cytokines that may act on interstitial myofibroblasts. |
| 1571 | 10751215 | Incubation of cultured tubular cells with recombinant human (rh) TGF-beta modestly raises expression of collagen type III, but rhHGF dose dependently blocks expression of this ECM protein. |
| 1572 | 10751215 | Both growth factors raise fibronectin expression up to fourfold and increase expression of platelet-derived growth factor (PDGF)-BB up to sixfold, but not of fibroblast growth factor-2. |
| 1573 | 10751215 | In the presence of neutralizing antibodies that block actions of HGF and TGF-beta, diabetic rat glomerular ultrafiltrate fails to increase tubular cell PDGF-BB expression. |
| 1574 | 10751215 | The findings provide evidence for ultrafiltered HGF and TGF-beta to contribute to interstitial accumulation of ECM proteins by direct effects on tubular cells as well as indirect mechanisms, via PDGF-BB and its action on myofibroblasts. |
| 1575 | 10751215 | In experimental diabetic glomerular sclerosis, there is translocation of high-molecular-weight growth factors, namely, hepatocyte growth factor (HGF) and transforming growth factor (TGF)-beta, from plasma into tubular fluid, both of which act on tubular cells through apical membrane receptors. |
| 1576 | 10751215 | In the present studies, the hypothesis is examined that ultrafiltered HGF and TGF-beta induce increased expression of extracellular matrix (ECM) proteins directly in tubular cells, or induce increased expression of cytokines that may act on interstitial myofibroblasts. |
| 1577 | 10751215 | Incubation of cultured tubular cells with recombinant human (rh) TGF-beta modestly raises expression of collagen type III, but rhHGF dose dependently blocks expression of this ECM protein. |
| 1578 | 10751215 | Both growth factors raise fibronectin expression up to fourfold and increase expression of platelet-derived growth factor (PDGF)-BB up to sixfold, but not of fibroblast growth factor-2. |
| 1579 | 10751215 | In the presence of neutralizing antibodies that block actions of HGF and TGF-beta, diabetic rat glomerular ultrafiltrate fails to increase tubular cell PDGF-BB expression. |
| 1580 | 10751215 | The findings provide evidence for ultrafiltered HGF and TGF-beta to contribute to interstitial accumulation of ECM proteins by direct effects on tubular cells as well as indirect mechanisms, via PDGF-BB and its action on myofibroblasts. |
| 1581 | 10751215 | In experimental diabetic glomerular sclerosis, there is translocation of high-molecular-weight growth factors, namely, hepatocyte growth factor (HGF) and transforming growth factor (TGF)-beta, from plasma into tubular fluid, both of which act on tubular cells through apical membrane receptors. |
| 1582 | 10751215 | In the present studies, the hypothesis is examined that ultrafiltered HGF and TGF-beta induce increased expression of extracellular matrix (ECM) proteins directly in tubular cells, or induce increased expression of cytokines that may act on interstitial myofibroblasts. |
| 1583 | 10751215 | Incubation of cultured tubular cells with recombinant human (rh) TGF-beta modestly raises expression of collagen type III, but rhHGF dose dependently blocks expression of this ECM protein. |
| 1584 | 10751215 | Both growth factors raise fibronectin expression up to fourfold and increase expression of platelet-derived growth factor (PDGF)-BB up to sixfold, but not of fibroblast growth factor-2. |
| 1585 | 10751215 | In the presence of neutralizing antibodies that block actions of HGF and TGF-beta, diabetic rat glomerular ultrafiltrate fails to increase tubular cell PDGF-BB expression. |
| 1586 | 10751215 | The findings provide evidence for ultrafiltered HGF and TGF-beta to contribute to interstitial accumulation of ECM proteins by direct effects on tubular cells as well as indirect mechanisms, via PDGF-BB and its action on myofibroblasts. |
| 1587 | 10751215 | In experimental diabetic glomerular sclerosis, there is translocation of high-molecular-weight growth factors, namely, hepatocyte growth factor (HGF) and transforming growth factor (TGF)-beta, from plasma into tubular fluid, both of which act on tubular cells through apical membrane receptors. |
| 1588 | 10751215 | In the present studies, the hypothesis is examined that ultrafiltered HGF and TGF-beta induce increased expression of extracellular matrix (ECM) proteins directly in tubular cells, or induce increased expression of cytokines that may act on interstitial myofibroblasts. |
| 1589 | 10751215 | Incubation of cultured tubular cells with recombinant human (rh) TGF-beta modestly raises expression of collagen type III, but rhHGF dose dependently blocks expression of this ECM protein. |
| 1590 | 10751215 | Both growth factors raise fibronectin expression up to fourfold and increase expression of platelet-derived growth factor (PDGF)-BB up to sixfold, but not of fibroblast growth factor-2. |
| 1591 | 10751215 | In the presence of neutralizing antibodies that block actions of HGF and TGF-beta, diabetic rat glomerular ultrafiltrate fails to increase tubular cell PDGF-BB expression. |
| 1592 | 10751215 | The findings provide evidence for ultrafiltered HGF and TGF-beta to contribute to interstitial accumulation of ECM proteins by direct effects on tubular cells as well as indirect mechanisms, via PDGF-BB and its action on myofibroblasts. |
| 1593 | 10751224 | Because increased proximal tubular transforming growth factor- beta1 (TGF-beta1) expression may mediate diabetic renal hypertrophy, we investigated the effects of antisense TGF-beta1 ODN on the high-glucose-induced proximal tubular epithelial cell hypertrophy in tissue culture and on diabetic renal hypertrophy in vivo. |
| 1594 | 10751224 | Treatment of diabetic mice with antisense ODN partially but significantly decreased kidney TGF-beta1 protein levels and attenuated the increase in kidney weight and the alpha1(IV) collagen and fibronectin mRNAs. |
| 1595 | 10751224 | Because increased proximal tubular transforming growth factor- beta1 (TGF-beta1) expression may mediate diabetic renal hypertrophy, we investigated the effects of antisense TGF-beta1 ODN on the high-glucose-induced proximal tubular epithelial cell hypertrophy in tissue culture and on diabetic renal hypertrophy in vivo. |
| 1596 | 10751224 | Treatment of diabetic mice with antisense ODN partially but significantly decreased kidney TGF-beta1 protein levels and attenuated the increase in kidney weight and the alpha1(IV) collagen and fibronectin mRNAs. |
| 1597 | 10770198 | Troglitazone, a novel oral insulin sensitizer, normalizes increased plasma activity of plasminogen activator inhibitor type 1 (PAI-1) in hyperinsulinemic patients such as women with polycystic ovary syndrome and patients with type 2 diabetes mellitus. |
| 1598 | 10770198 | The accumulation depended on the concentration of troglitazone, but not that of insulin (known to stimulate PAI-1 synthesis). |
| 1599 | 10770198 | By contrast, in human aortic smooth muscle cells, 3 microg/mL troglitazone decreased basal PAI-1 expression by 23% (P = 0.037) and decreased transforming growth factor-beta-induced expression by 34% (P = 0.026). |
| 1600 | 10770198 | In human endothelial cells, PAI-1 was diminished by 32% (P < 0.001), whereas tissue-type plasminogen activator was unaffected. |
| 1601 | 10770268 | One of the primary mechanisms of active cellular suppression is via secretion of suppressive cytokines such as TGF-beta, IL-4, and IL-10 following antigen-specific triggering. |
| 1602 | 10770268 | TGF-beta is produced both by CD4+ and CD8+ GALT-derived T cells and is an important mediator of the active suppression component of oral tolerance. |
| 1603 | 10770268 | One of the primary mechanisms of active cellular suppression is via secretion of suppressive cytokines such as TGF-beta, IL-4, and IL-10 following antigen-specific triggering. |
| 1604 | 10770268 | TGF-beta is produced both by CD4+ and CD8+ GALT-derived T cells and is an important mediator of the active suppression component of oral tolerance. |
| 1605 | 10773106 | We have therefore studied the influence of IL-1beta on the local production and secretion of parathyroid hormone-related protein (PTHrP) and transforming growth factor-beta (TGF-beta) from normal human osteoblast-like cells (hOB cells). |
| 1606 | 10773106 | Using a quantitative PCR-assay following reverse transcription of RNA, in situ hybridization, and a two-site immunofluorometric assay for PTHrP, we demonstrate that IL-1beta in a dose- and time-dependent manner increases PTHrP-mRNA expression and PTHrP-protein secretion. |
| 1607 | 10773106 | In addition, IL-1beta decreased the TGF-beta protein concentration in conditioned medium. |
| 1608 | 10773106 | Our results suggest that the actions of IL-1beta on bone may be mediated by novel mechanisms involving both local increase of PTHrP, a potent stimulator of bone resorption, and a decrease of TGF-beta, an important anabolic and coupling factor for bone turnover. |
| 1609 | 10773106 | We have therefore studied the influence of IL-1beta on the local production and secretion of parathyroid hormone-related protein (PTHrP) and transforming growth factor-beta (TGF-beta) from normal human osteoblast-like cells (hOB cells). |
| 1610 | 10773106 | Using a quantitative PCR-assay following reverse transcription of RNA, in situ hybridization, and a two-site immunofluorometric assay for PTHrP, we demonstrate that IL-1beta in a dose- and time-dependent manner increases PTHrP-mRNA expression and PTHrP-protein secretion. |
| 1611 | 10773106 | In addition, IL-1beta decreased the TGF-beta protein concentration in conditioned medium. |
| 1612 | 10773106 | Our results suggest that the actions of IL-1beta on bone may be mediated by novel mechanisms involving both local increase of PTHrP, a potent stimulator of bone resorption, and a decrease of TGF-beta, an important anabolic and coupling factor for bone turnover. |
| 1613 | 10773106 | We have therefore studied the influence of IL-1beta on the local production and secretion of parathyroid hormone-related protein (PTHrP) and transforming growth factor-beta (TGF-beta) from normal human osteoblast-like cells (hOB cells). |
| 1614 | 10773106 | Using a quantitative PCR-assay following reverse transcription of RNA, in situ hybridization, and a two-site immunofluorometric assay for PTHrP, we demonstrate that IL-1beta in a dose- and time-dependent manner increases PTHrP-mRNA expression and PTHrP-protein secretion. |
| 1615 | 10773106 | In addition, IL-1beta decreased the TGF-beta protein concentration in conditioned medium. |
| 1616 | 10773106 | Our results suggest that the actions of IL-1beta on bone may be mediated by novel mechanisms involving both local increase of PTHrP, a potent stimulator of bone resorption, and a decrease of TGF-beta, an important anabolic and coupling factor for bone turnover. |
| 1617 | 10775572 | We recently demonstrated that alpha(v)beta(3) integrins are involved in the mechanisms of angiotensin II (Ang II)-induced DNA synthesis and collagen gel contractions in rat cardiac fibroblasts (CFBs), cellular mechanisms that are relevant for cardiac remodeling. |
| 1618 | 10775572 | The alpha(v)beta(3) integrin receptor expression was significantly increased (P<0.05) at the mRNA level after treatment with Ang II, transforming growth factor-beta(1) (TGF-beta(1)), and platelet-derived growth factor (PDGF) for 8 and 16 hours. |
| 1619 | 10775572 | The present study demonstrates that the expression of alpha(v)beta(3) integrin is augmented by Ang II, PDGF, and TGF-beta(1) in neonatal CFBs. |
| 1620 | 10775572 | We recently demonstrated that alpha(v)beta(3) integrins are involved in the mechanisms of angiotensin II (Ang II)-induced DNA synthesis and collagen gel contractions in rat cardiac fibroblasts (CFBs), cellular mechanisms that are relevant for cardiac remodeling. |
| 1621 | 10775572 | The alpha(v)beta(3) integrin receptor expression was significantly increased (P<0.05) at the mRNA level after treatment with Ang II, transforming growth factor-beta(1) (TGF-beta(1)), and platelet-derived growth factor (PDGF) for 8 and 16 hours. |
| 1622 | 10775572 | The present study demonstrates that the expression of alpha(v)beta(3) integrin is augmented by Ang II, PDGF, and TGF-beta(1) in neonatal CFBs. |
| 1623 | 10778531 | GLUT-4, tumour necrosis factor, essential fatty acids and daf-genes and their role in glucose homeostasis, insulin resistance, non-insulin dependent diabetes mellitus, and longevity. |
| 1624 | 10778531 | GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes seem to play an important and essential role in the maintenance of glucose homeostasis, and in the pathobiology of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 1625 | 10778531 | Daf-genes encode for proteins which are 35% identical to the human insulin receptor, a transforming growth factor-beta (TGF-beta) type signal and can also enhance the expression of superoxide dismutase (SOD). |
| 1626 | 10778531 | On the other hand, EFAs and their metabolites can increase the cell membrane fluidity and thus, enhance the expression of GLUT-4 and insulin receptors. |
| 1627 | 10778531 | In addition, EFAs can suppress TNF-alpha production and secretion and thus, are capable of reversing insulin resistance. |
| 1628 | 10778531 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 1629 | 10778531 | Hence, it is likely that there is a close interaction between GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin that may have relevance to the development of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 1630 | 10778531 | GLUT-4, tumour necrosis factor, essential fatty acids and daf-genes and their role in glucose homeostasis, insulin resistance, non-insulin dependent diabetes mellitus, and longevity. |
| 1631 | 10778531 | GLUT-4 receptor, tumor necrosis factor-alpha (TNF-alpha), essential fatty acids (EFAs) and their metabolites and daf-genes seem to play an important and essential role in the maintenance of glucose homeostasis, and in the pathobiology of obesity and non-insulin dependent diabetes mellitus (NIDDM). |
| 1632 | 10778531 | Daf-genes encode for proteins which are 35% identical to the human insulin receptor, a transforming growth factor-beta (TGF-beta) type signal and can also enhance the expression of superoxide dismutase (SOD). |
| 1633 | 10778531 | On the other hand, EFAs and their metabolites can increase the cell membrane fluidity and thus, enhance the expression of GLUT-4 and insulin receptors. |
| 1634 | 10778531 | In addition, EFAs can suppress TNF-alpha production and secretion and thus, are capable of reversing insulin resistance. |
| 1635 | 10778531 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 1636 | 10778531 | Hence, it is likely that there is a close interaction between GLUT-4, TNF-alpha, EFAs, daf-genes, melatonin and leptin that may have relevance to the development of insulin resistance, obesity, NIDDM, complications due to NIDDM, longevity and ageing. |
| 1637 | 10807596 | Stimulation of TGF-beta type II receptor by high glucose in mouse mesangial cells and in diabetic kidney. |
| 1638 | 10807596 | Cells grown in high glucose demonstrated increased responsiveness to a relatively small dose of exogenous TGF-beta(1) (0.5 ng/ml): [(3)H]proline incorporation and alpha(1)(IV) collagen mRNA were significantly greater in cells cultured in high than in normal glucose. |
| 1639 | 10807596 | Stimulation of TGF-beta type II receptor by high glucose in mouse mesangial cells and in diabetic kidney. |
| 1640 | 10807596 | Cells grown in high glucose demonstrated increased responsiveness to a relatively small dose of exogenous TGF-beta(1) (0.5 ng/ml): [(3)H]proline incorporation and alpha(1)(IV) collagen mRNA were significantly greater in cells cultured in high than in normal glucose. |
| 1641 | 10814778 | Hsp60 expression was found to be enhanced in response to cytokines as diverse as IL-1beta, TNF-alpha, IL-4, IL-6 and IL-10. |
| 1642 | 10814778 | Upregulation of hsp27, however, was primarily induced by immunoregulatory cytokines like IL-4, IL-6 and TGF-beta whereas alphaB-crystallin expression was found to be enhanced by the pro-inflammatory cytokine TNF-alpha only. |
| 1643 | 10830291 | Vascular endothelial growth factor and transforming growth factor-beta1 regulate the expression of insulin-like growth factor-binding protein-3, -4, and -5 in large vessel endothelial cells. |
| 1644 | 10830291 | We investigated the effect of diabetes-associated growth factors on the expression of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGFBPs) in cultured endothelial cells from bovine aorta. |
| 1645 | 10830291 | Vascular endothelial growth factor inhibited IGFBP-3 mRNA (P < 0.01) and protein expression and increased IGFBP-5 mRNA (P < 0.001) and protein. |
| 1646 | 10830291 | Transforming growth factor-beta1 inhibited IGFBP-3 (P < 0.01), IGFBP-4 (P < 0.01), and IGF-I mRNA expression, whereas at the protein level only IGFBP-3 was significantly decreased. |
| 1647 | 10830291 | IGF-I, insulin, or angiotensin II did not affect IGF-I or IGFBP mRNA expression. |
| 1648 | 10830291 | At the protein level, IGF-I clearly increased IGFBP-5 levels in conditioned medium. |
| 1649 | 10830291 | In conclusion, vascular endothelial growth factor and transforming growth factor-beta1 regulate IGFBP expression in bovine aortic endothelial cells. |
| 1650 | 10830291 | Vascular endothelial growth factor and transforming growth factor-beta1 regulate the expression of insulin-like growth factor-binding protein-3, -4, and -5 in large vessel endothelial cells. |
| 1651 | 10830291 | We investigated the effect of diabetes-associated growth factors on the expression of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGFBPs) in cultured endothelial cells from bovine aorta. |
| 1652 | 10830291 | Vascular endothelial growth factor inhibited IGFBP-3 mRNA (P < 0.01) and protein expression and increased IGFBP-5 mRNA (P < 0.001) and protein. |
| 1653 | 10830291 | Transforming growth factor-beta1 inhibited IGFBP-3 (P < 0.01), IGFBP-4 (P < 0.01), and IGF-I mRNA expression, whereas at the protein level only IGFBP-3 was significantly decreased. |
| 1654 | 10830291 | IGF-I, insulin, or angiotensin II did not affect IGF-I or IGFBP mRNA expression. |
| 1655 | 10830291 | At the protein level, IGF-I clearly increased IGFBP-5 levels in conditioned medium. |
| 1656 | 10830291 | In conclusion, vascular endothelial growth factor and transforming growth factor-beta1 regulate IGFBP expression in bovine aortic endothelial cells. |
| 1657 | 10830291 | Vascular endothelial growth factor and transforming growth factor-beta1 regulate the expression of insulin-like growth factor-binding protein-3, -4, and -5 in large vessel endothelial cells. |
| 1658 | 10830291 | We investigated the effect of diabetes-associated growth factors on the expression of insulin-like growth factor-I (IGF-I) and IGF-binding proteins (IGFBPs) in cultured endothelial cells from bovine aorta. |
| 1659 | 10830291 | Vascular endothelial growth factor inhibited IGFBP-3 mRNA (P < 0.01) and protein expression and increased IGFBP-5 mRNA (P < 0.001) and protein. |
| 1660 | 10830291 | Transforming growth factor-beta1 inhibited IGFBP-3 (P < 0.01), IGFBP-4 (P < 0.01), and IGF-I mRNA expression, whereas at the protein level only IGFBP-3 was significantly decreased. |
| 1661 | 10830291 | IGF-I, insulin, or angiotensin II did not affect IGF-I or IGFBP mRNA expression. |
| 1662 | 10830291 | At the protein level, IGF-I clearly increased IGFBP-5 levels in conditioned medium. |
| 1663 | 10830291 | In conclusion, vascular endothelial growth factor and transforming growth factor-beta1 regulate IGFBP expression in bovine aortic endothelial cells. |
| 1664 | 10831181 | Effect of tumor necrosis factor alpha and transforming growth factor beta 1 on plasminogen activator inhibitor-1 secretion from subcutaneous and omental human fat cells in suspension culture. |
| 1665 | 10831181 | A 24-hour exposure to 1 nmol/L tumor necrosis factor alpha (TNF-alpha) slightly increased PAI-1 release from both subcutaneous and omental adipocytes (30% +/- 21% and 17% +/- 18%, respectively, nonsignificant [NS]). |
| 1666 | 10831181 | Transforming growth factor beta 1 (TGF-beta1) induced a significant dose-dependent increase of PAI-1 release into the medium. |
| 1667 | 10831181 | Exposure to 400 pmol/L TGF-beta1 of subcutaneous and omental fat cells from both obese and non-obese individuals elevated PAI-1 secretion by 2-fold. |
| 1668 | 10831181 | These data provide evidence that human fat cells release a substantial amount of PAI-1 in a depot-specific manner and that TGF-beta1 particularly contributes to the regulation of PAI-1 secretion. |
| 1669 | 10831181 | Effect of tumor necrosis factor alpha and transforming growth factor beta 1 on plasminogen activator inhibitor-1 secretion from subcutaneous and omental human fat cells in suspension culture. |
| 1670 | 10831181 | A 24-hour exposure to 1 nmol/L tumor necrosis factor alpha (TNF-alpha) slightly increased PAI-1 release from both subcutaneous and omental adipocytes (30% +/- 21% and 17% +/- 18%, respectively, nonsignificant [NS]). |
| 1671 | 10831181 | Transforming growth factor beta 1 (TGF-beta1) induced a significant dose-dependent increase of PAI-1 release into the medium. |
| 1672 | 10831181 | Exposure to 400 pmol/L TGF-beta1 of subcutaneous and omental fat cells from both obese and non-obese individuals elevated PAI-1 secretion by 2-fold. |
| 1673 | 10831181 | These data provide evidence that human fat cells release a substantial amount of PAI-1 in a depot-specific manner and that TGF-beta1 particularly contributes to the regulation of PAI-1 secretion. |
| 1674 | 10831181 | Effect of tumor necrosis factor alpha and transforming growth factor beta 1 on plasminogen activator inhibitor-1 secretion from subcutaneous and omental human fat cells in suspension culture. |
| 1675 | 10831181 | A 24-hour exposure to 1 nmol/L tumor necrosis factor alpha (TNF-alpha) slightly increased PAI-1 release from both subcutaneous and omental adipocytes (30% +/- 21% and 17% +/- 18%, respectively, nonsignificant [NS]). |
| 1676 | 10831181 | Transforming growth factor beta 1 (TGF-beta1) induced a significant dose-dependent increase of PAI-1 release into the medium. |
| 1677 | 10831181 | Exposure to 400 pmol/L TGF-beta1 of subcutaneous and omental fat cells from both obese and non-obese individuals elevated PAI-1 secretion by 2-fold. |
| 1678 | 10831181 | These data provide evidence that human fat cells release a substantial amount of PAI-1 in a depot-specific manner and that TGF-beta1 particularly contributes to the regulation of PAI-1 secretion. |
| 1679 | 10831181 | Effect of tumor necrosis factor alpha and transforming growth factor beta 1 on plasminogen activator inhibitor-1 secretion from subcutaneous and omental human fat cells in suspension culture. |
| 1680 | 10831181 | A 24-hour exposure to 1 nmol/L tumor necrosis factor alpha (TNF-alpha) slightly increased PAI-1 release from both subcutaneous and omental adipocytes (30% +/- 21% and 17% +/- 18%, respectively, nonsignificant [NS]). |
| 1681 | 10831181 | Transforming growth factor beta 1 (TGF-beta1) induced a significant dose-dependent increase of PAI-1 release into the medium. |
| 1682 | 10831181 | Exposure to 400 pmol/L TGF-beta1 of subcutaneous and omental fat cells from both obese and non-obese individuals elevated PAI-1 secretion by 2-fold. |
| 1683 | 10831181 | These data provide evidence that human fat cells release a substantial amount of PAI-1 in a depot-specific manner and that TGF-beta1 particularly contributes to the regulation of PAI-1 secretion. |
| 1684 | 10834427 | Urinary transforming growth factor-beta1 and alpha1-microglobulin in children and adolescents with type 1 diabetes. |
| 1685 | 10841915 | Particularly, de novo synthesis of transforming growth factor beta1 (TGF-beta1) is induced and TGF-beta1 appears also involved since blockage of this prosclerotic factor inhibits high glucose-induced collagen synthesis. |
| 1686 | 10841915 | Interestingly, it could be demonstrated that angiotensin II also stimulates TGF-beta1 production possibly via the same signal transduction pathway. |
| 1687 | 10841915 | Particularly, de novo synthesis of transforming growth factor beta1 (TGF-beta1) is induced and TGF-beta1 appears also involved since blockage of this prosclerotic factor inhibits high glucose-induced collagen synthesis. |
| 1688 | 10841915 | Interestingly, it could be demonstrated that angiotensin II also stimulates TGF-beta1 production possibly via the same signal transduction pathway. |
| 1689 | 10845889 | Transforming growth factor-beta1 (TGF-beta1) increased PAI-1 secretion in a dose- and time-dependent manner. |
| 1690 | 10845889 | PAI-1 protein increased by 3.2-fold and PAI-1 mRNA by 1.9-fold after a 6-hour exposure to 400 pmol/L TGF-beta1. |
| 1691 | 10845889 | Moreover, TNF-alpha and interkeukin-1beta (IL-1beta) also exerted a stimulatory effect on PAI-1 release and increased PAI-1 mRNA levels. |
| 1692 | 10845889 | As assessed by a semiquantitative reverse transcription-polymerase chain reaction technique, TGF-beta1 mRNA is expressed by differentiation of human preadipocytes and is moderately upregulated by TNF-alpha and IL-1beta. |
| 1693 | 10845889 | In conclusion, our results clearly indicate that TGF-beta1 is a potent inducer of PAI-1 production in subcutaneous human adipocytes. |
| 1694 | 10845889 | In addition, data suggest that TNF-alpha and IL-1beta also have stimulatory effects on PAI-1 protein secretion and may contribute to the elevated PAI-1 levels observed in obesity. |
| 1695 | 10845889 | Transforming growth factor-beta1 (TGF-beta1) increased PAI-1 secretion in a dose- and time-dependent manner. |
| 1696 | 10845889 | PAI-1 protein increased by 3.2-fold and PAI-1 mRNA by 1.9-fold after a 6-hour exposure to 400 pmol/L TGF-beta1. |
| 1697 | 10845889 | Moreover, TNF-alpha and interkeukin-1beta (IL-1beta) also exerted a stimulatory effect on PAI-1 release and increased PAI-1 mRNA levels. |
| 1698 | 10845889 | As assessed by a semiquantitative reverse transcription-polymerase chain reaction technique, TGF-beta1 mRNA is expressed by differentiation of human preadipocytes and is moderately upregulated by TNF-alpha and IL-1beta. |
| 1699 | 10845889 | In conclusion, our results clearly indicate that TGF-beta1 is a potent inducer of PAI-1 production in subcutaneous human adipocytes. |
| 1700 | 10845889 | In addition, data suggest that TNF-alpha and IL-1beta also have stimulatory effects on PAI-1 protein secretion and may contribute to the elevated PAI-1 levels observed in obesity. |
| 1701 | 10845889 | Transforming growth factor-beta1 (TGF-beta1) increased PAI-1 secretion in a dose- and time-dependent manner. |
| 1702 | 10845889 | PAI-1 protein increased by 3.2-fold and PAI-1 mRNA by 1.9-fold after a 6-hour exposure to 400 pmol/L TGF-beta1. |
| 1703 | 10845889 | Moreover, TNF-alpha and interkeukin-1beta (IL-1beta) also exerted a stimulatory effect on PAI-1 release and increased PAI-1 mRNA levels. |
| 1704 | 10845889 | As assessed by a semiquantitative reverse transcription-polymerase chain reaction technique, TGF-beta1 mRNA is expressed by differentiation of human preadipocytes and is moderately upregulated by TNF-alpha and IL-1beta. |
| 1705 | 10845889 | In conclusion, our results clearly indicate that TGF-beta1 is a potent inducer of PAI-1 production in subcutaneous human adipocytes. |
| 1706 | 10845889 | In addition, data suggest that TNF-alpha and IL-1beta also have stimulatory effects on PAI-1 protein secretion and may contribute to the elevated PAI-1 levels observed in obesity. |
| 1707 | 10845889 | Transforming growth factor-beta1 (TGF-beta1) increased PAI-1 secretion in a dose- and time-dependent manner. |
| 1708 | 10845889 | PAI-1 protein increased by 3.2-fold and PAI-1 mRNA by 1.9-fold after a 6-hour exposure to 400 pmol/L TGF-beta1. |
| 1709 | 10845889 | Moreover, TNF-alpha and interkeukin-1beta (IL-1beta) also exerted a stimulatory effect on PAI-1 release and increased PAI-1 mRNA levels. |
| 1710 | 10845889 | As assessed by a semiquantitative reverse transcription-polymerase chain reaction technique, TGF-beta1 mRNA is expressed by differentiation of human preadipocytes and is moderately upregulated by TNF-alpha and IL-1beta. |
| 1711 | 10845889 | In conclusion, our results clearly indicate that TGF-beta1 is a potent inducer of PAI-1 production in subcutaneous human adipocytes. |
| 1712 | 10845889 | In addition, data suggest that TNF-alpha and IL-1beta also have stimulatory effects on PAI-1 protein secretion and may contribute to the elevated PAI-1 levels observed in obesity. |
| 1713 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 1714 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 1715 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 1716 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 1717 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 1718 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 1719 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 1720 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 1721 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 1722 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 1723 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 1724 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 1725 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 1726 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 1727 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 1728 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 1729 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 1730 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 1731 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 1732 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 1733 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 1734 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 1735 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 1736 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 1737 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 1738 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 1739 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 1740 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 1741 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 1742 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 1743 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 1744 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 1745 | 10851311 | Loss of TGFbeta, Apoptosis, and Bcl-2 in Erectile Dysfunction and Upregulation of p53 and HIF-1alpha in Diabetes-Associated Erectile Dysfunction. |
| 1746 | 10851311 | Vasculogenic erectile dysfunction (ED) is associated with collagen replacement of the cavernosal smooth muscle, mediated by an increase in transforming growth factor (TGF)-production secondary to hypoxemia. |
| 1747 | 10851311 | We tested the hypothesis that human ED is the result of an increase in apoptosis of the cavernosal smooth muscle cells with replacement by collagen, mediated by the TGFbeta upregulation. |
| 1748 | 10851311 | Immunohistochemistry staining was used to detect TGFbeta and Bcl-2 expression, while Western blot analysis was used to detect expression of Bcl-2, p53, and hypoxia-inducible factor (HIF)-1a. |
| 1749 | 10851311 | In contrast, Western blotting demonstrated upregulation of p53 and HIF-1a expression in the cavernosal tissues from the men with ED and diabetes. |
| 1750 | 10851311 | Male ED follows an active process characterized by a loss of TGFb expression, apoptosis, and Bcl-2 expression. |
| 1751 | 10851311 | However, there is upregulation of p53 and HIF-1a in men with diabetes. |
| 1752 | 10851311 | These data support the possibility of hypoxia-mediated ED in diabetes via upregulation of p53 and HIF-1a but does not substantiate a role for TGFbeta in ED. |
| 1753 | 10859282 | Association of a T29-->C polymorphism of the transforming growth factor-beta1 gene with genetic susceptibility to myocardial infarction in Japanese. |
| 1754 | 10865847 | In this chapter, we summarize our studies on plasminogen activator inhibitor 1 (PAI-1), tissue factor, and transforming growth factor beta (TGF-beta) expression in obesity, using genetically obese mice as a model. |
| 1755 | 10866056 | Troglitazone was able to prevent not only diabetic glomerular hyperfiltration and albuminuria, but an increase in mRNA expression of extracellular matrix proteins and transforming growth factor-beta1 in glomeruli of diabetic rats, without changing blood glucose levels. |
| 1756 | 10866056 | Biochemically, an increase in diacylglycerol (DAG) contents and the activation of the protein kinase C (PKC)-extracellular signal-regulated kinase (ERK) pathway in glomeruli of diabetic rats were abrogated by troglitazone. |
| 1757 | 10871205 | Mechanical stretch-induced fibronectin and transforming growth factor-beta1 production in human mesangial cells is p38 mitogen-activated protein kinase-dependent. |
| 1758 | 10871205 | Hemodynamic abnormalities are important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomerulopathies. p38-Mitogen-activated protein (MAP) kinase, an important intracellular signaling molecule, is activated in the glomeruli of diabetic rats. |
| 1759 | 10871205 | We studied, in human mesangial cells, the effect of stretch on p38 MAP kinase activation and the role of p38 MAP kinase in stretch-induced fibronectin and transforming growth factor-beta1 (TGF-beta1) accumulation. p38 MAP kinase was activated by stretch in a rapid (11-fold increase at 30 min, P < 0.001) and sustained manner (3-fold increase at 33 h, P < 0.001); this activation was mediated by protein kinase C (PKC). |
| 1760 | 10871205 | Stretch-induced fibronectin and TGF-beta1 protein levels were completely abolished (100% inhibition, P < 0.001; and 92% inhibition, P < 0.01, respectively) by SB203580, a specific p38 MAP kinase inhibitor. |
| 1761 | 10871205 | At 33 h, TGF-beta1 blockade did not affect stretch-induced fibronectin production, but partially prevented stretch-induced p38 MAP kinase activation (59% inhibition, P < 0.05). |
| 1762 | 10871205 | TGF-beta1 induced fibronectin accumulation after 72 h of exposure via a p38 MAP kinase-dependent mechanism (30% increase over control, P < 0.01). |
| 1763 | 10871205 | In human mesangial cells, stretch activates, via a PKC-dependent mechanism, p38 MAP kinase, which independently induces TGF-beta1 and fibronectin. |
| 1764 | 10871205 | In turn, TGF-beta1 contributes to maintaining late p38 MAP kinase activation, which perpetuates fibronectin accumulation. |
| 1765 | 10871205 | Mechanical stretch-induced fibronectin and transforming growth factor-beta1 production in human mesangial cells is p38 mitogen-activated protein kinase-dependent. |
| 1766 | 10871205 | Hemodynamic abnormalities are important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomerulopathies. p38-Mitogen-activated protein (MAP) kinase, an important intracellular signaling molecule, is activated in the glomeruli of diabetic rats. |
| 1767 | 10871205 | We studied, in human mesangial cells, the effect of stretch on p38 MAP kinase activation and the role of p38 MAP kinase in stretch-induced fibronectin and transforming growth factor-beta1 (TGF-beta1) accumulation. p38 MAP kinase was activated by stretch in a rapid (11-fold increase at 30 min, P < 0.001) and sustained manner (3-fold increase at 33 h, P < 0.001); this activation was mediated by protein kinase C (PKC). |
| 1768 | 10871205 | Stretch-induced fibronectin and TGF-beta1 protein levels were completely abolished (100% inhibition, P < 0.001; and 92% inhibition, P < 0.01, respectively) by SB203580, a specific p38 MAP kinase inhibitor. |
| 1769 | 10871205 | At 33 h, TGF-beta1 blockade did not affect stretch-induced fibronectin production, but partially prevented stretch-induced p38 MAP kinase activation (59% inhibition, P < 0.05). |
| 1770 | 10871205 | TGF-beta1 induced fibronectin accumulation after 72 h of exposure via a p38 MAP kinase-dependent mechanism (30% increase over control, P < 0.01). |
| 1771 | 10871205 | In human mesangial cells, stretch activates, via a PKC-dependent mechanism, p38 MAP kinase, which independently induces TGF-beta1 and fibronectin. |
| 1772 | 10871205 | In turn, TGF-beta1 contributes to maintaining late p38 MAP kinase activation, which perpetuates fibronectin accumulation. |
| 1773 | 10871205 | Mechanical stretch-induced fibronectin and transforming growth factor-beta1 production in human mesangial cells is p38 mitogen-activated protein kinase-dependent. |
| 1774 | 10871205 | Hemodynamic abnormalities are important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomerulopathies. p38-Mitogen-activated protein (MAP) kinase, an important intracellular signaling molecule, is activated in the glomeruli of diabetic rats. |
| 1775 | 10871205 | We studied, in human mesangial cells, the effect of stretch on p38 MAP kinase activation and the role of p38 MAP kinase in stretch-induced fibronectin and transforming growth factor-beta1 (TGF-beta1) accumulation. p38 MAP kinase was activated by stretch in a rapid (11-fold increase at 30 min, P < 0.001) and sustained manner (3-fold increase at 33 h, P < 0.001); this activation was mediated by protein kinase C (PKC). |
| 1776 | 10871205 | Stretch-induced fibronectin and TGF-beta1 protein levels were completely abolished (100% inhibition, P < 0.001; and 92% inhibition, P < 0.01, respectively) by SB203580, a specific p38 MAP kinase inhibitor. |
| 1777 | 10871205 | At 33 h, TGF-beta1 blockade did not affect stretch-induced fibronectin production, but partially prevented stretch-induced p38 MAP kinase activation (59% inhibition, P < 0.05). |
| 1778 | 10871205 | TGF-beta1 induced fibronectin accumulation after 72 h of exposure via a p38 MAP kinase-dependent mechanism (30% increase over control, P < 0.01). |
| 1779 | 10871205 | In human mesangial cells, stretch activates, via a PKC-dependent mechanism, p38 MAP kinase, which independently induces TGF-beta1 and fibronectin. |
| 1780 | 10871205 | In turn, TGF-beta1 contributes to maintaining late p38 MAP kinase activation, which perpetuates fibronectin accumulation. |
| 1781 | 10871205 | Mechanical stretch-induced fibronectin and transforming growth factor-beta1 production in human mesangial cells is p38 mitogen-activated protein kinase-dependent. |
| 1782 | 10871205 | Hemodynamic abnormalities are important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomerulopathies. p38-Mitogen-activated protein (MAP) kinase, an important intracellular signaling molecule, is activated in the glomeruli of diabetic rats. |
| 1783 | 10871205 | We studied, in human mesangial cells, the effect of stretch on p38 MAP kinase activation and the role of p38 MAP kinase in stretch-induced fibronectin and transforming growth factor-beta1 (TGF-beta1) accumulation. p38 MAP kinase was activated by stretch in a rapid (11-fold increase at 30 min, P < 0.001) and sustained manner (3-fold increase at 33 h, P < 0.001); this activation was mediated by protein kinase C (PKC). |
| 1784 | 10871205 | Stretch-induced fibronectin and TGF-beta1 protein levels were completely abolished (100% inhibition, P < 0.001; and 92% inhibition, P < 0.01, respectively) by SB203580, a specific p38 MAP kinase inhibitor. |
| 1785 | 10871205 | At 33 h, TGF-beta1 blockade did not affect stretch-induced fibronectin production, but partially prevented stretch-induced p38 MAP kinase activation (59% inhibition, P < 0.05). |
| 1786 | 10871205 | TGF-beta1 induced fibronectin accumulation after 72 h of exposure via a p38 MAP kinase-dependent mechanism (30% increase over control, P < 0.01). |
| 1787 | 10871205 | In human mesangial cells, stretch activates, via a PKC-dependent mechanism, p38 MAP kinase, which independently induces TGF-beta1 and fibronectin. |
| 1788 | 10871205 | In turn, TGF-beta1 contributes to maintaining late p38 MAP kinase activation, which perpetuates fibronectin accumulation. |
| 1789 | 10871205 | Mechanical stretch-induced fibronectin and transforming growth factor-beta1 production in human mesangial cells is p38 mitogen-activated protein kinase-dependent. |
| 1790 | 10871205 | Hemodynamic abnormalities are important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomerulopathies. p38-Mitogen-activated protein (MAP) kinase, an important intracellular signaling molecule, is activated in the glomeruli of diabetic rats. |
| 1791 | 10871205 | We studied, in human mesangial cells, the effect of stretch on p38 MAP kinase activation and the role of p38 MAP kinase in stretch-induced fibronectin and transforming growth factor-beta1 (TGF-beta1) accumulation. p38 MAP kinase was activated by stretch in a rapid (11-fold increase at 30 min, P < 0.001) and sustained manner (3-fold increase at 33 h, P < 0.001); this activation was mediated by protein kinase C (PKC). |
| 1792 | 10871205 | Stretch-induced fibronectin and TGF-beta1 protein levels were completely abolished (100% inhibition, P < 0.001; and 92% inhibition, P < 0.01, respectively) by SB203580, a specific p38 MAP kinase inhibitor. |
| 1793 | 10871205 | At 33 h, TGF-beta1 blockade did not affect stretch-induced fibronectin production, but partially prevented stretch-induced p38 MAP kinase activation (59% inhibition, P < 0.05). |
| 1794 | 10871205 | TGF-beta1 induced fibronectin accumulation after 72 h of exposure via a p38 MAP kinase-dependent mechanism (30% increase over control, P < 0.01). |
| 1795 | 10871205 | In human mesangial cells, stretch activates, via a PKC-dependent mechanism, p38 MAP kinase, which independently induces TGF-beta1 and fibronectin. |
| 1796 | 10871205 | In turn, TGF-beta1 contributes to maintaining late p38 MAP kinase activation, which perpetuates fibronectin accumulation. |
| 1797 | 10871205 | Mechanical stretch-induced fibronectin and transforming growth factor-beta1 production in human mesangial cells is p38 mitogen-activated protein kinase-dependent. |
| 1798 | 10871205 | Hemodynamic abnormalities are important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomerulopathies. p38-Mitogen-activated protein (MAP) kinase, an important intracellular signaling molecule, is activated in the glomeruli of diabetic rats. |
| 1799 | 10871205 | We studied, in human mesangial cells, the effect of stretch on p38 MAP kinase activation and the role of p38 MAP kinase in stretch-induced fibronectin and transforming growth factor-beta1 (TGF-beta1) accumulation. p38 MAP kinase was activated by stretch in a rapid (11-fold increase at 30 min, P < 0.001) and sustained manner (3-fold increase at 33 h, P < 0.001); this activation was mediated by protein kinase C (PKC). |
| 1800 | 10871205 | Stretch-induced fibronectin and TGF-beta1 protein levels were completely abolished (100% inhibition, P < 0.001; and 92% inhibition, P < 0.01, respectively) by SB203580, a specific p38 MAP kinase inhibitor. |
| 1801 | 10871205 | At 33 h, TGF-beta1 blockade did not affect stretch-induced fibronectin production, but partially prevented stretch-induced p38 MAP kinase activation (59% inhibition, P < 0.05). |
| 1802 | 10871205 | TGF-beta1 induced fibronectin accumulation after 72 h of exposure via a p38 MAP kinase-dependent mechanism (30% increase over control, P < 0.01). |
| 1803 | 10871205 | In human mesangial cells, stretch activates, via a PKC-dependent mechanism, p38 MAP kinase, which independently induces TGF-beta1 and fibronectin. |
| 1804 | 10871205 | In turn, TGF-beta1 contributes to maintaining late p38 MAP kinase activation, which perpetuates fibronectin accumulation. |
| 1805 | 10871205 | Mechanical stretch-induced fibronectin and transforming growth factor-beta1 production in human mesangial cells is p38 mitogen-activated protein kinase-dependent. |
| 1806 | 10871205 | Hemodynamic abnormalities are important in the pathogenesis of the excess mesangial matrix deposition of diabetic and other glomerulopathies. p38-Mitogen-activated protein (MAP) kinase, an important intracellular signaling molecule, is activated in the glomeruli of diabetic rats. |
| 1807 | 10871205 | We studied, in human mesangial cells, the effect of stretch on p38 MAP kinase activation and the role of p38 MAP kinase in stretch-induced fibronectin and transforming growth factor-beta1 (TGF-beta1) accumulation. p38 MAP kinase was activated by stretch in a rapid (11-fold increase at 30 min, P < 0.001) and sustained manner (3-fold increase at 33 h, P < 0.001); this activation was mediated by protein kinase C (PKC). |
| 1808 | 10871205 | Stretch-induced fibronectin and TGF-beta1 protein levels were completely abolished (100% inhibition, P < 0.001; and 92% inhibition, P < 0.01, respectively) by SB203580, a specific p38 MAP kinase inhibitor. |
| 1809 | 10871205 | At 33 h, TGF-beta1 blockade did not affect stretch-induced fibronectin production, but partially prevented stretch-induced p38 MAP kinase activation (59% inhibition, P < 0.05). |
| 1810 | 10871205 | TGF-beta1 induced fibronectin accumulation after 72 h of exposure via a p38 MAP kinase-dependent mechanism (30% increase over control, P < 0.01). |
| 1811 | 10871205 | In human mesangial cells, stretch activates, via a PKC-dependent mechanism, p38 MAP kinase, which independently induces TGF-beta1 and fibronectin. |
| 1812 | 10871205 | In turn, TGF-beta1 contributes to maintaining late p38 MAP kinase activation, which perpetuates fibronectin accumulation. |
| 1813 | 10878408 | Furthermore, AST-120 administration reduced the interstitial expression of transforming growth factor (TGF)-beta(1) and tissue inhibitor of metalloproteinase (TIMP)-1, as well as interstitial infiltration of macrophages. |
| 1814 | 10878408 | In conclusion, AST-120 reduced the interstitial expression of TGF-beta(1) and TIMP-1, and the interstitial infiltration of macrophages, and ameliorates the progression of diabetic nephropathy in OLETF rats. |
| 1815 | 10884438 | As shown most recently, TGF-beta stimulates the expression of a distinct serine/threonine kinase (hSGK) which had previously been cloned as an early gene transcriptionally regulated by cell volume alterations. |
| 1816 | 10884438 | As shown by Northern blotting, an increase of extracellular glucose concentration increased hSGK mRNA levels in cultured cells, an effect qualitatively mimicked by osmotic cell shrinkage or treatment with TGF-beta (2 microgram/liter), phorbol 12,13-didecanoate (1 microM), or the Ca(2+) ionophore ionomycin (1 microM) and blunted by high concentrations of nifedipine (10 and 100 microM). |
| 1817 | 10884438 | According to voltage clamp and tracer flux studies in Xenopus oocytes expressing the renal epithelial Na(+) channel ENaC or the mouse thick ascending limb Na(+),K(+),2Cl(-) cotransporter BSC-1, coexpression with hSGK stimulated ENaC and BSC-1 11-fold and 6-fold, respectively, effects reversed by kinase inhibitors staurosporine (1 microM) and chelerythrine (1 microM) and not elicited by inactive hSGK. |
| 1818 | 10884438 | As shown most recently, TGF-beta stimulates the expression of a distinct serine/threonine kinase (hSGK) which had previously been cloned as an early gene transcriptionally regulated by cell volume alterations. |
| 1819 | 10884438 | As shown by Northern blotting, an increase of extracellular glucose concentration increased hSGK mRNA levels in cultured cells, an effect qualitatively mimicked by osmotic cell shrinkage or treatment with TGF-beta (2 microgram/liter), phorbol 12,13-didecanoate (1 microM), or the Ca(2+) ionophore ionomycin (1 microM) and blunted by high concentrations of nifedipine (10 and 100 microM). |
| 1820 | 10884438 | According to voltage clamp and tracer flux studies in Xenopus oocytes expressing the renal epithelial Na(+) channel ENaC or the mouse thick ascending limb Na(+),K(+),2Cl(-) cotransporter BSC-1, coexpression with hSGK stimulated ENaC and BSC-1 11-fold and 6-fold, respectively, effects reversed by kinase inhibitors staurosporine (1 microM) and chelerythrine (1 microM) and not elicited by inactive hSGK. |
| 1821 | 10892881 | TGF-beta1, TGF-beta receptor II and ED-A fibronectin expression in myofibroblast of vitreoretinopathy. |
| 1822 | 10907122 | Effects of diabetes and hypoxia on gene markers of angiogenesis (HGF, cMET, uPA and uPAR, TGF-alpha, TGF-beta, bFGF and Vimentin) in cultured and transplanted rat islets. |
| 1823 | 10953029 | PSF expression was constitutive in retinal pericytes (RPCs) but could be modulated in bovine retinal capillary endothelial cells (RECs) by cell confluency, hypoxia, serum starvation, high glucose concentrations, or inversely by soluble factors present in early vs. late retinopathy, such as TGF-beta, VEGF, or bFGF. |
| 1824 | 10953913 | Genes encoding transforming growth factor beta, interleukin-4 (IL-4) and IL-10 are most frequently protective. |
| 1825 | 10953913 | Autoimmune/ inflammatory diseases are associated with excessive production of inflammatory cytokines such as IL-1, IL-12, tumor necrosis factor alpha (TNFalpha) and interferon gamma (IFNgamma). |
| 1826 | 10953913 | Vectors encoding inhibitors of these cytokines, such as IL-1 receptor antagonist, soluble IL-1 receptors, IL-12p40, soluble TNFalpha receptors or IFNgamma-receptor/IgG-Fc fusion proteins are protective in models of either arthritis, Type 1 DM, SLE or EAE. |
| 1827 | 10965906 | This study examined the effects of one agent, 5-thio-D-glucose (5TG) on renal hypertrophy and transforming growth factor beta1 (TGF-beta1). |
| 1828 | 10971090 | As to nephropathy, insulin-like growth factor I (IGF-I) seems to be implicated in the earlier stages of the disease, while transforming growth factor beta (TGF beta) is involved both in the early and later stages, being responsible, at least in part, for extracellular matrix (ECM) accumulation. |
| 1829 | 10971090 | Finally, deficiency of several neurotrophic factors, namely nerve growth factor (NGF) and IGF-I has been related to the degeneration or impaired regeneration occurring in diabetic neuropathy. |
| 1830 | 10972540 | High plasma concentrations of prorenin in a transgenic animal model of nephropathy with overexpression of transforming growth factor-beta1 in the kidneys. |
| 1831 | 10975990 | We found that after 2 and 12 h exposure to 75% reduced amino acids, the release of basic fibroblast growth factor (bFGF) and transforming growth factor beta1 (TGF beta 1) from VSMC was significantly greater than that from cells maintained in control medium [2572.0 (546.3) vs 602.1 (241.7), P=0.001 and 16 028.0 (2192. 4) vs 13 027.3 (1233.5) pg/10(6)cells, P=0.022 respectively]. |
| 1832 | 10976005 | This was shown by increased proliferation to antigenic stimulus, increased production of IFN-gamma and decreased secretion of TGF-beta. |
| 1833 | 10978417 | GLUT-1 and TGF-beta: the link between hyperglycaemia and diabetic nephropathy. |
| 1834 | 10997685 | Furthermore, stable overexpression of GFAT increased levels of TGF-beta1 protein, mRNA, and promoter activity. |
| 1835 | 10997685 | Inasmuch as stimulation or inhibition of GFAT increased or decreased high glucose-stimulated activity of protein kinase C (PKC), respectively, the observed effects appear to be transduced by PKC. |
| 1836 | 10997685 | In similar experiments, involvement of the hexosamine pathway in hyperglycemia-induced production of cytokines (TGF-alpha and basic fibroblast growth factor [bFGF]) was demonstrated in vascular smooth muscle cells. |
| 1837 | 10997689 | When added to the incubation media of glomerular mesangial and endothelial cells, glycated albumin stimulates protein kinase C (PKC) activity, increases transforming growth factor-beta (TGF-beta) bioactivity, and induces gene overexpression and enhanced production of extracellular matrix proteins. |
| 1838 | 10997691 | Mechanism of transforming growth factor-beta1 signaling:. |
| 1839 | 10997691 | Mechanism of transforming growth factor-beta1 signaling: Role of the mitogen-activated protein kinase. |
| 1840 | 10997691 | Transforming growth factor-beta1 (TGF-beta1) regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. |
| 1841 | 10997691 | Initiation of signaling requires binding of TGF-beta1 to TGF-beta type II receptor (TbetaR-II), a constitutively active serine/threonine kinase, which subsequently transphosphorylates TGF-beta type I receptor (TbetaR-I). |
| 1842 | 10997691 | An emerging body of evidence implicates the mitogen-activated protein kinase (MAPK) as an important TGF-beta1 signaling pathway. |
| 1843 | 10997691 | Mechanism of transforming growth factor-beta1 signaling:. |
| 1844 | 10997691 | Mechanism of transforming growth factor-beta1 signaling: Role of the mitogen-activated protein kinase. |
| 1845 | 10997691 | Transforming growth factor-beta1 (TGF-beta1) regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. |
| 1846 | 10997691 | Initiation of signaling requires binding of TGF-beta1 to TGF-beta type II receptor (TbetaR-II), a constitutively active serine/threonine kinase, which subsequently transphosphorylates TGF-beta type I receptor (TbetaR-I). |
| 1847 | 10997691 | An emerging body of evidence implicates the mitogen-activated protein kinase (MAPK) as an important TGF-beta1 signaling pathway. |
| 1848 | 10997691 | Mechanism of transforming growth factor-beta1 signaling:. |
| 1849 | 10997691 | Mechanism of transforming growth factor-beta1 signaling: Role of the mitogen-activated protein kinase. |
| 1850 | 10997691 | Transforming growth factor-beta1 (TGF-beta1) regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. |
| 1851 | 10997691 | Initiation of signaling requires binding of TGF-beta1 to TGF-beta type II receptor (TbetaR-II), a constitutively active serine/threonine kinase, which subsequently transphosphorylates TGF-beta type I receptor (TbetaR-I). |
| 1852 | 10997691 | An emerging body of evidence implicates the mitogen-activated protein kinase (MAPK) as an important TGF-beta1 signaling pathway. |
| 1853 | 10997691 | Mechanism of transforming growth factor-beta1 signaling:. |
| 1854 | 10997691 | Mechanism of transforming growth factor-beta1 signaling: Role of the mitogen-activated protein kinase. |
| 1855 | 10997691 | Transforming growth factor-beta1 (TGF-beta1) regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. |
| 1856 | 10997691 | Initiation of signaling requires binding of TGF-beta1 to TGF-beta type II receptor (TbetaR-II), a constitutively active serine/threonine kinase, which subsequently transphosphorylates TGF-beta type I receptor (TbetaR-I). |
| 1857 | 10997691 | An emerging body of evidence implicates the mitogen-activated protein kinase (MAPK) as an important TGF-beta1 signaling pathway. |
| 1858 | 10997691 | Mechanism of transforming growth factor-beta1 signaling:. |
| 1859 | 10997691 | Mechanism of transforming growth factor-beta1 signaling: Role of the mitogen-activated protein kinase. |
| 1860 | 10997691 | Transforming growth factor-beta1 (TGF-beta1) regulates diverse biologic activities including cell growth, cell death or apoptosis, cell differentiation, and extracellular matrix (ECM) synthesis. |
| 1861 | 10997691 | Initiation of signaling requires binding of TGF-beta1 to TGF-beta type II receptor (TbetaR-II), a constitutively active serine/threonine kinase, which subsequently transphosphorylates TGF-beta type I receptor (TbetaR-I). |
| 1862 | 10997691 | An emerging body of evidence implicates the mitogen-activated protein kinase (MAPK) as an important TGF-beta1 signaling pathway. |
| 1863 | 10997692 | High glucose, transforming growth factor-beta (TGF-beta), angiotensin II, and probably other factors induce inhibitors of cyclin-dependent kinases (CDK) including p21Cip1 and p27KiP1. |
| 1864 | 10997692 | Treatment of diabetic rats with angiotensin-converting enzyme inhibitors attenuates glomerular hypertrophy and abolishes the glomerular expression of the CDK-inhibitors p16INK4 and p27KiP1, thus indicating that the cell cycle arrest can be therapeutically influenced. |
| 1865 | 10997697 | Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) receptor blockers (ARBs) can attenuate progressive glomerulosclerosis in disease models and can slow disease progression in humans. |
| 1866 | 10997697 | Glucose increases expression of the angiotensinogen gene in proximal tubule cells and Ang II production in primary mesangial cell culture, which indicates that high glucose itself can activate the renin-angiotensin system. |
| 1867 | 10997697 | The effects of glucose and Ang II on mesangial matrix metabolism may be mediated by transforming growth factor-beta (TGF-beta). |
| 1868 | 10997697 | Exposure of mesangial cells to glucose or Ang II increases TGF-beta expression and secretion. |
| 1869 | 10997697 | Taken together, these findings support the hypothesis that the high-glucose milieu of diabetes increases Ang II production by renal, and especially, mesangial cells, which results in stimulation of TGF-beta secretion, leading to increased synthesis and decreased degradation of matrix proteins, thus producing matrix accumulation. |
| 1870 | 10997697 | Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) receptor blockers (ARBs) can attenuate progressive glomerulosclerosis in disease models and can slow disease progression in humans. |
| 1871 | 10997697 | Glucose increases expression of the angiotensinogen gene in proximal tubule cells and Ang II production in primary mesangial cell culture, which indicates that high glucose itself can activate the renin-angiotensin system. |
| 1872 | 10997697 | The effects of glucose and Ang II on mesangial matrix metabolism may be mediated by transforming growth factor-beta (TGF-beta). |
| 1873 | 10997697 | Exposure of mesangial cells to glucose or Ang II increases TGF-beta expression and secretion. |
| 1874 | 10997697 | Taken together, these findings support the hypothesis that the high-glucose milieu of diabetes increases Ang II production by renal, and especially, mesangial cells, which results in stimulation of TGF-beta secretion, leading to increased synthesis and decreased degradation of matrix proteins, thus producing matrix accumulation. |
| 1875 | 10997697 | Angiotensin-converting enzyme (ACE) inhibitors and angiotensin II (Ang II) receptor blockers (ARBs) can attenuate progressive glomerulosclerosis in disease models and can slow disease progression in humans. |
| 1876 | 10997697 | Glucose increases expression of the angiotensinogen gene in proximal tubule cells and Ang II production in primary mesangial cell culture, which indicates that high glucose itself can activate the renin-angiotensin system. |
| 1877 | 10997697 | The effects of glucose and Ang II on mesangial matrix metabolism may be mediated by transforming growth factor-beta (TGF-beta). |
| 1878 | 10997697 | Exposure of mesangial cells to glucose or Ang II increases TGF-beta expression and secretion. |
| 1879 | 10997697 | Taken together, these findings support the hypothesis that the high-glucose milieu of diabetes increases Ang II production by renal, and especially, mesangial cells, which results in stimulation of TGF-beta secretion, leading to increased synthesis and decreased degradation of matrix proteins, thus producing matrix accumulation. |
| 1880 | 10997698 | Regulation of inositol 1,4,5-trisphosphate receptors by transforming growth factor-beta: implications for vascular dysfunction in diabetes. |
| 1881 | 10997698 | Earlier studies have demonstrated that vascular smooth muscle cells and mesangial cells pretreated with TGF-beta have impaired calcium mobilization to inositol 1,4,5-trisphosphate (IP3) generating agonists, such as platelet-derived growth factor (PDGF) and Angiotensin I1 (Ang II). |
| 1882 | 10997698 | We postulated that this action of TGF-beta may be caused by regulation of the key intracellular calcium channel, the inositol 1,4,5-trisphosphate receptor (IP3R). |
| 1883 | 10997698 | Short-term exposure of mesangial cells to TGF-beta (15-60 min) leads to phosphorylation of the type I IP3R at specific serine residues. |
| 1884 | 10997698 | Long-term exposure of mesangial cells to TGF-beta (24 hours) leads to down-regulation of protein levels of both types I and III IP3Rs as assessed by Western blot and confocal analysis. |
| 1885 | 10997698 | We conclude that the vascular dysfunction of diabetes leading to glomerular hypertrophy is mediated, in part, by TGF-beta-induced regulation of IP3Rs. |
| 1886 | 10997698 | Regulation of inositol 1,4,5-trisphosphate receptors by transforming growth factor-beta: implications for vascular dysfunction in diabetes. |
| 1887 | 10997698 | Earlier studies have demonstrated that vascular smooth muscle cells and mesangial cells pretreated with TGF-beta have impaired calcium mobilization to inositol 1,4,5-trisphosphate (IP3) generating agonists, such as platelet-derived growth factor (PDGF) and Angiotensin I1 (Ang II). |
| 1888 | 10997698 | We postulated that this action of TGF-beta may be caused by regulation of the key intracellular calcium channel, the inositol 1,4,5-trisphosphate receptor (IP3R). |
| 1889 | 10997698 | Short-term exposure of mesangial cells to TGF-beta (15-60 min) leads to phosphorylation of the type I IP3R at specific serine residues. |
| 1890 | 10997698 | Long-term exposure of mesangial cells to TGF-beta (24 hours) leads to down-regulation of protein levels of both types I and III IP3Rs as assessed by Western blot and confocal analysis. |
| 1891 | 10997698 | We conclude that the vascular dysfunction of diabetes leading to glomerular hypertrophy is mediated, in part, by TGF-beta-induced regulation of IP3Rs. |
| 1892 | 10997698 | Regulation of inositol 1,4,5-trisphosphate receptors by transforming growth factor-beta: implications for vascular dysfunction in diabetes. |
| 1893 | 10997698 | Earlier studies have demonstrated that vascular smooth muscle cells and mesangial cells pretreated with TGF-beta have impaired calcium mobilization to inositol 1,4,5-trisphosphate (IP3) generating agonists, such as platelet-derived growth factor (PDGF) and Angiotensin I1 (Ang II). |
| 1894 | 10997698 | We postulated that this action of TGF-beta may be caused by regulation of the key intracellular calcium channel, the inositol 1,4,5-trisphosphate receptor (IP3R). |
| 1895 | 10997698 | Short-term exposure of mesangial cells to TGF-beta (15-60 min) leads to phosphorylation of the type I IP3R at specific serine residues. |
| 1896 | 10997698 | Long-term exposure of mesangial cells to TGF-beta (24 hours) leads to down-regulation of protein levels of both types I and III IP3Rs as assessed by Western blot and confocal analysis. |
| 1897 | 10997698 | We conclude that the vascular dysfunction of diabetes leading to glomerular hypertrophy is mediated, in part, by TGF-beta-induced regulation of IP3Rs. |
| 1898 | 10997698 | Regulation of inositol 1,4,5-trisphosphate receptors by transforming growth factor-beta: implications for vascular dysfunction in diabetes. |
| 1899 | 10997698 | Earlier studies have demonstrated that vascular smooth muscle cells and mesangial cells pretreated with TGF-beta have impaired calcium mobilization to inositol 1,4,5-trisphosphate (IP3) generating agonists, such as platelet-derived growth factor (PDGF) and Angiotensin I1 (Ang II). |
| 1900 | 10997698 | We postulated that this action of TGF-beta may be caused by regulation of the key intracellular calcium channel, the inositol 1,4,5-trisphosphate receptor (IP3R). |
| 1901 | 10997698 | Short-term exposure of mesangial cells to TGF-beta (15-60 min) leads to phosphorylation of the type I IP3R at specific serine residues. |
| 1902 | 10997698 | Long-term exposure of mesangial cells to TGF-beta (24 hours) leads to down-regulation of protein levels of both types I and III IP3Rs as assessed by Western blot and confocal analysis. |
| 1903 | 10997698 | We conclude that the vascular dysfunction of diabetes leading to glomerular hypertrophy is mediated, in part, by TGF-beta-induced regulation of IP3Rs. |
| 1904 | 10997698 | Regulation of inositol 1,4,5-trisphosphate receptors by transforming growth factor-beta: implications for vascular dysfunction in diabetes. |
| 1905 | 10997698 | Earlier studies have demonstrated that vascular smooth muscle cells and mesangial cells pretreated with TGF-beta have impaired calcium mobilization to inositol 1,4,5-trisphosphate (IP3) generating agonists, such as platelet-derived growth factor (PDGF) and Angiotensin I1 (Ang II). |
| 1906 | 10997698 | We postulated that this action of TGF-beta may be caused by regulation of the key intracellular calcium channel, the inositol 1,4,5-trisphosphate receptor (IP3R). |
| 1907 | 10997698 | Short-term exposure of mesangial cells to TGF-beta (15-60 min) leads to phosphorylation of the type I IP3R at specific serine residues. |
| 1908 | 10997698 | Long-term exposure of mesangial cells to TGF-beta (24 hours) leads to down-regulation of protein levels of both types I and III IP3Rs as assessed by Western blot and confocal analysis. |
| 1909 | 10997698 | We conclude that the vascular dysfunction of diabetes leading to glomerular hypertrophy is mediated, in part, by TGF-beta-induced regulation of IP3Rs. |
| 1910 | 10997698 | Regulation of inositol 1,4,5-trisphosphate receptors by transforming growth factor-beta: implications for vascular dysfunction in diabetes. |
| 1911 | 10997698 | Earlier studies have demonstrated that vascular smooth muscle cells and mesangial cells pretreated with TGF-beta have impaired calcium mobilization to inositol 1,4,5-trisphosphate (IP3) generating agonists, such as platelet-derived growth factor (PDGF) and Angiotensin I1 (Ang II). |
| 1912 | 10997698 | We postulated that this action of TGF-beta may be caused by regulation of the key intracellular calcium channel, the inositol 1,4,5-trisphosphate receptor (IP3R). |
| 1913 | 10997698 | Short-term exposure of mesangial cells to TGF-beta (15-60 min) leads to phosphorylation of the type I IP3R at specific serine residues. |
| 1914 | 10997698 | Long-term exposure of mesangial cells to TGF-beta (24 hours) leads to down-regulation of protein levels of both types I and III IP3Rs as assessed by Western blot and confocal analysis. |
| 1915 | 10997698 | We conclude that the vascular dysfunction of diabetes leading to glomerular hypertrophy is mediated, in part, by TGF-beta-induced regulation of IP3Rs. |
| 1916 | 11050244 | Hyperglycemia-induced mitochondrial superoxide overproduction activates the hexosamine pathway and induces plasminogen activator inhibitor-1 expression by increasing Sp1 glycosylation. |
| 1917 | 11050244 | Both decreased glyceraldehyde-3-phosphate dehydrogenase activity and increased hexosamine pathway activity were prevented completely by an inhibitor of electron transport complex II (thenoyltrifluoroacetone), an uncoupler of oxidative phosphorylation (carbonyl cyanide m-chlorophenylhydrazone), a superoxide dismutase mimetic [manganese (III) tetrakis(4-benzoic acid) porphyrin], overexpression of either uncoupling protein 1 or manganese superoxide dismutase, and azaserine, an inhibitor of the rate-limiting enzyme in the hexosamine pathway (glutamine:fructose-6-phosphate amidotransferase). |
| 1918 | 11050244 | Hyperglycemia increased expression from a transforming growth factor-beta(1) promoter luciferase reporter by 2-fold and increased expression from a (-740 to +44) plasminogen activator inhibitor-1 promoter luciferase reporter gene by nearly 3-fold. |
| 1919 | 11050244 | Hyperglycemia increased expression from an 85-bp truncated plasminogen activator inhibitor-1 (PAI-1) promoter luciferase reporter containing two Sp1 sites in a similar fashion (3.8-fold). |
| 1920 | 11078447 | Testicular sertoli cells protect islet beta-cells from autoimmune destruction in NOD mice by a transforming growth factor-beta1-dependent mechanism. |
| 1921 | 11078447 | The aim of this study was to determine whether Fas ligand (FasL) and/or transforming growth factor (TGF)-beta, immunoregulatory proteins produced by Sertoli cells, might mediate the protective effects of these cells against autoimmune destruction of islet beta-cells. |
| 1922 | 11078447 | Immunohistochemical examination of Sertoli cell grafts in normoglycemic mice revealed that TGF-beta1 expression by Sertoli cells remained high, whereas FasL expression by Sertoli cells decreased progressively posttransplantation. |
| 1923 | 11078447 | Islet graft destruction in anti-TGF-beta1-treated mice was associated with increases in interferon (IFN)-gamma-producing cells and decreases in interleukin (IL)-4-producing cells in the islet grafts. |
| 1924 | 11078447 | We conclude that 1) Sertoli cell production of TGF-beta1, not FasL, protects islet beta-cells from autoimmune destruction and 2) TGF-beta1 diverts islet-infiltrating cells from a beta-cell-destructive (IFN-gamma+) phenotype to a nondestructive (IL-4+) phenotype. |
| 1925 | 11078447 | Testicular sertoli cells protect islet beta-cells from autoimmune destruction in NOD mice by a transforming growth factor-beta1-dependent mechanism. |
| 1926 | 11078447 | The aim of this study was to determine whether Fas ligand (FasL) and/or transforming growth factor (TGF)-beta, immunoregulatory proteins produced by Sertoli cells, might mediate the protective effects of these cells against autoimmune destruction of islet beta-cells. |
| 1927 | 11078447 | Immunohistochemical examination of Sertoli cell grafts in normoglycemic mice revealed that TGF-beta1 expression by Sertoli cells remained high, whereas FasL expression by Sertoli cells decreased progressively posttransplantation. |
| 1928 | 11078447 | Islet graft destruction in anti-TGF-beta1-treated mice was associated with increases in interferon (IFN)-gamma-producing cells and decreases in interleukin (IL)-4-producing cells in the islet grafts. |
| 1929 | 11078447 | We conclude that 1) Sertoli cell production of TGF-beta1, not FasL, protects islet beta-cells from autoimmune destruction and 2) TGF-beta1 diverts islet-infiltrating cells from a beta-cell-destructive (IFN-gamma+) phenotype to a nondestructive (IL-4+) phenotype. |
| 1930 | 11078447 | Testicular sertoli cells protect islet beta-cells from autoimmune destruction in NOD mice by a transforming growth factor-beta1-dependent mechanism. |
| 1931 | 11078447 | The aim of this study was to determine whether Fas ligand (FasL) and/or transforming growth factor (TGF)-beta, immunoregulatory proteins produced by Sertoli cells, might mediate the protective effects of these cells against autoimmune destruction of islet beta-cells. |
| 1932 | 11078447 | Immunohistochemical examination of Sertoli cell grafts in normoglycemic mice revealed that TGF-beta1 expression by Sertoli cells remained high, whereas FasL expression by Sertoli cells decreased progressively posttransplantation. |
| 1933 | 11078447 | Islet graft destruction in anti-TGF-beta1-treated mice was associated with increases in interferon (IFN)-gamma-producing cells and decreases in interleukin (IL)-4-producing cells in the islet grafts. |
| 1934 | 11078447 | We conclude that 1) Sertoli cell production of TGF-beta1, not FasL, protects islet beta-cells from autoimmune destruction and 2) TGF-beta1 diverts islet-infiltrating cells from a beta-cell-destructive (IFN-gamma+) phenotype to a nondestructive (IL-4+) phenotype. |
| 1935 | 11079738 | In particular, growth hormone (GH)/insulin-like growth factors (IGFs), transforming growth factor beta (TGF-beta), vascular endothelial growth factor (VEGF) and epidermal growth factor (EGF) have measurable effects on the development of experimental diabetic kidney disease through complex intra-renal systems. |
| 1936 | 11126235 | Molecular mechanisms of insulin resistance and the role of the adipocyte. |
| 1937 | 11126235 | The role of TNFalpha in insulin resistance and other pathologies associated with obesity, have been examined in several experimental systems including obese mice with homozygous null mutations at the TNFalpha or TNF receptor loci. |
| 1938 | 11126235 | Analysis of these animals demonstrated that the genetic absence of TNF signaling in obesity: (i) significantly improves insulin receptor signaling capacity and consequently insulin sensitivity; (ii) prevents brown adipose tissue atrophy and beta3-adrenoreceptor deficiency and improves thermo-adaptive responses, (iii) decreases the elevated PAI-1 and TGFbeta production; and (iv) lowers hyperlipidemia and hyperleptinemia. |
| 1939 | 11134258 | At 2 mo, inulin clearance, urinary albumin excretion, fractional albumin clearance, glomerular volume, and glomerular content of immunoreactive transforming growth factor-beta (TGF-beta) and collagen alpha1 (IV) all were significantly increased in unsupplemented D compared with age-matched nondiabetic controls. |
| 1940 | 11134258 | VC suppressed urinary albumin excretion, fractional albumin clearance, and glomerular volume but not glomerular or tubular TGF-beta or glomerular collagen alpha1 (IV) content. |
| 1941 | 11134258 | At 2 mo, inulin clearance, urinary albumin excretion, fractional albumin clearance, glomerular volume, and glomerular content of immunoreactive transforming growth factor-beta (TGF-beta) and collagen alpha1 (IV) all were significantly increased in unsupplemented D compared with age-matched nondiabetic controls. |
| 1942 | 11134258 | VC suppressed urinary albumin excretion, fractional albumin clearance, and glomerular volume but not glomerular or tubular TGF-beta or glomerular collagen alpha1 (IV) content. |
| 1943 | 11145922 | The major putative angiogenic factor, vascular endothelial growth factor (VEGF), seems to increase to a greater extent and more consistently than other measured angiogenic factors, such as fibroblast growth factor-2 (FGF-2) and transforming growth factor-beta1 (TGF-beta1). |
| 1944 | 11180921 | Tumor necrosis factor-alpha (TNF alpha), interleukin 1beta (IL-1beta), platelet-derived growth factor BB (PDGF-BB) and transforming growth factor-beta1 (TGF-beta1) in cytoplasm were quantified by enzyme-linked immunosorbent assays (ELISA). |
| 1945 | 11180921 | Alkaline phosphatase (ALP) activity was standardized by the DNA content of the cells. |
| 1946 | 11259366 | Small proteoglycans in human diabetic nephropathy: discrepancy between glomerular expression and protein accumulation of decorin, biglycan, lumican, and fibromodulin. |
| 1947 | 11259366 | Small leucine-rich proteoglycans (SLRPs), for example, decorin, biglycan, fibromodulin, and lumican, are extracellular matrix organizers and binding partners of TGF-b. |
| 1948 | 11259366 | Biglycan was expressed by glomerular endothelial cells and, together with fibromodulin, by distal tubular cells and in collecting ducts. |
| 1949 | 11259366 | Decorin and lumican became expressed in tubuli. |
| 1950 | 11259366 | In severe glomerulosclerosis, increased decorin concentrations were found in plasma and urine, and urinary TGF-b/decorin complexes could be demonstrated indirectly. |
| 1951 | 11259366 | Small proteoglycans in human diabetic nephropathy: discrepancy between glomerular expression and protein accumulation of decorin, biglycan, lumican, and fibromodulin. |
| 1952 | 11259366 | Small leucine-rich proteoglycans (SLRPs), for example, decorin, biglycan, fibromodulin, and lumican, are extracellular matrix organizers and binding partners of TGF-b. |
| 1953 | 11259366 | Biglycan was expressed by glomerular endothelial cells and, together with fibromodulin, by distal tubular cells and in collecting ducts. |
| 1954 | 11259366 | Decorin and lumican became expressed in tubuli. |
| 1955 | 11259366 | In severe glomerulosclerosis, increased decorin concentrations were found in plasma and urine, and urinary TGF-b/decorin complexes could be demonstrated indirectly. |
| 1956 | 11264900 | There was a decrease in the activity of Mn-superoxide dismutase (SOD), suggesting abnormal mitochondrial metabolism of reactive oxygen species. |
| 1957 | 11264900 | The expression of transforming growth factor-beta1 (TGF-beta1), known as a growth factor and a suppressor of GSH synthesis, elevated in DM rat hearts. |
| 1958 | 11264900 | Collectively, it was suggested a linkage between mitochondrial damage to generate reactive oxygen species and inactivation of Mn-SOD and elevation of the expression of TGF-beta1 to lead suppression of GSH synthesis and induction of fibrous change for the consequent cardiac dysfunction in DM. |
| 1959 | 11264900 | There was a decrease in the activity of Mn-superoxide dismutase (SOD), suggesting abnormal mitochondrial metabolism of reactive oxygen species. |
| 1960 | 11264900 | The expression of transforming growth factor-beta1 (TGF-beta1), known as a growth factor and a suppressor of GSH synthesis, elevated in DM rat hearts. |
| 1961 | 11264900 | Collectively, it was suggested a linkage between mitochondrial damage to generate reactive oxygen species and inactivation of Mn-SOD and elevation of the expression of TGF-beta1 to lead suppression of GSH synthesis and induction of fibrous change for the consequent cardiac dysfunction in DM. |
| 1962 | 11279102 | Sorting nexin 6, a novel SNX, interacts with the transforming growth factor-beta family of receptor serine-threonine kinases. |
| 1963 | 11279102 | Human SNX1, -2, and -4 have been proposed to play a role in receptor trafficking and have been shown to bind to several receptor tyrosine kinases, including receptors for epidermal growth factor, platelet-derived growth factor, and insulin as well as the long form of the leptin receptor, a glycoprotein 130-associated receptor. |
| 1964 | 11279102 | We now describe a novel member of this family, SNX6, which interacts with members of the transforming growth factor-beta family of receptor serine-threonine kinases. |
| 1965 | 11279102 | Of the type II receptors, SNX6 was found to interact strongly with ActRIIB and more moderately with wild type and kinase-defective mutants of TbetaRII. |
| 1966 | 11279102 | Conversely, SNX6 behaved similarly to the other SNX proteins in its interactions with receptor tyrosine kinases. |
| 1967 | 11279102 | Sorting nexin 6, a novel SNX, interacts with the transforming growth factor-beta family of receptor serine-threonine kinases. |
| 1968 | 11279102 | Human SNX1, -2, and -4 have been proposed to play a role in receptor trafficking and have been shown to bind to several receptor tyrosine kinases, including receptors for epidermal growth factor, platelet-derived growth factor, and insulin as well as the long form of the leptin receptor, a glycoprotein 130-associated receptor. |
| 1969 | 11279102 | We now describe a novel member of this family, SNX6, which interacts with members of the transforming growth factor-beta family of receptor serine-threonine kinases. |
| 1970 | 11279102 | Of the type II receptors, SNX6 was found to interact strongly with ActRIIB and more moderately with wild type and kinase-defective mutants of TbetaRII. |
| 1971 | 11279102 | Conversely, SNX6 behaved similarly to the other SNX proteins in its interactions with receptor tyrosine kinases. |
| 1972 | 11285272 | TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage. |
| 1973 | 11285272 | In this study, we showed that TGF-beta/Smad3 signals inhibit terminal hypertrophic differentiation of chondrocyte and are essential for maintaining articular cartilage. |
| 1974 | 11285272 | Mutant mice homozygous for a targeted disruption of Smad3 exon 8 (Smad3(ex8/ex8)) developed degenerative joint disease resembling human osteoarthritis, as characterized by progressive loss of articular cartilage, formation of large osteophytes, decreased production of proteoglycans, and abnormally increased number of type X collagen-expressing chondrocytes in synovial joints. |
| 1975 | 11285272 | These data suggest that TGF-beta/Smad3 signals are essential for repressing articular chondrocyte differentiation. |
| 1976 | 11285272 | TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage. |
| 1977 | 11285272 | In this study, we showed that TGF-beta/Smad3 signals inhibit terminal hypertrophic differentiation of chondrocyte and are essential for maintaining articular cartilage. |
| 1978 | 11285272 | Mutant mice homozygous for a targeted disruption of Smad3 exon 8 (Smad3(ex8/ex8)) developed degenerative joint disease resembling human osteoarthritis, as characterized by progressive loss of articular cartilage, formation of large osteophytes, decreased production of proteoglycans, and abnormally increased number of type X collagen-expressing chondrocytes in synovial joints. |
| 1979 | 11285272 | These data suggest that TGF-beta/Smad3 signals are essential for repressing articular chondrocyte differentiation. |
| 1980 | 11285272 | TGF-beta/Smad3 signals repress chondrocyte hypertrophic differentiation and are required for maintaining articular cartilage. |
| 1981 | 11285272 | In this study, we showed that TGF-beta/Smad3 signals inhibit terminal hypertrophic differentiation of chondrocyte and are essential for maintaining articular cartilage. |
| 1982 | 11285272 | Mutant mice homozygous for a targeted disruption of Smad3 exon 8 (Smad3(ex8/ex8)) developed degenerative joint disease resembling human osteoarthritis, as characterized by progressive loss of articular cartilage, formation of large osteophytes, decreased production of proteoglycans, and abnormally increased number of type X collagen-expressing chondrocytes in synovial joints. |
| 1983 | 11285272 | These data suggest that TGF-beta/Smad3 signals are essential for repressing articular chondrocyte differentiation. |
| 1984 | 11309160 | The aim of this study was to evaluate possible changes in the circulating levels of interferon (IFN)-gamma, interleukin (IL)-4 and transforming growth factor (TGF)-beta in association with the autoimmune process leading to type 1 diabetes. |
| 1985 | 11309160 | Newly diagnosed diabetic children had lower levels of IFN-gamma, IL-4 and TGF-beta 1 signals compared to their age- and sex-matched controls (P < 0.02, P < 0.005 and P < 0.005, respectively) and also the autoantibody-positive subjects had significantly lower levels of IL-4 and TGF-beta 1 in comparison with their matched controls (P = 0.0013 and P = 0.012). |
| 1986 | 11309160 | Our results suggest a systemic bias towards reduced production of T-helper cell type 2 cytokines (IL-4 and TGF-beta 1) during the autoimmune process, but there was also a reduced level of IFN-gamma expression in the periphery at the onset of clinical diabetes. |
| 1987 | 11309160 | The aim of this study was to evaluate possible changes in the circulating levels of interferon (IFN)-gamma, interleukin (IL)-4 and transforming growth factor (TGF)-beta in association with the autoimmune process leading to type 1 diabetes. |
| 1988 | 11309160 | Newly diagnosed diabetic children had lower levels of IFN-gamma, IL-4 and TGF-beta 1 signals compared to their age- and sex-matched controls (P < 0.02, P < 0.005 and P < 0.005, respectively) and also the autoantibody-positive subjects had significantly lower levels of IL-4 and TGF-beta 1 in comparison with their matched controls (P = 0.0013 and P = 0.012). |
| 1989 | 11309160 | Our results suggest a systemic bias towards reduced production of T-helper cell type 2 cytokines (IL-4 and TGF-beta 1) during the autoimmune process, but there was also a reduced level of IFN-gamma expression in the periphery at the onset of clinical diabetes. |
| 1990 | 11316739 | Advanced glycosylation end products up-regulate connective tissue growth factor (insulin-like growth factor-binding protein-related protein 2) in human fibroblasts: a potential mechanism for expansion of extracellular matrix in diabetes mellitus. |
| 1991 | 11316739 | Connective tissue growth factor (CTGF), also known as insulin-like growth factor-binding protein-related protein-2 (IGFBP-rP2), is a potent inducer of extracellular matrix synthesis and angiogenesis and is increased in tissues from rodent models of diabetes. |
| 1992 | 11316739 | In contrast, mRNAs for other IGFBP superfamily members, IGFBP-rP1 (mac 25) and IGFBP-3, were not up-regulated by AGE. |
| 1993 | 11316739 | Reactive oxygen species as well as endogenous transforming growth factor-beta1 could not explain the AGE effect on CTGF mRNA. |
| 1994 | 11337363 | Increased glomerular and tubular expression of transforming growth factor-beta1, its type II receptor, and activation of the Smad signaling pathway in the db/db mouse. |
| 1995 | 11337363 | To establish the role of the TGF-beta system in type 2 diabetic nephropathy, we examined the intrarenal localization and expression of the TGF-beta1 isoform, the TGF-beta type II receptor, and the Smad signaling pathway in the 16-week-old db/db mouse, a genetic model of type 2 diabetes that exhibits mesangial matrix expansion, glomerular basement membrane thickening, and renal insufficiency that closely resemble the human disease. |
| 1996 | 11337363 | In situ hybridization and immunohistochemical staining for the TGF-beta type II receptor revealed concordant and significant increases of both mRNA and protein in the glomerular and tubular compartments of diabetic animals. |
| 1997 | 11337363 | Increased glomerular and tubular expression of transforming growth factor-beta1, its type II receptor, and activation of the Smad signaling pathway in the db/db mouse. |
| 1998 | 11337363 | To establish the role of the TGF-beta system in type 2 diabetic nephropathy, we examined the intrarenal localization and expression of the TGF-beta1 isoform, the TGF-beta type II receptor, and the Smad signaling pathway in the 16-week-old db/db mouse, a genetic model of type 2 diabetes that exhibits mesangial matrix expansion, glomerular basement membrane thickening, and renal insufficiency that closely resemble the human disease. |
| 1999 | 11337363 | In situ hybridization and immunohistochemical staining for the TGF-beta type II receptor revealed concordant and significant increases of both mRNA and protein in the glomerular and tubular compartments of diabetic animals. |
| 2000 | 11337363 | Increased glomerular and tubular expression of transforming growth factor-beta1, its type II receptor, and activation of the Smad signaling pathway in the db/db mouse. |
| 2001 | 11337363 | To establish the role of the TGF-beta system in type 2 diabetic nephropathy, we examined the intrarenal localization and expression of the TGF-beta1 isoform, the TGF-beta type II receptor, and the Smad signaling pathway in the 16-week-old db/db mouse, a genetic model of type 2 diabetes that exhibits mesangial matrix expansion, glomerular basement membrane thickening, and renal insufficiency that closely resemble the human disease. |
| 2002 | 11337363 | In situ hybridization and immunohistochemical staining for the TGF-beta type II receptor revealed concordant and significant increases of both mRNA and protein in the glomerular and tubular compartments of diabetic animals. |
| 2003 | 11353688 | Transforming growth factor-beta1 (TGF-beta1) immunostaining revealed that DH kidneys showed the highest glomerular expression. |
| 2004 | 11357481 | Angiotensin converting enzyme inhibitor suppresses glomerular transforming growth factor beta receptor expression in experimental diabetes in rats. |
| 2005 | 11359854 | Several studies have provided indirect evidence in support of a role for beta cell-specific Th2 cells in regulating insulin-dependent diabetes (IDDM). |
| 2006 | 11359854 | Adoptive transfer of a GAD65-specific Th2 cell clone (characterized by the secretion of IL-4, IL-5, and IL-10, but not IFN-gamma or TGF-beta) into 2- or 12-wk-old NOD female recipients prevented the progression of insulitis and subsequent development of overt IDDM. |
| 2007 | 11359854 | The immunoregulatory function of a given Th cell clone was dependent on the relative levels of IFN-gamma vs IL-4 and IL-10 secreted. |
| 2008 | 11369711 | Treatment of (PL/J x SJL)F(1) mice with low-dose oral myelin basic protein (MBP) (0.5 mg) and simultaneous oral IL-10 given 3 times reduced the severity and incidence of experimental autoimmune encephalomyelitis (EAE), whereas administration of oral IL-10 alone or MBP alone given in these doses had no effect. |
| 2009 | 11369711 | Lymphocytes from mice treated orally with MBP and IL-10 proliferated less, and produced decreased amounts of IFN-gamma and IL-2 and increased amounts of IL-10 and transforming growth factor-beta upon in vitro stimulation with MBP. |
| 2010 | 11369711 | Nasal administration of antigen and IL-10 reduced proliferative responses and IFN-gamma production, increased IL-10 production, and enhanced protection from EAE. |
| 2011 | 11369711 | In addition, oral IL-10 combined with oral myelin oligodendrocyte glycoprotein (MOG) 35-55 reduced relapses in MOG-induced EAE in the NOD mouse, as well as enhanced the protective effect of oral insulin in the NOD model of diabetes. |
| 2012 | 11384198 | Citrulline formed by the NOS reaction is recycled to arginine by the citrulline-NO cycle, which is composed of NOS, argininosuccinate synthetase (AS), and argininosuccinate lyase. |
| 2013 | 11384198 | Cationic amino acid transporter (CAT)-1 mRNA remained little changed, and CAT-2 mRNA was not detected. |
| 2014 | 11384198 | Transforming growth factor-beta1 (TGF-beta1) mRNA in the aorta was also induced. |
| 2015 | 11384198 | TGF-beta1 induced eNOS and AS mRNAs in human umbilical vein endothelial cells but inhibited the proliferation of HUVEC. |
| 2016 | 11384198 | These results indicate that eNOS and AS are coinduced in the aorta in early stages of STZ-induced diabetic rats and that the induction is mediated by TGF-beta1. |
| 2017 | 11384198 | Citrulline formed by the NOS reaction is recycled to arginine by the citrulline-NO cycle, which is composed of NOS, argininosuccinate synthetase (AS), and argininosuccinate lyase. |
| 2018 | 11384198 | Cationic amino acid transporter (CAT)-1 mRNA remained little changed, and CAT-2 mRNA was not detected. |
| 2019 | 11384198 | Transforming growth factor-beta1 (TGF-beta1) mRNA in the aorta was also induced. |
| 2020 | 11384198 | TGF-beta1 induced eNOS and AS mRNAs in human umbilical vein endothelial cells but inhibited the proliferation of HUVEC. |
| 2021 | 11384198 | These results indicate that eNOS and AS are coinduced in the aorta in early stages of STZ-induced diabetic rats and that the induction is mediated by TGF-beta1. |
| 2022 | 11384198 | Citrulline formed by the NOS reaction is recycled to arginine by the citrulline-NO cycle, which is composed of NOS, argininosuccinate synthetase (AS), and argininosuccinate lyase. |
| 2023 | 11384198 | Cationic amino acid transporter (CAT)-1 mRNA remained little changed, and CAT-2 mRNA was not detected. |
| 2024 | 11384198 | Transforming growth factor-beta1 (TGF-beta1) mRNA in the aorta was also induced. |
| 2025 | 11384198 | TGF-beta1 induced eNOS and AS mRNAs in human umbilical vein endothelial cells but inhibited the proliferation of HUVEC. |
| 2026 | 11384198 | These results indicate that eNOS and AS are coinduced in the aorta in early stages of STZ-induced diabetic rats and that the induction is mediated by TGF-beta1. |
| 2027 | 11397695 | Diabetic kidney demonstrated increased numbers of EN-RAGE-expressing inflammatory cells infiltrating the glomerulus and enhanced mRNA for transforming growth factor-beta, fibronectin, and alpha(1) (IV) collagen. |
| 2028 | 11423724 | High glucose decreases matrix metalloproteinase-2 activity in rat mesangial cells via transforming growth factor-beta1. |
| 2029 | 11423724 | The present studies were designed to investigate if the cytokine transforming growth factor-beta1 (TGF-beta1) mediates this effect of glucose. |
| 2030 | 11423724 | The activity of 72 kDa type IV collagenase, also known as matrix metalloproteinase-2 (MMP-2), was assessed using three methods: (1) fluoresceinated gelatin degradation assay to detect free enzyme activity (activity which is present in excess of TIMP-inhibited activity); (2) zymography to measure total (free + TIMP-bound) enzyme activity; (3) ELISA using specific antibodies to measure MMP-2 levels. |
| 2031 | 11423724 | TGF-beta1 and TIMP-2 levels were also determined by ELISA. |
| 2032 | 11423724 | Incubation of primary cultures of rat mesangial cells for 5 days in 30 vs. 5 mM glucose resulted in a 3-fold increase in production of total TGF-beta1, a significant decrease in MMP-2 activity and immunoreactive MMP-2 levels, and an increase in TIMP-2 levels. |
| 2033 | 11423724 | Addition of exogenous TGF-beta1 to mesangial cells incubated in 5 mM glucose replicated the high glucose effect by producing a significant decrease in MMP-2 levels with a concurrent increase in TIMP-2 levels. |
| 2034 | 11423724 | Furthermore, glucose-induced inhibition of MMP-2 activity was completely blocked by neutralization of TGF-beta1 with anti-TGF-beta1 antibody. |
| 2035 | 11423724 | We conclude that the decrease in MMP-2 activity induced by glucose loading is mediated via TGF-beta1. |
| 2036 | 11423724 | High glucose decreases matrix metalloproteinase-2 activity in rat mesangial cells via transforming growth factor-beta1. |
| 2037 | 11423724 | The present studies were designed to investigate if the cytokine transforming growth factor-beta1 (TGF-beta1) mediates this effect of glucose. |
| 2038 | 11423724 | The activity of 72 kDa type IV collagenase, also known as matrix metalloproteinase-2 (MMP-2), was assessed using three methods: (1) fluoresceinated gelatin degradation assay to detect free enzyme activity (activity which is present in excess of TIMP-inhibited activity); (2) zymography to measure total (free + TIMP-bound) enzyme activity; (3) ELISA using specific antibodies to measure MMP-2 levels. |
| 2039 | 11423724 | TGF-beta1 and TIMP-2 levels were also determined by ELISA. |
| 2040 | 11423724 | Incubation of primary cultures of rat mesangial cells for 5 days in 30 vs. 5 mM glucose resulted in a 3-fold increase in production of total TGF-beta1, a significant decrease in MMP-2 activity and immunoreactive MMP-2 levels, and an increase in TIMP-2 levels. |
| 2041 | 11423724 | Addition of exogenous TGF-beta1 to mesangial cells incubated in 5 mM glucose replicated the high glucose effect by producing a significant decrease in MMP-2 levels with a concurrent increase in TIMP-2 levels. |
| 2042 | 11423724 | Furthermore, glucose-induced inhibition of MMP-2 activity was completely blocked by neutralization of TGF-beta1 with anti-TGF-beta1 antibody. |
| 2043 | 11423724 | We conclude that the decrease in MMP-2 activity induced by glucose loading is mediated via TGF-beta1. |
| 2044 | 11423724 | High glucose decreases matrix metalloproteinase-2 activity in rat mesangial cells via transforming growth factor-beta1. |
| 2045 | 11423724 | The present studies were designed to investigate if the cytokine transforming growth factor-beta1 (TGF-beta1) mediates this effect of glucose. |
| 2046 | 11423724 | The activity of 72 kDa type IV collagenase, also known as matrix metalloproteinase-2 (MMP-2), was assessed using three methods: (1) fluoresceinated gelatin degradation assay to detect free enzyme activity (activity which is present in excess of TIMP-inhibited activity); (2) zymography to measure total (free + TIMP-bound) enzyme activity; (3) ELISA using specific antibodies to measure MMP-2 levels. |
| 2047 | 11423724 | TGF-beta1 and TIMP-2 levels were also determined by ELISA. |
| 2048 | 11423724 | Incubation of primary cultures of rat mesangial cells for 5 days in 30 vs. 5 mM glucose resulted in a 3-fold increase in production of total TGF-beta1, a significant decrease in MMP-2 activity and immunoreactive MMP-2 levels, and an increase in TIMP-2 levels. |
| 2049 | 11423724 | Addition of exogenous TGF-beta1 to mesangial cells incubated in 5 mM glucose replicated the high glucose effect by producing a significant decrease in MMP-2 levels with a concurrent increase in TIMP-2 levels. |
| 2050 | 11423724 | Furthermore, glucose-induced inhibition of MMP-2 activity was completely blocked by neutralization of TGF-beta1 with anti-TGF-beta1 antibody. |
| 2051 | 11423724 | We conclude that the decrease in MMP-2 activity induced by glucose loading is mediated via TGF-beta1. |
| 2052 | 11423724 | High glucose decreases matrix metalloproteinase-2 activity in rat mesangial cells via transforming growth factor-beta1. |
| 2053 | 11423724 | The present studies were designed to investigate if the cytokine transforming growth factor-beta1 (TGF-beta1) mediates this effect of glucose. |
| 2054 | 11423724 | The activity of 72 kDa type IV collagenase, also known as matrix metalloproteinase-2 (MMP-2), was assessed using three methods: (1) fluoresceinated gelatin degradation assay to detect free enzyme activity (activity which is present in excess of TIMP-inhibited activity); (2) zymography to measure total (free + TIMP-bound) enzyme activity; (3) ELISA using specific antibodies to measure MMP-2 levels. |
| 2055 | 11423724 | TGF-beta1 and TIMP-2 levels were also determined by ELISA. |
| 2056 | 11423724 | Incubation of primary cultures of rat mesangial cells for 5 days in 30 vs. 5 mM glucose resulted in a 3-fold increase in production of total TGF-beta1, a significant decrease in MMP-2 activity and immunoreactive MMP-2 levels, and an increase in TIMP-2 levels. |
| 2057 | 11423724 | Addition of exogenous TGF-beta1 to mesangial cells incubated in 5 mM glucose replicated the high glucose effect by producing a significant decrease in MMP-2 levels with a concurrent increase in TIMP-2 levels. |
| 2058 | 11423724 | Furthermore, glucose-induced inhibition of MMP-2 activity was completely blocked by neutralization of TGF-beta1 with anti-TGF-beta1 antibody. |
| 2059 | 11423724 | We conclude that the decrease in MMP-2 activity induced by glucose loading is mediated via TGF-beta1. |
| 2060 | 11423724 | High glucose decreases matrix metalloproteinase-2 activity in rat mesangial cells via transforming growth factor-beta1. |
| 2061 | 11423724 | The present studies were designed to investigate if the cytokine transforming growth factor-beta1 (TGF-beta1) mediates this effect of glucose. |
| 2062 | 11423724 | The activity of 72 kDa type IV collagenase, also known as matrix metalloproteinase-2 (MMP-2), was assessed using three methods: (1) fluoresceinated gelatin degradation assay to detect free enzyme activity (activity which is present in excess of TIMP-inhibited activity); (2) zymography to measure total (free + TIMP-bound) enzyme activity; (3) ELISA using specific antibodies to measure MMP-2 levels. |
| 2063 | 11423724 | TGF-beta1 and TIMP-2 levels were also determined by ELISA. |
| 2064 | 11423724 | Incubation of primary cultures of rat mesangial cells for 5 days in 30 vs. 5 mM glucose resulted in a 3-fold increase in production of total TGF-beta1, a significant decrease in MMP-2 activity and immunoreactive MMP-2 levels, and an increase in TIMP-2 levels. |
| 2065 | 11423724 | Addition of exogenous TGF-beta1 to mesangial cells incubated in 5 mM glucose replicated the high glucose effect by producing a significant decrease in MMP-2 levels with a concurrent increase in TIMP-2 levels. |
| 2066 | 11423724 | Furthermore, glucose-induced inhibition of MMP-2 activity was completely blocked by neutralization of TGF-beta1 with anti-TGF-beta1 antibody. |
| 2067 | 11423724 | We conclude that the decrease in MMP-2 activity induced by glucose loading is mediated via TGF-beta1. |
| 2068 | 11423724 | High glucose decreases matrix metalloproteinase-2 activity in rat mesangial cells via transforming growth factor-beta1. |
| 2069 | 11423724 | The present studies were designed to investigate if the cytokine transforming growth factor-beta1 (TGF-beta1) mediates this effect of glucose. |
| 2070 | 11423724 | The activity of 72 kDa type IV collagenase, also known as matrix metalloproteinase-2 (MMP-2), was assessed using three methods: (1) fluoresceinated gelatin degradation assay to detect free enzyme activity (activity which is present in excess of TIMP-inhibited activity); (2) zymography to measure total (free + TIMP-bound) enzyme activity; (3) ELISA using specific antibodies to measure MMP-2 levels. |
| 2071 | 11423724 | TGF-beta1 and TIMP-2 levels were also determined by ELISA. |
| 2072 | 11423724 | Incubation of primary cultures of rat mesangial cells for 5 days in 30 vs. 5 mM glucose resulted in a 3-fold increase in production of total TGF-beta1, a significant decrease in MMP-2 activity and immunoreactive MMP-2 levels, and an increase in TIMP-2 levels. |
| 2073 | 11423724 | Addition of exogenous TGF-beta1 to mesangial cells incubated in 5 mM glucose replicated the high glucose effect by producing a significant decrease in MMP-2 levels with a concurrent increase in TIMP-2 levels. |
| 2074 | 11423724 | Furthermore, glucose-induced inhibition of MMP-2 activity was completely blocked by neutralization of TGF-beta1 with anti-TGF-beta1 antibody. |
| 2075 | 11423724 | We conclude that the decrease in MMP-2 activity induced by glucose loading is mediated via TGF-beta1. |
| 2076 | 11423724 | High glucose decreases matrix metalloproteinase-2 activity in rat mesangial cells via transforming growth factor-beta1. |
| 2077 | 11423724 | The present studies were designed to investigate if the cytokine transforming growth factor-beta1 (TGF-beta1) mediates this effect of glucose. |
| 2078 | 11423724 | The activity of 72 kDa type IV collagenase, also known as matrix metalloproteinase-2 (MMP-2), was assessed using three methods: (1) fluoresceinated gelatin degradation assay to detect free enzyme activity (activity which is present in excess of TIMP-inhibited activity); (2) zymography to measure total (free + TIMP-bound) enzyme activity; (3) ELISA using specific antibodies to measure MMP-2 levels. |
| 2079 | 11423724 | TGF-beta1 and TIMP-2 levels were also determined by ELISA. |
| 2080 | 11423724 | Incubation of primary cultures of rat mesangial cells for 5 days in 30 vs. 5 mM glucose resulted in a 3-fold increase in production of total TGF-beta1, a significant decrease in MMP-2 activity and immunoreactive MMP-2 levels, and an increase in TIMP-2 levels. |
| 2081 | 11423724 | Addition of exogenous TGF-beta1 to mesangial cells incubated in 5 mM glucose replicated the high glucose effect by producing a significant decrease in MMP-2 levels with a concurrent increase in TIMP-2 levels. |
| 2082 | 11423724 | Furthermore, glucose-induced inhibition of MMP-2 activity was completely blocked by neutralization of TGF-beta1 with anti-TGF-beta1 antibody. |
| 2083 | 11423724 | We conclude that the decrease in MMP-2 activity induced by glucose loading is mediated via TGF-beta1. |
| 2084 | 11436183 | High glucose stimulates hyaluronan production by renal interstitial fibroblasts through the protein kinase C and transforming growth factor-beta cascade. |
| 2085 | 11436183 | The involvement of protein kinase C (PKC) and transforming growth factor-beta (TGF-beta) in this response was also examined. |
| 2086 | 11436183 | High glucose stimulates hyaluronan production by renal interstitial fibroblasts through the protein kinase C and transforming growth factor-beta cascade. |
| 2087 | 11436183 | The involvement of protein kinase C (PKC) and transforming growth factor-beta (TGF-beta) in this response was also examined. |
| 2088 | 11438667 | Smad proteins and hepatocyte growth factor control parallel regulatory pathways that converge on beta1-integrin to promote normal liver development. |
| 2089 | 11438667 | Mice lacking one copy each of Smad2 and Smad3 suffered midgestation lethality due to liver hypoplasia and anemia, suggesting essential dosage requirements of TGF-beta signal components. |
| 2090 | 11438667 | These pathways merge at the beta1-integrin, the level of which was increased by HGF in the cultured mutant livers. |
| 2091 | 11438667 | HGF treatment reversed the defects in cell proliferation and hepatic architecture in the Smad2(+/-); Smad3(+/-) livers. |
| 2092 | 11440360 | The hallmark of nephropathy is an abnormal accumulation of extracellular matrix within the mesangium, sustained by an upregulation of TGF-beta, possibly triggered by a local activation of the renin-angiotensin system. |
| 2093 | 11454519 | Effects of IGF-I and -II, IGF binding protein-3 (IGFBP-3), and transforming growth factor-beta (TGF-beta) on growth and apoptosis of human osteosarcoma Saos-2/B-10 cells: lack of IGF-independent IGFBP-3 effects. |
| 2094 | 11457671 | This study was performed to clarify the relationship between protein kinase C (PKC) activity and activation of TGF-beta1 and TSP-1 production in cultured human MCs exposed to high glucose levels. |
| 2095 | 11499561 | Exposure of MC to rhCTGF significantly increased fibronectin and collagen type I secretion. |
| 2096 | 11499561 | However, exposure to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in glomerulosclerosis, markedly induced the expression of CTGF transcripts. |
| 2097 | 11499561 | TGF-beta also induced abundant quantities of a small molecular weight form of CTGF (18 kDa). |
| 2098 | 11499561 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta neutralizing antibody blocked this stimulation. |
| 2099 | 11499561 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation in both diabetic and non-diabetic glomerulosclerosis, acting downstream of TGF-beta. |
| 2100 | 11499561 | Exposure of MC to rhCTGF significantly increased fibronectin and collagen type I secretion. |
| 2101 | 11499561 | However, exposure to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in glomerulosclerosis, markedly induced the expression of CTGF transcripts. |
| 2102 | 11499561 | TGF-beta also induced abundant quantities of a small molecular weight form of CTGF (18 kDa). |
| 2103 | 11499561 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta neutralizing antibody blocked this stimulation. |
| 2104 | 11499561 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation in both diabetic and non-diabetic glomerulosclerosis, acting downstream of TGF-beta. |
| 2105 | 11499561 | Exposure of MC to rhCTGF significantly increased fibronectin and collagen type I secretion. |
| 2106 | 11499561 | However, exposure to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in glomerulosclerosis, markedly induced the expression of CTGF transcripts. |
| 2107 | 11499561 | TGF-beta also induced abundant quantities of a small molecular weight form of CTGF (18 kDa). |
| 2108 | 11499561 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta neutralizing antibody blocked this stimulation. |
| 2109 | 11499561 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation in both diabetic and non-diabetic glomerulosclerosis, acting downstream of TGF-beta. |
| 2110 | 11499561 | Exposure of MC to rhCTGF significantly increased fibronectin and collagen type I secretion. |
| 2111 | 11499561 | However, exposure to TGF-beta, increased glucose concentrations, or cyclic mechanical strain, all causal factors in glomerulosclerosis, markedly induced the expression of CTGF transcripts. |
| 2112 | 11499561 | TGF-beta also induced abundant quantities of a small molecular weight form of CTGF (18 kDa). |
| 2113 | 11499561 | The induction of CTGF protein by a high glucose concentration was mediated by TGF-beta, since a TGF-beta neutralizing antibody blocked this stimulation. |
| 2114 | 11499561 | These results suggest that CTGF upregulation is an important factor in the pathogenesis of mesangial matrix accumulation in both diabetic and non-diabetic glomerulosclerosis, acting downstream of TGF-beta. |
| 2115 | 11521435 | Ten cytokines (alpha-IFN, gamma-IFN, GM-CSF, TGF-beta 1, Il-1, Il-4, Il-6, Il-6sR, TNF alpha) were measured in the serum, lacrimal fluid, and vitreous and subretinal fluid collected during operations. |
| 2116 | 11521435 | The data indicate that excessive or insufficient local and/or systemic production of at least seven cytokines (TNF alpha, gamma-IFN, Il-6, Il-pR, alpha-IFN, Il-8, and RGF-beta 1) can affect the retinal involvement in the pathological process and development of proliferative retinopathy in patients with insulin-dependent diabetes mellitus. |
| 2117 | 11522679 | In both SOD and D-SOD mice, renal cortical SOD-1 activity was twofold higher than values in the WT mice; blood glucose and glycosylated hemoglobin (GHb) levels did not differ in the two diabetic groups. |
| 2118 | 11522679 | Urinary albumin excretion, fractional albumin clearance, urinary transforming growth factor-beta (TGF-beta) excretion, glomerular volume, glomerular content of immunoreactive TGF-beta, and collagen alpha1 (IV) and renal cortical malondialdehyde (MDA) levels were significantly higher in D-WT mice compared with corresponding values in D-SOD mice. |
| 2119 | 11522679 | Glomerular volume, glomerular content of TGF-beta and collagen IV, renal cortical MDA, and urinary excretion of TGF-beta in D-SOD mice did not differ significantly from corresponding values in either the nondiabetic SOD or WT mice. |
| 2120 | 11522679 | In vitro infection of mesangial cells (MC) with a recombinant adenovirus encoding human SOD-1 increased SOD-1 activity threefold over control cells and prevented the reduction of aconitase activity, an index of cellular superoxide, and the increase in collagen synthesis that otherwise occurred in control MC in response to culture with 300 or 500 mg/dl glucose. |
| 2121 | 11522679 | In both SOD and D-SOD mice, renal cortical SOD-1 activity was twofold higher than values in the WT mice; blood glucose and glycosylated hemoglobin (GHb) levels did not differ in the two diabetic groups. |
| 2122 | 11522679 | Urinary albumin excretion, fractional albumin clearance, urinary transforming growth factor-beta (TGF-beta) excretion, glomerular volume, glomerular content of immunoreactive TGF-beta, and collagen alpha1 (IV) and renal cortical malondialdehyde (MDA) levels were significantly higher in D-WT mice compared with corresponding values in D-SOD mice. |
| 2123 | 11522679 | Glomerular volume, glomerular content of TGF-beta and collagen IV, renal cortical MDA, and urinary excretion of TGF-beta in D-SOD mice did not differ significantly from corresponding values in either the nondiabetic SOD or WT mice. |
| 2124 | 11522679 | In vitro infection of mesangial cells (MC) with a recombinant adenovirus encoding human SOD-1 increased SOD-1 activity threefold over control cells and prevented the reduction of aconitase activity, an index of cellular superoxide, and the increase in collagen synthesis that otherwise occurred in control MC in response to culture with 300 or 500 mg/dl glucose. |
| 2125 | 11562408 | At 6 mo, experimental diabetes was associated with a three-fold increase in expression of transforming growth factor (TGF)-beta1 (P < 0.01 versus control) and five-fold increase in platelet-derived growth factor (PDGF)-B gene expression (P < 0.01 versus control) in the tubulointerstitium. |
| 2126 | 11562408 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and PDGF-B mRNA in renal tubules. |
| 2127 | 11562408 | Aminoguanidine attenuated not only the overexpression of TGF-beta1 and PDGF-B but also reduced type IV collagen deposition in diabetic rats (P < 0.05). |
| 2128 | 11562408 | TGF-beta1 and PDGF mRNA within glomeruli were also similarly increased with diabetes and attenuated with aminoguanidine. |
| 2129 | 11562408 | At 6 mo, experimental diabetes was associated with a three-fold increase in expression of transforming growth factor (TGF)-beta1 (P < 0.01 versus control) and five-fold increase in platelet-derived growth factor (PDGF)-B gene expression (P < 0.01 versus control) in the tubulointerstitium. |
| 2130 | 11562408 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and PDGF-B mRNA in renal tubules. |
| 2131 | 11562408 | Aminoguanidine attenuated not only the overexpression of TGF-beta1 and PDGF-B but also reduced type IV collagen deposition in diabetic rats (P < 0.05). |
| 2132 | 11562408 | TGF-beta1 and PDGF mRNA within glomeruli were also similarly increased with diabetes and attenuated with aminoguanidine. |
| 2133 | 11562408 | At 6 mo, experimental diabetes was associated with a three-fold increase in expression of transforming growth factor (TGF)-beta1 (P < 0.01 versus control) and five-fold increase in platelet-derived growth factor (PDGF)-B gene expression (P < 0.01 versus control) in the tubulointerstitium. |
| 2134 | 11562408 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and PDGF-B mRNA in renal tubules. |
| 2135 | 11562408 | Aminoguanidine attenuated not only the overexpression of TGF-beta1 and PDGF-B but also reduced type IV collagen deposition in diabetic rats (P < 0.05). |
| 2136 | 11562408 | TGF-beta1 and PDGF mRNA within glomeruli were also similarly increased with diabetes and attenuated with aminoguanidine. |
| 2137 | 11563971 | Transient transfection of a transformed human mesangial cell line with a CTGF-V5 epitope fusion protein markedly increased fibronectin and plasminogen activator inhibitor-1 synthesis in cultures maintained in normal glucose (4 mM) conditions; a CTGF-antisense construct reduced the elevated synthesis of these proteins in high glucose (30 mM) cultures. |
| 2138 | 11563971 | Culture of primary human mesangial cells for 14 days in high glucose, or in low glucose supplemented with recombinant CTGF or transforming growth factor beta1, markedly increased CTGF mRNA levels and fibronectin synthesis. |
| 2139 | 11563971 | Nevertheless CTGF expression in diabetic kidneys is likely to be a key event in the development of glomerulosclerosis by affecting both matrix synthesis and, potentially through plasminogen activator inhibitor-1, its turnover. |
| 2140 | 11576932 | In mesangial and endothelial cells, the AGE-RAGE interaction caused enhanced formation of oxygen radicals with subsequent activation of nuclear factor-kappaB and release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-alpha), growth factors (transforming growth factor-beta1 [TGF-beta1], insulin-like growth factor-1), and adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). |
| 2141 | 11576932 | In tubular cells, incubation with AGE albumin was followed by stimulation of the mitogen-activating protein (MAP) kinase pathway and its downstream target, the activating protien-1 (AP-1) complex, TGF-beta1 overexpression, enhanced protein kinase C activity, decreased cell proliferation, and impaired protein degradation rate, in part caused by decreased cathepsin activities. |
| 2142 | 11576932 | The pathogenic relevance of AGEs was further verified by in vivo experiments in euglycemic rats and mice by the parenteral administration of AGE albumin, leading in the glomeruli to TGF-beta1 overproduction, enhanced gene expression of ECM proteins, and morphological lesions similar to those of DN. |
| 2143 | 11576932 | In mesangial and endothelial cells, the AGE-RAGE interaction caused enhanced formation of oxygen radicals with subsequent activation of nuclear factor-kappaB and release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-alpha), growth factors (transforming growth factor-beta1 [TGF-beta1], insulin-like growth factor-1), and adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). |
| 2144 | 11576932 | In tubular cells, incubation with AGE albumin was followed by stimulation of the mitogen-activating protein (MAP) kinase pathway and its downstream target, the activating protien-1 (AP-1) complex, TGF-beta1 overexpression, enhanced protein kinase C activity, decreased cell proliferation, and impaired protein degradation rate, in part caused by decreased cathepsin activities. |
| 2145 | 11576932 | The pathogenic relevance of AGEs was further verified by in vivo experiments in euglycemic rats and mice by the parenteral administration of AGE albumin, leading in the glomeruli to TGF-beta1 overproduction, enhanced gene expression of ECM proteins, and morphological lesions similar to those of DN. |
| 2146 | 11576932 | In mesangial and endothelial cells, the AGE-RAGE interaction caused enhanced formation of oxygen radicals with subsequent activation of nuclear factor-kappaB and release of pro-inflammatory cytokines (interleukin-6, tumor necrosis factor-alpha), growth factors (transforming growth factor-beta1 [TGF-beta1], insulin-like growth factor-1), and adhesion molecules (vascular cell adhesion molecule-1, intercellular adhesion molecule-1). |
| 2147 | 11576932 | In tubular cells, incubation with AGE albumin was followed by stimulation of the mitogen-activating protein (MAP) kinase pathway and its downstream target, the activating protien-1 (AP-1) complex, TGF-beta1 overexpression, enhanced protein kinase C activity, decreased cell proliferation, and impaired protein degradation rate, in part caused by decreased cathepsin activities. |
| 2148 | 11576932 | The pathogenic relevance of AGEs was further verified by in vivo experiments in euglycemic rats and mice by the parenteral administration of AGE albumin, leading in the glomeruli to TGF-beta1 overproduction, enhanced gene expression of ECM proteins, and morphological lesions similar to those of DN. |
| 2149 | 11576951 | Association of transforming growth factor-beta1 T29C polymorphism with the progression of diabetic nephropathy. |
| 2150 | 11576951 | Because transforming growth factor (TGF)-beta promotes extracellular matrix production in response to high glucose, TGF-beta is considered to play a central role in the pathogenesis of diabetic nephropathy. |
| 2151 | 11576951 | Association of transforming growth factor-beta1 T29C polymorphism with the progression of diabetic nephropathy. |
| 2152 | 11576951 | Because transforming growth factor (TGF)-beta promotes extracellular matrix production in response to high glucose, TGF-beta is considered to play a central role in the pathogenesis of diabetic nephropathy. |
| 2153 | 11576955 | Increased peritoneal expression of vascular endothelial growth factor and transforming growth factor-beta1 and excessive accumulation of advanced glycosylation end products may be involved in the progressive increase in membrane permeability, loss of ultrafiltration, and peritoneal fibrosis. |
| 2154 | 11675415 | Bone morphogenetic protein-7 (BMP7), a member of the transforming growth factor-beta (TGF-beta) superfamily of cytokines, is highly expressed in renal tubules and generally promotes maintenance of epithelial phenotype. |
| 2155 | 11675415 | Renal expression of the high-affinity BMP type II receptor and the type I receptor Alk2 (activin receptor-like kinase-2) decreased. |
| 2156 | 11675415 | Alk3 tended to decrease, but Alk6 remained unchanged. |
| 2157 | 11675415 | In cultured tubular cells, TGF-beta reduced BMP7 and Alk3 expression and increased gremlin but did not interrupt BMP7-induced activation of smad5 or Erk1 and -2. |
| 2158 | 11675415 | In contrast, BMP7 did not alter TGF-beta expression. |
| 2159 | 11675415 | Neutralization of endogenous BMP7 in cultured proximal tubular cells raised the expression of fibronectin and tended to increase collagen alpha(1) III mRNA levels. |
| 2160 | 11675415 | In conclusion, in experimental diabetic nephropathy, renal tubular BMP7 and some of its receptors decreased and gremlin, a secreted BMP antagonist, increased. |
| 2161 | 11675415 | Bone morphogenetic protein-7 (BMP7), a member of the transforming growth factor-beta (TGF-beta) superfamily of cytokines, is highly expressed in renal tubules and generally promotes maintenance of epithelial phenotype. |
| 2162 | 11675415 | Renal expression of the high-affinity BMP type II receptor and the type I receptor Alk2 (activin receptor-like kinase-2) decreased. |
| 2163 | 11675415 | Alk3 tended to decrease, but Alk6 remained unchanged. |
| 2164 | 11675415 | In cultured tubular cells, TGF-beta reduced BMP7 and Alk3 expression and increased gremlin but did not interrupt BMP7-induced activation of smad5 or Erk1 and -2. |
| 2165 | 11675415 | In contrast, BMP7 did not alter TGF-beta expression. |
| 2166 | 11675415 | Neutralization of endogenous BMP7 in cultured proximal tubular cells raised the expression of fibronectin and tended to increase collagen alpha(1) III mRNA levels. |
| 2167 | 11675415 | In conclusion, in experimental diabetic nephropathy, renal tubular BMP7 and some of its receptors decreased and gremlin, a secreted BMP antagonist, increased. |
| 2168 | 11675415 | Bone morphogenetic protein-7 (BMP7), a member of the transforming growth factor-beta (TGF-beta) superfamily of cytokines, is highly expressed in renal tubules and generally promotes maintenance of epithelial phenotype. |
| 2169 | 11675415 | Renal expression of the high-affinity BMP type II receptor and the type I receptor Alk2 (activin receptor-like kinase-2) decreased. |
| 2170 | 11675415 | Alk3 tended to decrease, but Alk6 remained unchanged. |
| 2171 | 11675415 | In cultured tubular cells, TGF-beta reduced BMP7 and Alk3 expression and increased gremlin but did not interrupt BMP7-induced activation of smad5 or Erk1 and -2. |
| 2172 | 11675415 | In contrast, BMP7 did not alter TGF-beta expression. |
| 2173 | 11675415 | Neutralization of endogenous BMP7 in cultured proximal tubular cells raised the expression of fibronectin and tended to increase collagen alpha(1) III mRNA levels. |
| 2174 | 11675415 | In conclusion, in experimental diabetic nephropathy, renal tubular BMP7 and some of its receptors decreased and gremlin, a secreted BMP antagonist, increased. |
| 2175 | 11695846 | Transforming growth factor (beta1) in testes of aged and diabetic rats: correlation with testicular function. |
| 2176 | 11695846 | This study was conducted to evaluate the expression of transforming growth factor-beta1 (TGF-beta1) in testis with aging and progress of diabetes mellitus (DM) and correlated this with testicular function. |
| 2177 | 11695846 | Transforming growth factor (beta1) in testes of aged and diabetic rats: correlation with testicular function. |
| 2178 | 11695846 | This study was conducted to evaluate the expression of transforming growth factor-beta1 (TGF-beta1) in testis with aging and progress of diabetes mellitus (DM) and correlated this with testicular function. |
| 2179 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2180 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2181 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2182 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2183 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2184 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2185 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2186 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2187 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2188 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2189 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2190 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2191 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2192 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2193 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2194 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2195 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2196 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2197 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2198 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2199 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2200 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2201 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2202 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2203 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2204 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2205 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2206 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2207 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2208 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2209 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2210 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2211 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2212 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2213 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2214 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2215 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2216 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2217 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2218 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2219 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2220 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2221 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2222 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2223 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2224 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2225 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2226 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2227 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2228 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2229 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2230 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2231 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2232 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2233 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2234 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2235 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2236 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2237 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2238 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2239 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2240 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2241 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2242 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2243 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2244 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2245 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2246 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2247 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2248 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2249 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2250 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2251 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2252 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2253 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2254 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2255 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2256 | 11696451 | Translational regulation of renal proximal tubular epithelial cell transforming growth factor-beta1 generation by insulin. |
| 2257 | 11696451 | The aim of the current study was to examine the effect of insulin on the generation of TGF-beta1 by proximal tubular cells. |
| 2258 | 11696451 | HK-2 cells were grown to confluence in the absence of insulin, and serum deprived for 48 hours before all experimental manipulations. |
| 2259 | 11696451 | Addition of insulin (5 microg/ml) to the culture medium led to a time-dependent increase in TGF-beta1 concentration in the cell culture supernatant, and increased incorporation of radiolabeled amino acids into TGF-beta1 suggestive of de novo TGF-beta1 protein synthesis. |
| 2260 | 11696451 | Addition of insulin did not alter TGF-beta1 mRNA expression as assessed by reverse transcriptase-polymerase chain reaction or Northern analysis. |
| 2261 | 11696451 | Insulin-induced increase in TGF-beta1 concentration was not abrogated by actinomycin D, however, stimulation by insulin, in the presence of cycloheximide led to a dose-dependent decrease in TGF-beta1 production. |
| 2262 | 11696451 | Addition of insulin had no effect on TGF-beta1 mRNA stability as assessed by actinomycin D chase, but led to increased binding of a cytoplasmic protein to a putative stem loop structure in the 5'-UTR of TGF-beta1 mRNA, previously implicated in the posttranscriptional control of TGF-beta1 synthesis. |
| 2263 | 11696451 | To address the functional significance of insulin-induced alteration in TGF-beta1 synthesis, we examined its effect on matrix turnover. |
| 2264 | 11696451 | Insulin stimulated type IV collagen gene expression and an increase in the concentrations of the type IV collagen laid down in the extracellular matrix. |
| 2265 | 11696451 | This increase in type IV collagen was abrogated when cells were stimulated by insulin in the presence of an anti-TGF-beta1-blocking antibody. |
| 2266 | 11696451 | In conclusion the data demonstrate that insulin may directly alter the production of TGF-beta1 by renal proximal tubular cells by a posttranscriptional mechanism, and that this may have implications for the increase in extracellular matrix that accompanies diabetic nephropathy. |
| 2267 | 11706299 | Pathogenesis of diabetic nephropathy: focus on transforming growth factor-beta and connective tissue growth factor. |
| 2268 | 11706299 | Although considerable improvement in the prognosis of diabetic nephropathy has been achieved in recent years due to intensive insulin and angiotensin-converting enzyme inhibitor treatment, these approaches do not provide complete protection against progression of diabetic nephropathy. |
| 2269 | 11706299 | An urgent need for additional novel therapies to prevent or further slow the progression of diabetic nephropathy motivated us to provide an up-to-date review with particular emphasis on the potential role of two growth factors--transforming growth factor-beta and connective tissue growth factor--in the pathogenesis of diabetic nephropathy. |
| 2270 | 11706299 | Recently, attention has focused on connective tissue growth factor, which mimics the biological activity of transforming growth factor-beta in profibrotic tissue formation. |
| 2271 | 11706299 | Thus, acting as a downstream mediator of the profibrotic activity of transforming growth factor-beta, connective tissue growth factor may constitute a more specific target for future antifibrotic therapies. |
| 2272 | 11706299 | Pathogenesis of diabetic nephropathy: focus on transforming growth factor-beta and connective tissue growth factor. |
| 2273 | 11706299 | Although considerable improvement in the prognosis of diabetic nephropathy has been achieved in recent years due to intensive insulin and angiotensin-converting enzyme inhibitor treatment, these approaches do not provide complete protection against progression of diabetic nephropathy. |
| 2274 | 11706299 | An urgent need for additional novel therapies to prevent or further slow the progression of diabetic nephropathy motivated us to provide an up-to-date review with particular emphasis on the potential role of two growth factors--transforming growth factor-beta and connective tissue growth factor--in the pathogenesis of diabetic nephropathy. |
| 2275 | 11706299 | Recently, attention has focused on connective tissue growth factor, which mimics the biological activity of transforming growth factor-beta in profibrotic tissue formation. |
| 2276 | 11706299 | Thus, acting as a downstream mediator of the profibrotic activity of transforming growth factor-beta, connective tissue growth factor may constitute a more specific target for future antifibrotic therapies. |
| 2277 | 11706299 | Pathogenesis of diabetic nephropathy: focus on transforming growth factor-beta and connective tissue growth factor. |
| 2278 | 11706299 | Although considerable improvement in the prognosis of diabetic nephropathy has been achieved in recent years due to intensive insulin and angiotensin-converting enzyme inhibitor treatment, these approaches do not provide complete protection against progression of diabetic nephropathy. |
| 2279 | 11706299 | An urgent need for additional novel therapies to prevent or further slow the progression of diabetic nephropathy motivated us to provide an up-to-date review with particular emphasis on the potential role of two growth factors--transforming growth factor-beta and connective tissue growth factor--in the pathogenesis of diabetic nephropathy. |
| 2280 | 11706299 | Recently, attention has focused on connective tissue growth factor, which mimics the biological activity of transforming growth factor-beta in profibrotic tissue formation. |
| 2281 | 11706299 | Thus, acting as a downstream mediator of the profibrotic activity of transforming growth factor-beta, connective tissue growth factor may constitute a more specific target for future antifibrotic therapies. |
| 2282 | 11706299 | Pathogenesis of diabetic nephropathy: focus on transforming growth factor-beta and connective tissue growth factor. |
| 2283 | 11706299 | Although considerable improvement in the prognosis of diabetic nephropathy has been achieved in recent years due to intensive insulin and angiotensin-converting enzyme inhibitor treatment, these approaches do not provide complete protection against progression of diabetic nephropathy. |
| 2284 | 11706299 | An urgent need for additional novel therapies to prevent or further slow the progression of diabetic nephropathy motivated us to provide an up-to-date review with particular emphasis on the potential role of two growth factors--transforming growth factor-beta and connective tissue growth factor--in the pathogenesis of diabetic nephropathy. |
| 2285 | 11706299 | Recently, attention has focused on connective tissue growth factor, which mimics the biological activity of transforming growth factor-beta in profibrotic tissue formation. |
| 2286 | 11706299 | Thus, acting as a downstream mediator of the profibrotic activity of transforming growth factor-beta, connective tissue growth factor may constitute a more specific target for future antifibrotic therapies. |
| 2287 | 11719827 | These haemodynamic pathways, independently and with metabolic pathways, activate intracellular second messengers such as protein kinase C and MAP kinase, nuclear transcription factors such as NF-kappaB and various growth factors such as the prosclerotic cytokine, TGF-beta and the angiogenic, permeability enhancing growth factor, VEGF. |
| 2288 | 11719827 | More novel strategies to influence vasoactive hormone action or to inhibit various metabolic pathways such as inhibitors of advanced glycation, specific protein kinase C isoforms and aldose reductase are at present under experimental and clinical investigation. |
| 2289 | 11726533 | The vitamin D hormone stimulates transforming growth factor TGFbeta-1 and interleukin 4 (IL-4) production, which in turn may suppress inflammatory T cell activity. |
| 2290 | 11733869 | Increased renal GLUT1 abundance and urinary TGF-beta 1 in streptozotocin-induced diabetic rats: implications for the development of nephropathy complicating diabetes. |
| 2291 | 11733869 | Increased expression of transforming growth factor beta-1 (TGF-beta 1) and glucose transporter (GLUT1) has been implicated in the genesis of diabetic nephropathy. |
| 2292 | 11733869 | The aim of this study was to evaluate GLUT1 protein levels in the renal cortex of a rat model of diabetes as well as its relationship to urinary albumin and TGF-beta1. |
| 2293 | 11733869 | Streptozotocin-injected rats (n = 13) and controls (n = 13) were compared for their urinary albumin, and TGF-beta 1 and for renal cortical and medullar GLUT1 protein abundance. |
| 2294 | 11733869 | GLUT1 protein content was determined by optical densitometry after Western blotting using an anti-GLUT1 antibody; urinary albumin was measured using electroimmunoassay, urinary TGF-beta 1 using ELISA. |
| 2295 | 11733869 | Forty-five days of diabetes resulted in increased albuminuria (p < 0.05), urinary TGF-beta 1 (p < 0.05) and GLUT1 protein abundance (p < 0.05). |
| 2296 | 11733869 | Increased renal GLUT1 abundance and urinary TGF-beta 1 in streptozotocin-induced diabetic rats: implications for the development of nephropathy complicating diabetes. |
| 2297 | 11733869 | Increased expression of transforming growth factor beta-1 (TGF-beta 1) and glucose transporter (GLUT1) has been implicated in the genesis of diabetic nephropathy. |
| 2298 | 11733869 | The aim of this study was to evaluate GLUT1 protein levels in the renal cortex of a rat model of diabetes as well as its relationship to urinary albumin and TGF-beta1. |
| 2299 | 11733869 | Streptozotocin-injected rats (n = 13) and controls (n = 13) were compared for their urinary albumin, and TGF-beta 1 and for renal cortical and medullar GLUT1 protein abundance. |
| 2300 | 11733869 | GLUT1 protein content was determined by optical densitometry after Western blotting using an anti-GLUT1 antibody; urinary albumin was measured using electroimmunoassay, urinary TGF-beta 1 using ELISA. |
| 2301 | 11733869 | Forty-five days of diabetes resulted in increased albuminuria (p < 0.05), urinary TGF-beta 1 (p < 0.05) and GLUT1 protein abundance (p < 0.05). |
| 2302 | 11733869 | Increased renal GLUT1 abundance and urinary TGF-beta 1 in streptozotocin-induced diabetic rats: implications for the development of nephropathy complicating diabetes. |
| 2303 | 11733869 | Increased expression of transforming growth factor beta-1 (TGF-beta 1) and glucose transporter (GLUT1) has been implicated in the genesis of diabetic nephropathy. |
| 2304 | 11733869 | The aim of this study was to evaluate GLUT1 protein levels in the renal cortex of a rat model of diabetes as well as its relationship to urinary albumin and TGF-beta1. |
| 2305 | 11733869 | Streptozotocin-injected rats (n = 13) and controls (n = 13) were compared for their urinary albumin, and TGF-beta 1 and for renal cortical and medullar GLUT1 protein abundance. |
| 2306 | 11733869 | GLUT1 protein content was determined by optical densitometry after Western blotting using an anti-GLUT1 antibody; urinary albumin was measured using electroimmunoassay, urinary TGF-beta 1 using ELISA. |
| 2307 | 11733869 | Forty-five days of diabetes resulted in increased albuminuria (p < 0.05), urinary TGF-beta 1 (p < 0.05) and GLUT1 protein abundance (p < 0.05). |
| 2308 | 11733869 | Increased renal GLUT1 abundance and urinary TGF-beta 1 in streptozotocin-induced diabetic rats: implications for the development of nephropathy complicating diabetes. |
| 2309 | 11733869 | Increased expression of transforming growth factor beta-1 (TGF-beta 1) and glucose transporter (GLUT1) has been implicated in the genesis of diabetic nephropathy. |
| 2310 | 11733869 | The aim of this study was to evaluate GLUT1 protein levels in the renal cortex of a rat model of diabetes as well as its relationship to urinary albumin and TGF-beta1. |
| 2311 | 11733869 | Streptozotocin-injected rats (n = 13) and controls (n = 13) were compared for their urinary albumin, and TGF-beta 1 and for renal cortical and medullar GLUT1 protein abundance. |
| 2312 | 11733869 | GLUT1 protein content was determined by optical densitometry after Western blotting using an anti-GLUT1 antibody; urinary albumin was measured using electroimmunoassay, urinary TGF-beta 1 using ELISA. |
| 2313 | 11733869 | Forty-five days of diabetes resulted in increased albuminuria (p < 0.05), urinary TGF-beta 1 (p < 0.05) and GLUT1 protein abundance (p < 0.05). |
| 2314 | 11733869 | Increased renal GLUT1 abundance and urinary TGF-beta 1 in streptozotocin-induced diabetic rats: implications for the development of nephropathy complicating diabetes. |
| 2315 | 11733869 | Increased expression of transforming growth factor beta-1 (TGF-beta 1) and glucose transporter (GLUT1) has been implicated in the genesis of diabetic nephropathy. |
| 2316 | 11733869 | The aim of this study was to evaluate GLUT1 protein levels in the renal cortex of a rat model of diabetes as well as its relationship to urinary albumin and TGF-beta1. |
| 2317 | 11733869 | Streptozotocin-injected rats (n = 13) and controls (n = 13) were compared for their urinary albumin, and TGF-beta 1 and for renal cortical and medullar GLUT1 protein abundance. |
| 2318 | 11733869 | GLUT1 protein content was determined by optical densitometry after Western blotting using an anti-GLUT1 antibody; urinary albumin was measured using electroimmunoassay, urinary TGF-beta 1 using ELISA. |
| 2319 | 11733869 | Forty-five days of diabetes resulted in increased albuminuria (p < 0.05), urinary TGF-beta 1 (p < 0.05) and GLUT1 protein abundance (p < 0.05). |
| 2320 | 11733869 | Increased renal GLUT1 abundance and urinary TGF-beta 1 in streptozotocin-induced diabetic rats: implications for the development of nephropathy complicating diabetes. |
| 2321 | 11733869 | Increased expression of transforming growth factor beta-1 (TGF-beta 1) and glucose transporter (GLUT1) has been implicated in the genesis of diabetic nephropathy. |
| 2322 | 11733869 | The aim of this study was to evaluate GLUT1 protein levels in the renal cortex of a rat model of diabetes as well as its relationship to urinary albumin and TGF-beta1. |
| 2323 | 11733869 | Streptozotocin-injected rats (n = 13) and controls (n = 13) were compared for their urinary albumin, and TGF-beta 1 and for renal cortical and medullar GLUT1 protein abundance. |
| 2324 | 11733869 | GLUT1 protein content was determined by optical densitometry after Western blotting using an anti-GLUT1 antibody; urinary albumin was measured using electroimmunoassay, urinary TGF-beta 1 using ELISA. |
| 2325 | 11733869 | Forty-five days of diabetes resulted in increased albuminuria (p < 0.05), urinary TGF-beta 1 (p < 0.05) and GLUT1 protein abundance (p < 0.05). |
| 2326 | 11752027 | Compared with control rats, D developed increased urinary excretion of albumin and transforming growth factor beta, renal insufficiency, glomerular mesangial matrix expansion, and glomerulosclerosis in association with depletion of glutathione and accumulation of malondialdehyde in renal cortex. |
| 2327 | 11752027 | Despite superior longitudinal glycemic control in D-INS, urinary excretion of albumin and transforming growth factor beta, glomerular mesangial matrix expansion, the extent of glomerulosclerosis, and renal cortical malondialdehyde content were all significantly greater, whereas cortical glutathione content was lower than corresponding values in D given LA. |
| 2328 | 11752027 | Compared with control rats, D developed increased urinary excretion of albumin and transforming growth factor beta, renal insufficiency, glomerular mesangial matrix expansion, and glomerulosclerosis in association with depletion of glutathione and accumulation of malondialdehyde in renal cortex. |
| 2329 | 11752027 | Despite superior longitudinal glycemic control in D-INS, urinary excretion of albumin and transforming growth factor beta, glomerular mesangial matrix expansion, the extent of glomerulosclerosis, and renal cortical malondialdehyde content were all significantly greater, whereas cortical glutathione content was lower than corresponding values in D given LA. |
| 2330 | 11755473 | Although the cytokine TGF-beta is secreted from regulatory T-cells (Th3), and is related to oral tolerance, the interleukin-2 (IL-2, Th1)/IL-4 (Th2) ratio in the patient group was significantly elevated (P<0.001), which might indicate that the oral tolerance is impaired in patients. |
| 2331 | 11756325 | In separate studies, 5-day-old BBdp rat pups were administered the aforementioned treatments, and expression of intestinal mRNA for gamma-interferon (IFN-gamma) or transforming growth factor-beta (TGF-beta) was quantified using reverse transcriptase-polymerase chain reaction. |
| 2332 | 11756325 | Oral exposure to diabetes-promoting food antigens or LPS downregulated the Th1 cytokine IFN-gamma and decreased the IFN-gamma/TGF-beta ratio. |
| 2333 | 11756325 | In separate studies, 5-day-old BBdp rat pups were administered the aforementioned treatments, and expression of intestinal mRNA for gamma-interferon (IFN-gamma) or transforming growth factor-beta (TGF-beta) was quantified using reverse transcriptase-polymerase chain reaction. |
| 2334 | 11756325 | Oral exposure to diabetes-promoting food antigens or LPS downregulated the Th1 cytokine IFN-gamma and decreased the IFN-gamma/TGF-beta ratio. |
| 2335 | 11774095 | Moreover, leptin exerts several other important metabolic effects on peripheral tissue, including modification of insulin action, induction of angiogenesis, and modulation of the immune system. |
| 2336 | 11774095 | In glomerular endothelial cells, leptin stimulates cellular proliferation, transforming growth factor-beta1 (TGF-beta1) synthesis, and type IV collagen production. |
| 2337 | 11774095 | Conversely, in mesangial cells, leptin upregulates synthesis of the TGF-beta type II receptor, but not TGF-beta1, and stimulates glucose transport and type I collagen production through signal transduction pathways involving phosphatidylinositol-3-kinase. |
| 2338 | 11774095 | These data suggest that leptin triggers a paracrine interaction in which glomerular endothelial cells secrete TGF-beta, to which sensitized mesangial cells may respond. |
| 2339 | 11774095 | Moreover, leptin exerts several other important metabolic effects on peripheral tissue, including modification of insulin action, induction of angiogenesis, and modulation of the immune system. |
| 2340 | 11774095 | In glomerular endothelial cells, leptin stimulates cellular proliferation, transforming growth factor-beta1 (TGF-beta1) synthesis, and type IV collagen production. |
| 2341 | 11774095 | Conversely, in mesangial cells, leptin upregulates synthesis of the TGF-beta type II receptor, but not TGF-beta1, and stimulates glucose transport and type I collagen production through signal transduction pathways involving phosphatidylinositol-3-kinase. |
| 2342 | 11774095 | These data suggest that leptin triggers a paracrine interaction in which glomerular endothelial cells secrete TGF-beta, to which sensitized mesangial cells may respond. |
| 2343 | 11774095 | Moreover, leptin exerts several other important metabolic effects on peripheral tissue, including modification of insulin action, induction of angiogenesis, and modulation of the immune system. |
| 2344 | 11774095 | In glomerular endothelial cells, leptin stimulates cellular proliferation, transforming growth factor-beta1 (TGF-beta1) synthesis, and type IV collagen production. |
| 2345 | 11774095 | Conversely, in mesangial cells, leptin upregulates synthesis of the TGF-beta type II receptor, but not TGF-beta1, and stimulates glucose transport and type I collagen production through signal transduction pathways involving phosphatidylinositol-3-kinase. |
| 2346 | 11774095 | These data suggest that leptin triggers a paracrine interaction in which glomerular endothelial cells secrete TGF-beta, to which sensitized mesangial cells may respond. |
| 2347 | 11784718 | The induction of actin cytoskeleton regulatory gene expression by high glucose was attenuated by the inhibitor of reactive oxygen species generation, carbonyl cyanide m-chlorophenylhydrazone but not by the protein kinase C inhibitor GF 109203X and was not mimicked by the addition of transforming growth factor beta. |
| 2348 | 11784718 | In aggregate, these results suggest that the induction of genes encoding actin cytoskeleton regulatory proteins (a) is a prominent component of the mesangial cell transcriptomic response in diabetic nephropathy and (b) is dependent on oxidative stress, is independent of protein kinase C and transforming growth factor-beta, and represents an adaptive response to actin cytoskeleton disassembly. |
| 2349 | 11784718 | The induction of actin cytoskeleton regulatory gene expression by high glucose was attenuated by the inhibitor of reactive oxygen species generation, carbonyl cyanide m-chlorophenylhydrazone but not by the protein kinase C inhibitor GF 109203X and was not mimicked by the addition of transforming growth factor beta. |
| 2350 | 11784718 | In aggregate, these results suggest that the induction of genes encoding actin cytoskeleton regulatory proteins (a) is a prominent component of the mesangial cell transcriptomic response in diabetic nephropathy and (b) is dependent on oxidative stress, is independent of protein kinase C and transforming growth factor-beta, and represents an adaptive response to actin cytoskeleton disassembly. |
| 2351 | 11788461 | Proteoglycans synthesized by arterial smooth muscle cells in the presence of transforming growth factor-beta1 exhibit increased binding to LDLs. |
| 2352 | 11793095 | Puberty permits increased expression of renal transforming growth factor-beta1 in experimental diabetes. |
| 2353 | 11793095 | Transforming growth factor-beta1 (TGF-beta1) is a major mediator of diabetic kidney disease. |
| 2354 | 11793095 | Puberty permits increased expression of renal transforming growth factor-beta1 in experimental diabetes. |
| 2355 | 11793095 | Transforming growth factor-beta1 (TGF-beta1) is a major mediator of diabetic kidney disease. |
| 2356 | 11807812 | Insulin-like growth factor binding protein-2 mediates the inhibition of DNA synthesis by transforming growth factor-beta in mink lung epithelial cells. |
| 2357 | 11807812 | Insulin-like growth factor binding protein-3 (IGFBP-3) has been proposed to mediate the growth inhibitory effects of transforming growth factor (TGF)-beta in breast and prostate cancer cells. |
| 2358 | 11807812 | Both TGF-beta and exogenous IGFBP-3 inhibit DNA synthesis in Mv1 mink lung epithelial cells (CCL64). |
| 2359 | 11807812 | Leu(60)-IGF-I also decreased the inhibition of CCL64 DNA synthesis by TGF-beta by up to 70%, whereas Long-R3-IGF-I, an IGF-I analog with higher affinity for IGF-I receptors than for IGFBPs, did not decrease inhibition, suggesting that the effect of Leu(60)-IGF-I resulted from its forming complexes with endogenous IGFBPs. |
| 2360 | 11807812 | Leu(60)-IGF-I did not decrease TGF-beta stimulation of a Smad3-dependent reporter gene. |
| 2361 | 11807812 | If exogenous and secreted IGFBP-2 must bind to CCL64 cells to inhibit DNA synthesis, Leu(60)-IGF-I might reduce the inhibition of DNA synthesis by bIGFBP-2 or TGF-beta by inhibiting the association of IGFBP-2 in the media with CCL64 cells. |
| 2362 | 11807812 | Since TGF-beta does not increase IGFBP-2 abundance, we propose that TGF-beta sensitizes CCL64 cells to the latent growth inhibitory activity of endogenous IGFBP-2 by potentiating an intracellular IGFBP-2 signaling pathway or by promoting the association of secreted IGFBP-2 with the plasma membrane. |
| 2363 | 11807812 | Insulin-like growth factor binding protein-2 mediates the inhibition of DNA synthesis by transforming growth factor-beta in mink lung epithelial cells. |
| 2364 | 11807812 | Insulin-like growth factor binding protein-3 (IGFBP-3) has been proposed to mediate the growth inhibitory effects of transforming growth factor (TGF)-beta in breast and prostate cancer cells. |
| 2365 | 11807812 | Both TGF-beta and exogenous IGFBP-3 inhibit DNA synthesis in Mv1 mink lung epithelial cells (CCL64). |
| 2366 | 11807812 | Leu(60)-IGF-I also decreased the inhibition of CCL64 DNA synthesis by TGF-beta by up to 70%, whereas Long-R3-IGF-I, an IGF-I analog with higher affinity for IGF-I receptors than for IGFBPs, did not decrease inhibition, suggesting that the effect of Leu(60)-IGF-I resulted from its forming complexes with endogenous IGFBPs. |
| 2367 | 11807812 | Leu(60)-IGF-I did not decrease TGF-beta stimulation of a Smad3-dependent reporter gene. |
| 2368 | 11807812 | If exogenous and secreted IGFBP-2 must bind to CCL64 cells to inhibit DNA synthesis, Leu(60)-IGF-I might reduce the inhibition of DNA synthesis by bIGFBP-2 or TGF-beta by inhibiting the association of IGFBP-2 in the media with CCL64 cells. |
| 2369 | 11807812 | Since TGF-beta does not increase IGFBP-2 abundance, we propose that TGF-beta sensitizes CCL64 cells to the latent growth inhibitory activity of endogenous IGFBP-2 by potentiating an intracellular IGFBP-2 signaling pathway or by promoting the association of secreted IGFBP-2 with the plasma membrane. |
| 2370 | 11807812 | Insulin-like growth factor binding protein-2 mediates the inhibition of DNA synthesis by transforming growth factor-beta in mink lung epithelial cells. |
| 2371 | 11807812 | Insulin-like growth factor binding protein-3 (IGFBP-3) has been proposed to mediate the growth inhibitory effects of transforming growth factor (TGF)-beta in breast and prostate cancer cells. |
| 2372 | 11807812 | Both TGF-beta and exogenous IGFBP-3 inhibit DNA synthesis in Mv1 mink lung epithelial cells (CCL64). |
| 2373 | 11807812 | Leu(60)-IGF-I also decreased the inhibition of CCL64 DNA synthesis by TGF-beta by up to 70%, whereas Long-R3-IGF-I, an IGF-I analog with higher affinity for IGF-I receptors than for IGFBPs, did not decrease inhibition, suggesting that the effect of Leu(60)-IGF-I resulted from its forming complexes with endogenous IGFBPs. |
| 2374 | 11807812 | Leu(60)-IGF-I did not decrease TGF-beta stimulation of a Smad3-dependent reporter gene. |
| 2375 | 11807812 | If exogenous and secreted IGFBP-2 must bind to CCL64 cells to inhibit DNA synthesis, Leu(60)-IGF-I might reduce the inhibition of DNA synthesis by bIGFBP-2 or TGF-beta by inhibiting the association of IGFBP-2 in the media with CCL64 cells. |
| 2376 | 11807812 | Since TGF-beta does not increase IGFBP-2 abundance, we propose that TGF-beta sensitizes CCL64 cells to the latent growth inhibitory activity of endogenous IGFBP-2 by potentiating an intracellular IGFBP-2 signaling pathway or by promoting the association of secreted IGFBP-2 with the plasma membrane. |
| 2377 | 11807812 | Insulin-like growth factor binding protein-2 mediates the inhibition of DNA synthesis by transforming growth factor-beta in mink lung epithelial cells. |
| 2378 | 11807812 | Insulin-like growth factor binding protein-3 (IGFBP-3) has been proposed to mediate the growth inhibitory effects of transforming growth factor (TGF)-beta in breast and prostate cancer cells. |
| 2379 | 11807812 | Both TGF-beta and exogenous IGFBP-3 inhibit DNA synthesis in Mv1 mink lung epithelial cells (CCL64). |
| 2380 | 11807812 | Leu(60)-IGF-I also decreased the inhibition of CCL64 DNA synthesis by TGF-beta by up to 70%, whereas Long-R3-IGF-I, an IGF-I analog with higher affinity for IGF-I receptors than for IGFBPs, did not decrease inhibition, suggesting that the effect of Leu(60)-IGF-I resulted from its forming complexes with endogenous IGFBPs. |
| 2381 | 11807812 | Leu(60)-IGF-I did not decrease TGF-beta stimulation of a Smad3-dependent reporter gene. |
| 2382 | 11807812 | If exogenous and secreted IGFBP-2 must bind to CCL64 cells to inhibit DNA synthesis, Leu(60)-IGF-I might reduce the inhibition of DNA synthesis by bIGFBP-2 or TGF-beta by inhibiting the association of IGFBP-2 in the media with CCL64 cells. |
| 2383 | 11807812 | Since TGF-beta does not increase IGFBP-2 abundance, we propose that TGF-beta sensitizes CCL64 cells to the latent growth inhibitory activity of endogenous IGFBP-2 by potentiating an intracellular IGFBP-2 signaling pathway or by promoting the association of secreted IGFBP-2 with the plasma membrane. |
| 2384 | 11807812 | Insulin-like growth factor binding protein-2 mediates the inhibition of DNA synthesis by transforming growth factor-beta in mink lung epithelial cells. |
| 2385 | 11807812 | Insulin-like growth factor binding protein-3 (IGFBP-3) has been proposed to mediate the growth inhibitory effects of transforming growth factor (TGF)-beta in breast and prostate cancer cells. |
| 2386 | 11807812 | Both TGF-beta and exogenous IGFBP-3 inhibit DNA synthesis in Mv1 mink lung epithelial cells (CCL64). |
| 2387 | 11807812 | Leu(60)-IGF-I also decreased the inhibition of CCL64 DNA synthesis by TGF-beta by up to 70%, whereas Long-R3-IGF-I, an IGF-I analog with higher affinity for IGF-I receptors than for IGFBPs, did not decrease inhibition, suggesting that the effect of Leu(60)-IGF-I resulted from its forming complexes with endogenous IGFBPs. |
| 2388 | 11807812 | Leu(60)-IGF-I did not decrease TGF-beta stimulation of a Smad3-dependent reporter gene. |
| 2389 | 11807812 | If exogenous and secreted IGFBP-2 must bind to CCL64 cells to inhibit DNA synthesis, Leu(60)-IGF-I might reduce the inhibition of DNA synthesis by bIGFBP-2 or TGF-beta by inhibiting the association of IGFBP-2 in the media with CCL64 cells. |
| 2390 | 11807812 | Since TGF-beta does not increase IGFBP-2 abundance, we propose that TGF-beta sensitizes CCL64 cells to the latent growth inhibitory activity of endogenous IGFBP-2 by potentiating an intracellular IGFBP-2 signaling pathway or by promoting the association of secreted IGFBP-2 with the plasma membrane. |
| 2391 | 11807812 | Insulin-like growth factor binding protein-2 mediates the inhibition of DNA synthesis by transforming growth factor-beta in mink lung epithelial cells. |
| 2392 | 11807812 | Insulin-like growth factor binding protein-3 (IGFBP-3) has been proposed to mediate the growth inhibitory effects of transforming growth factor (TGF)-beta in breast and prostate cancer cells. |
| 2393 | 11807812 | Both TGF-beta and exogenous IGFBP-3 inhibit DNA synthesis in Mv1 mink lung epithelial cells (CCL64). |
| 2394 | 11807812 | Leu(60)-IGF-I also decreased the inhibition of CCL64 DNA synthesis by TGF-beta by up to 70%, whereas Long-R3-IGF-I, an IGF-I analog with higher affinity for IGF-I receptors than for IGFBPs, did not decrease inhibition, suggesting that the effect of Leu(60)-IGF-I resulted from its forming complexes with endogenous IGFBPs. |
| 2395 | 11807812 | Leu(60)-IGF-I did not decrease TGF-beta stimulation of a Smad3-dependent reporter gene. |
| 2396 | 11807812 | If exogenous and secreted IGFBP-2 must bind to CCL64 cells to inhibit DNA synthesis, Leu(60)-IGF-I might reduce the inhibition of DNA synthesis by bIGFBP-2 or TGF-beta by inhibiting the association of IGFBP-2 in the media with CCL64 cells. |
| 2397 | 11807812 | Since TGF-beta does not increase IGFBP-2 abundance, we propose that TGF-beta sensitizes CCL64 cells to the latent growth inhibitory activity of endogenous IGFBP-2 by potentiating an intracellular IGFBP-2 signaling pathway or by promoting the association of secreted IGFBP-2 with the plasma membrane. |
| 2398 | 11812761 | Matrix metalloproteinase-2 (MMP-2) and transforming growth factor-beta(1) (TGF-beta(1)) levels increased in B6 MC exposed to 25 mmol/l glucose but returned to baseline levels when the glucose concentration was reduced to 6 mmol/l. |
| 2399 | 11812761 | MMP-2 and TGF-beta(1) were higher in ROP MC at baseline and increased in response to 25 mmol/l glucose, but remained elevated when glucose concentration was reduced. |
| 2400 | 11812761 | Thus, 25 mmol/l glucose induced reversible changes in MMP-2, TGF-beta(1), and type I collagen in MC of sclerosis-resistant mice but not in MC from sclerosis-prone mice. |
| 2401 | 11812761 | Matrix metalloproteinase-2 (MMP-2) and transforming growth factor-beta(1) (TGF-beta(1)) levels increased in B6 MC exposed to 25 mmol/l glucose but returned to baseline levels when the glucose concentration was reduced to 6 mmol/l. |
| 2402 | 11812761 | MMP-2 and TGF-beta(1) were higher in ROP MC at baseline and increased in response to 25 mmol/l glucose, but remained elevated when glucose concentration was reduced. |
| 2403 | 11812761 | Thus, 25 mmol/l glucose induced reversible changes in MMP-2, TGF-beta(1), and type I collagen in MC of sclerosis-resistant mice but not in MC from sclerosis-prone mice. |
| 2404 | 11812761 | Matrix metalloproteinase-2 (MMP-2) and transforming growth factor-beta(1) (TGF-beta(1)) levels increased in B6 MC exposed to 25 mmol/l glucose but returned to baseline levels when the glucose concentration was reduced to 6 mmol/l. |
| 2405 | 11812761 | MMP-2 and TGF-beta(1) were higher in ROP MC at baseline and increased in response to 25 mmol/l glucose, but remained elevated when glucose concentration was reduced. |
| 2406 | 11812761 | Thus, 25 mmol/l glucose induced reversible changes in MMP-2, TGF-beta(1), and type I collagen in MC of sclerosis-resistant mice but not in MC from sclerosis-prone mice. |
| 2407 | 11822224 | Moreover, proteolytic enzymes may accelerate the removal of TGF-beta 1 from renal tissue via a protease-induced activation of alpha 2-macroglobulin (alpha 2M). |
| 2408 | 11823504 | We have analyzed the effects of CTB on macrophages in vitro and have found that preincubation with CTB (10 microg/ml) suppresses the proinflammatory reaction to LPS challenge, as demonstrated by suppressed production of TNF-alpha, IL-6, IL-12(p70), and NO (p < 0.01) in cells of macrophage lines. |
| 2409 | 11823504 | Pre-exposure to CTB also suppresses LPS-induced TNF-alpha and IL-12(p70) formation in human PBMC. |
| 2410 | 11823504 | The suppression of TNF-alpha and IL-6 production could be counteracted by the addition of Abs to IL-10 and TGF-beta. |
| 2411 | 11872661 | In addition, Th1-type cells (gamma-interferon-positive and IL-2(+)) were decreased the most, and Th2-type cells (IL-4(+) and IL-10(+)) and Th3-type cells (transforming growth factor-beta1(+)) were increased the most in islet grafts of sirolimus and IL-2-treated mice. |
| 2412 | 11875060 | Role of sterol regulatory element-binding protein 1 in regulation of renal lipid metabolism and glomerulosclerosis in diabetes mellitus. |
| 2413 | 11875060 | In streptozotocin-induced diabetes in the rat, there were marked increases in SREBP-1 and fatty acid synthase (FAS) expression, resulting in increased triglyceride (TG) accumulation. |
| 2414 | 11875060 | Treatment of diabetic rats with insulin prevented the increased renal expression of SREBP-1 and the accumulation of TG. |
| 2415 | 11875060 | High glucose induced increased expression of SREBP-1a and -1c mRNA, SREBP-1 protein, and FAS, resulting in increased TG content. |
| 2416 | 11875060 | The increase in SREBP-1 was associated with increased expression of FAS and acetyl CoA carboxylase, resulting in increased TG content, increased expression of transforming growth factor beta1 and vascular endothelial growth factor, mesangial expansion, glomerulosclerosis, and proteinuria. |
| 2417 | 11875060 | Our study therefore indicates that renal SREBP-1 expression is increased in diabetes and that SREBP-1 plays an important role in the increased lipid synthesis, TG accumulation, mesangial expansion, glomerulosclerosis, and proteinuria by increasing the expression of transforming growth factor beta and vascular endothelial growth factor. |
| 2418 | 11875060 | Role of sterol regulatory element-binding protein 1 in regulation of renal lipid metabolism and glomerulosclerosis in diabetes mellitus. |
| 2419 | 11875060 | In streptozotocin-induced diabetes in the rat, there were marked increases in SREBP-1 and fatty acid synthase (FAS) expression, resulting in increased triglyceride (TG) accumulation. |
| 2420 | 11875060 | Treatment of diabetic rats with insulin prevented the increased renal expression of SREBP-1 and the accumulation of TG. |
| 2421 | 11875060 | High glucose induced increased expression of SREBP-1a and -1c mRNA, SREBP-1 protein, and FAS, resulting in increased TG content. |
| 2422 | 11875060 | The increase in SREBP-1 was associated with increased expression of FAS and acetyl CoA carboxylase, resulting in increased TG content, increased expression of transforming growth factor beta1 and vascular endothelial growth factor, mesangial expansion, glomerulosclerosis, and proteinuria. |
| 2423 | 11875060 | Our study therefore indicates that renal SREBP-1 expression is increased in diabetes and that SREBP-1 plays an important role in the increased lipid synthesis, TG accumulation, mesangial expansion, glomerulosclerosis, and proteinuria by increasing the expression of transforming growth factor beta and vascular endothelial growth factor. |
| 2424 | 11877467 | Myostatin is a TGF-beta family member that acts as a negative regulator of muscle growth. |
| 2425 | 11877467 | To investigate whether myostatin might be an effective target for suppressing the development of obesity in settings of abnormal fat accumulation, we analyzed the effect of the Mstn mutation in two genetic models of obesity, agouti lethal yellow (A(y)) and obese (Lep(ob/ob)). |
| 2426 | 11879191 | Decorin suppresses transforming growth factor-beta-induced expression of plasminogen activator inhibitor-1 in human mesangial cells through a mechanism that involves Ca2+-dependent phosphorylation of Smad2 at serine-240. |
| 2427 | 11879191 | One of the main target cells for TGFbeta in the kidney are glomerular mesangial cells, which respond by increasing expression of ECM proteins, such as collagens, laminin and fibronectin, while suppressing the expression of ECM-degrading proteases and increasing the synthesis of ECM protease inhibitors, including plasminogen activator inhibitor-1. |
| 2428 | 11879191 | While the mechanism by which TGFbeta stimulates gene expression via the Smad signal-transduction pathway is becoming clear, the precise mechanism by which decorin may impinge upon TGFbeta activity remains to be established. |
| 2429 | 11879191 | In this study, for the first time we provide evidence that decorin can disrupt glucose- and TGFbeta/Smad-dependent transcriptional events in human mesangial cells through a mechanism that involves an increase in Ca(2+) signalling, the activation of Ca(2+)/calmodulin-dependent protein kinase II and ensuing phosphorylation of Smad2 at Ser-240. |
| 2430 | 11879191 | We show that decorin also induces Ser-240 phospho-Smad hetero-oligomerization with Smad4 and the nuclear localization of this complex independently of TGFbeta receptor activation. |
| 2431 | 11879191 | Thus, in human mesangial cells, the mechanism of decorin-mediated inhibition of TGFbeta signalling may involve activation of Ca(2+) signalling, the subsequent phosphorylation of Smad2 at a key regulatory site, and the sequestration of Smad4 in the nucleus. |
| 2432 | 11879191 | Decorin suppresses transforming growth factor-beta-induced expression of plasminogen activator inhibitor-1 in human mesangial cells through a mechanism that involves Ca2+-dependent phosphorylation of Smad2 at serine-240. |
| 2433 | 11879191 | One of the main target cells for TGFbeta in the kidney are glomerular mesangial cells, which respond by increasing expression of ECM proteins, such as collagens, laminin and fibronectin, while suppressing the expression of ECM-degrading proteases and increasing the synthesis of ECM protease inhibitors, including plasminogen activator inhibitor-1. |
| 2434 | 11879191 | While the mechanism by which TGFbeta stimulates gene expression via the Smad signal-transduction pathway is becoming clear, the precise mechanism by which decorin may impinge upon TGFbeta activity remains to be established. |
| 2435 | 11879191 | In this study, for the first time we provide evidence that decorin can disrupt glucose- and TGFbeta/Smad-dependent transcriptional events in human mesangial cells through a mechanism that involves an increase in Ca(2+) signalling, the activation of Ca(2+)/calmodulin-dependent protein kinase II and ensuing phosphorylation of Smad2 at Ser-240. |
| 2436 | 11879191 | We show that decorin also induces Ser-240 phospho-Smad hetero-oligomerization with Smad4 and the nuclear localization of this complex independently of TGFbeta receptor activation. |
| 2437 | 11879191 | Thus, in human mesangial cells, the mechanism of decorin-mediated inhibition of TGFbeta signalling may involve activation of Ca(2+) signalling, the subsequent phosphorylation of Smad2 at a key regulatory site, and the sequestration of Smad4 in the nucleus. |
| 2438 | 11879191 | Decorin suppresses transforming growth factor-beta-induced expression of plasminogen activator inhibitor-1 in human mesangial cells through a mechanism that involves Ca2+-dependent phosphorylation of Smad2 at serine-240. |
| 2439 | 11879191 | One of the main target cells for TGFbeta in the kidney are glomerular mesangial cells, which respond by increasing expression of ECM proteins, such as collagens, laminin and fibronectin, while suppressing the expression of ECM-degrading proteases and increasing the synthesis of ECM protease inhibitors, including plasminogen activator inhibitor-1. |
| 2440 | 11879191 | While the mechanism by which TGFbeta stimulates gene expression via the Smad signal-transduction pathway is becoming clear, the precise mechanism by which decorin may impinge upon TGFbeta activity remains to be established. |
| 2441 | 11879191 | In this study, for the first time we provide evidence that decorin can disrupt glucose- and TGFbeta/Smad-dependent transcriptional events in human mesangial cells through a mechanism that involves an increase in Ca(2+) signalling, the activation of Ca(2+)/calmodulin-dependent protein kinase II and ensuing phosphorylation of Smad2 at Ser-240. |
| 2442 | 11879191 | We show that decorin also induces Ser-240 phospho-Smad hetero-oligomerization with Smad4 and the nuclear localization of this complex independently of TGFbeta receptor activation. |
| 2443 | 11879191 | Thus, in human mesangial cells, the mechanism of decorin-mediated inhibition of TGFbeta signalling may involve activation of Ca(2+) signalling, the subsequent phosphorylation of Smad2 at a key regulatory site, and the sequestration of Smad4 in the nucleus. |
| 2444 | 11879191 | Decorin suppresses transforming growth factor-beta-induced expression of plasminogen activator inhibitor-1 in human mesangial cells through a mechanism that involves Ca2+-dependent phosphorylation of Smad2 at serine-240. |
| 2445 | 11879191 | One of the main target cells for TGFbeta in the kidney are glomerular mesangial cells, which respond by increasing expression of ECM proteins, such as collagens, laminin and fibronectin, while suppressing the expression of ECM-degrading proteases and increasing the synthesis of ECM protease inhibitors, including plasminogen activator inhibitor-1. |
| 2446 | 11879191 | While the mechanism by which TGFbeta stimulates gene expression via the Smad signal-transduction pathway is becoming clear, the precise mechanism by which decorin may impinge upon TGFbeta activity remains to be established. |
| 2447 | 11879191 | In this study, for the first time we provide evidence that decorin can disrupt glucose- and TGFbeta/Smad-dependent transcriptional events in human mesangial cells through a mechanism that involves an increase in Ca(2+) signalling, the activation of Ca(2+)/calmodulin-dependent protein kinase II and ensuing phosphorylation of Smad2 at Ser-240. |
| 2448 | 11879191 | We show that decorin also induces Ser-240 phospho-Smad hetero-oligomerization with Smad4 and the nuclear localization of this complex independently of TGFbeta receptor activation. |
| 2449 | 11879191 | Thus, in human mesangial cells, the mechanism of decorin-mediated inhibition of TGFbeta signalling may involve activation of Ca(2+) signalling, the subsequent phosphorylation of Smad2 at a key regulatory site, and the sequestration of Smad4 in the nucleus. |
| 2450 | 11879191 | Decorin suppresses transforming growth factor-beta-induced expression of plasminogen activator inhibitor-1 in human mesangial cells through a mechanism that involves Ca2+-dependent phosphorylation of Smad2 at serine-240. |
| 2451 | 11879191 | One of the main target cells for TGFbeta in the kidney are glomerular mesangial cells, which respond by increasing expression of ECM proteins, such as collagens, laminin and fibronectin, while suppressing the expression of ECM-degrading proteases and increasing the synthesis of ECM protease inhibitors, including plasminogen activator inhibitor-1. |
| 2452 | 11879191 | While the mechanism by which TGFbeta stimulates gene expression via the Smad signal-transduction pathway is becoming clear, the precise mechanism by which decorin may impinge upon TGFbeta activity remains to be established. |
| 2453 | 11879191 | In this study, for the first time we provide evidence that decorin can disrupt glucose- and TGFbeta/Smad-dependent transcriptional events in human mesangial cells through a mechanism that involves an increase in Ca(2+) signalling, the activation of Ca(2+)/calmodulin-dependent protein kinase II and ensuing phosphorylation of Smad2 at Ser-240. |
| 2454 | 11879191 | We show that decorin also induces Ser-240 phospho-Smad hetero-oligomerization with Smad4 and the nuclear localization of this complex independently of TGFbeta receptor activation. |
| 2455 | 11879191 | Thus, in human mesangial cells, the mechanism of decorin-mediated inhibition of TGFbeta signalling may involve activation of Ca(2+) signalling, the subsequent phosphorylation of Smad2 at a key regulatory site, and the sequestration of Smad4 in the nucleus. |
| 2456 | 11879191 | Decorin suppresses transforming growth factor-beta-induced expression of plasminogen activator inhibitor-1 in human mesangial cells through a mechanism that involves Ca2+-dependent phosphorylation of Smad2 at serine-240. |
| 2457 | 11879191 | One of the main target cells for TGFbeta in the kidney are glomerular mesangial cells, which respond by increasing expression of ECM proteins, such as collagens, laminin and fibronectin, while suppressing the expression of ECM-degrading proteases and increasing the synthesis of ECM protease inhibitors, including plasminogen activator inhibitor-1. |
| 2458 | 11879191 | While the mechanism by which TGFbeta stimulates gene expression via the Smad signal-transduction pathway is becoming clear, the precise mechanism by which decorin may impinge upon TGFbeta activity remains to be established. |
| 2459 | 11879191 | In this study, for the first time we provide evidence that decorin can disrupt glucose- and TGFbeta/Smad-dependent transcriptional events in human mesangial cells through a mechanism that involves an increase in Ca(2+) signalling, the activation of Ca(2+)/calmodulin-dependent protein kinase II and ensuing phosphorylation of Smad2 at Ser-240. |
| 2460 | 11879191 | We show that decorin also induces Ser-240 phospho-Smad hetero-oligomerization with Smad4 and the nuclear localization of this complex independently of TGFbeta receptor activation. |
| 2461 | 11879191 | Thus, in human mesangial cells, the mechanism of decorin-mediated inhibition of TGFbeta signalling may involve activation of Ca(2+) signalling, the subsequent phosphorylation of Smad2 at a key regulatory site, and the sequestration of Smad4 in the nucleus. |
| 2462 | 11880325 | Upregulation of type I collagen by TGF-beta in mesangial cells is blocked by PPARgamma activation. |
| 2463 | 11880325 | Because mesangial cells play an important role in diabetic nephropathy, we examined regulation of type I collagen expression by PPARgamma and transforming growth factor-beta(1) (TGF-beta(1)) in mouse mesangial cells in the presence of 6 and 25 mM glucose. |
| 2464 | 11880325 | Exposure to 25 mM glucose resulted in reduced PPARgamma expression and transcriptional activity, accompanied by increased type I collagen expression. |
| 2465 | 11880325 | Restoration of PPARgamma activity to normal levels in cells cultured in 25 mM glucose, by transfection with a PPARgamma expression construct and treatment with the PPARgamma agonist troglitazone, returned type I collagen levels toward normal values. |
| 2466 | 11880325 | Activation of PPARgamma by troglitazone also decreased type I collagen mRNA and blocked TGF-beta(1)-mediated upregulation of type I collagen mRNA and protein. |
| 2467 | 11880325 | Moreover, PPARgamma activation suppressed basal and activated TGF-beta(1) responses in mesangial cells. |
| 2468 | 11880325 | In summary, PPARgamma suppresses the increased type I collagen mRNA and protein expression mediated by TGF-beta(1) in mesangial cells. |
| 2469 | 11880325 | Upregulation of type I collagen by TGF-beta in mesangial cells is blocked by PPARgamma activation. |
| 2470 | 11880325 | Because mesangial cells play an important role in diabetic nephropathy, we examined regulation of type I collagen expression by PPARgamma and transforming growth factor-beta(1) (TGF-beta(1)) in mouse mesangial cells in the presence of 6 and 25 mM glucose. |
| 2471 | 11880325 | Exposure to 25 mM glucose resulted in reduced PPARgamma expression and transcriptional activity, accompanied by increased type I collagen expression. |
| 2472 | 11880325 | Restoration of PPARgamma activity to normal levels in cells cultured in 25 mM glucose, by transfection with a PPARgamma expression construct and treatment with the PPARgamma agonist troglitazone, returned type I collagen levels toward normal values. |
| 2473 | 11880325 | Activation of PPARgamma by troglitazone also decreased type I collagen mRNA and blocked TGF-beta(1)-mediated upregulation of type I collagen mRNA and protein. |
| 2474 | 11880325 | Moreover, PPARgamma activation suppressed basal and activated TGF-beta(1) responses in mesangial cells. |
| 2475 | 11880325 | In summary, PPARgamma suppresses the increased type I collagen mRNA and protein expression mediated by TGF-beta(1) in mesangial cells. |
| 2476 | 11880325 | Upregulation of type I collagen by TGF-beta in mesangial cells is blocked by PPARgamma activation. |
| 2477 | 11880325 | Because mesangial cells play an important role in diabetic nephropathy, we examined regulation of type I collagen expression by PPARgamma and transforming growth factor-beta(1) (TGF-beta(1)) in mouse mesangial cells in the presence of 6 and 25 mM glucose. |
| 2478 | 11880325 | Exposure to 25 mM glucose resulted in reduced PPARgamma expression and transcriptional activity, accompanied by increased type I collagen expression. |
| 2479 | 11880325 | Restoration of PPARgamma activity to normal levels in cells cultured in 25 mM glucose, by transfection with a PPARgamma expression construct and treatment with the PPARgamma agonist troglitazone, returned type I collagen levels toward normal values. |
| 2480 | 11880325 | Activation of PPARgamma by troglitazone also decreased type I collagen mRNA and blocked TGF-beta(1)-mediated upregulation of type I collagen mRNA and protein. |
| 2481 | 11880325 | Moreover, PPARgamma activation suppressed basal and activated TGF-beta(1) responses in mesangial cells. |
| 2482 | 11880325 | In summary, PPARgamma suppresses the increased type I collagen mRNA and protein expression mediated by TGF-beta(1) in mesangial cells. |
| 2483 | 11880325 | Upregulation of type I collagen by TGF-beta in mesangial cells is blocked by PPARgamma activation. |
| 2484 | 11880325 | Because mesangial cells play an important role in diabetic nephropathy, we examined regulation of type I collagen expression by PPARgamma and transforming growth factor-beta(1) (TGF-beta(1)) in mouse mesangial cells in the presence of 6 and 25 mM glucose. |
| 2485 | 11880325 | Exposure to 25 mM glucose resulted in reduced PPARgamma expression and transcriptional activity, accompanied by increased type I collagen expression. |
| 2486 | 11880325 | Restoration of PPARgamma activity to normal levels in cells cultured in 25 mM glucose, by transfection with a PPARgamma expression construct and treatment with the PPARgamma agonist troglitazone, returned type I collagen levels toward normal values. |
| 2487 | 11880325 | Activation of PPARgamma by troglitazone also decreased type I collagen mRNA and blocked TGF-beta(1)-mediated upregulation of type I collagen mRNA and protein. |
| 2488 | 11880325 | Moreover, PPARgamma activation suppressed basal and activated TGF-beta(1) responses in mesangial cells. |
| 2489 | 11880325 | In summary, PPARgamma suppresses the increased type I collagen mRNA and protein expression mediated by TGF-beta(1) in mesangial cells. |
| 2490 | 11880325 | Upregulation of type I collagen by TGF-beta in mesangial cells is blocked by PPARgamma activation. |
| 2491 | 11880325 | Because mesangial cells play an important role in diabetic nephropathy, we examined regulation of type I collagen expression by PPARgamma and transforming growth factor-beta(1) (TGF-beta(1)) in mouse mesangial cells in the presence of 6 and 25 mM glucose. |
| 2492 | 11880325 | Exposure to 25 mM glucose resulted in reduced PPARgamma expression and transcriptional activity, accompanied by increased type I collagen expression. |
| 2493 | 11880325 | Restoration of PPARgamma activity to normal levels in cells cultured in 25 mM glucose, by transfection with a PPARgamma expression construct and treatment with the PPARgamma agonist troglitazone, returned type I collagen levels toward normal values. |
| 2494 | 11880325 | Activation of PPARgamma by troglitazone also decreased type I collagen mRNA and blocked TGF-beta(1)-mediated upregulation of type I collagen mRNA and protein. |
| 2495 | 11880325 | Moreover, PPARgamma activation suppressed basal and activated TGF-beta(1) responses in mesangial cells. |
| 2496 | 11880325 | In summary, PPARgamma suppresses the increased type I collagen mRNA and protein expression mediated by TGF-beta(1) in mesangial cells. |
| 2497 | 11903419 | Insulin-like growth factor I, epidermal growth factor and transforming growth factor beta expression and their association with intrauterine fetal growth retardation, such as development during human pregnancy. |
| 2498 | 11937760 | Recently, transforming growth factor beta driven secreted proteins, i.e., connective tissue growth factor and gremlin (bone morphogenetic protein 2), have been identified, and their expression has been correlated with the tissue changes seen in diabetic nephropathy in the adult population. |
| 2499 | 11937760 | They included: (1) a translocase inner mitochondrial membrane 44 that is involved in the ATP-dependent import of preproteins from the cytosol into the mitochondrial matrix; (2) a kidney-specific aldo-keto reductase that utilizes NADPH and NADH as cofactors in the reduction of aromatic aldehydes and aldohexoses; (3) Rap1b, a Ras-related small GTP-binding protein that behaves as a GTPase and cycles between GTP-bound (active) and GDP-bound (inactive) states associated with conformational change, and (4) a fusion protein of ubiquitin polypeptide and ribosomal protein L40 (UbA(52) or ubiquitin/60) that is intimately involved in the ubiquitin-dependent proteasome pathway related to the accelerated degradation of proteins under various stress conditions, such as those seen in patients with cancer and diabetes mellitus. |
| 2500 | 11947899 | We evaluated the correlation of arterial proliferation with plasma levels of TGF-beta 1 and TGF-beta receptor type II, respectively, in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new strain of spontaneous non-insulin-dependent diabetes mellitus (NIDDM) models. |
| 2501 | 11947899 | Plasma TGF-beta1 and insulin were determined by enzyme-linked immunosorbent assay. |
| 2502 | 11947899 | There are significant linear relations between plasma TGF-beta 1 antigen and aorta wall section area, and plasma TGF-beta 1 antigen and fasting insulin level (P<0.001, respectively). |
| 2503 | 11947899 | We evaluated the correlation of arterial proliferation with plasma levels of TGF-beta 1 and TGF-beta receptor type II, respectively, in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new strain of spontaneous non-insulin-dependent diabetes mellitus (NIDDM) models. |
| 2504 | 11947899 | Plasma TGF-beta1 and insulin were determined by enzyme-linked immunosorbent assay. |
| 2505 | 11947899 | There are significant linear relations between plasma TGF-beta 1 antigen and aorta wall section area, and plasma TGF-beta 1 antigen and fasting insulin level (P<0.001, respectively). |
| 2506 | 11947899 | We evaluated the correlation of arterial proliferation with plasma levels of TGF-beta 1 and TGF-beta receptor type II, respectively, in Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new strain of spontaneous non-insulin-dependent diabetes mellitus (NIDDM) models. |
| 2507 | 11947899 | Plasma TGF-beta1 and insulin were determined by enzyme-linked immunosorbent assay. |
| 2508 | 11947899 | There are significant linear relations between plasma TGF-beta 1 antigen and aorta wall section area, and plasma TGF-beta 1 antigen and fasting insulin level (P<0.001, respectively). |
| 2509 | 11992481 | Associations of the genetic polymorphisms in the promoter region and the signal peptide sequence of the transforming growth factor-beta (TGF-beta1) gene with proliferative diabetic retinopathy (PDR) in patients with non-insulin-dependent diabetes mellitus (NIDDM) were studied. |
| 2510 | 11997313 | In both diabetic rodent models of diabetes and cultured mesangial cells, PKC-beta appears to be the key isozyme required for the enhanced expression of transforming growth factor-beta(1), initiation of early accumulation of mesangial matrix protein, and increased microalbuminuria. |
| 2511 | 11997313 | Enhanced collagen IV expression by mesangial cells in response to vasoactive peptide hormone stimulation, e.g., endothelin-1, requires PKC-beta, -delta, -epsilon and -zeta. |
| 2512 | 11999343 | In the nonobese diabetic (NOD) mouse, the T helper (Th)1-type inflammatory cytokines interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha play a critical role in the development of type 1 diabetes, whereas the Th2-type anti-inflammatory cytokines interleukin (IL)-4 and IL-10 operate counterregulatory. |
| 2513 | 11999343 | Therefore, we used islets to study ex vivo effects of MLD-STZ and in vitro effects of STZ on IFN-gamma, TNF-alpha, IL-4, and IL-10 on both levels of protein-producing cells and the mRNA expression, as well as the mRNA expression of the Th3-type cytokine transforming growth factor TGF-beta1. |
| 2514 | 11999343 | In islets of C57BL/6 mice of both genders MLD-STZ similarly stimulated production of IFN-gamma and TNF-alpha, but significantly reduced IL-4 and IL-10 levels in male mice only. |
| 2515 | 11999343 | Here, MLD-STZ markedly decreased the levels of IFN-gamma and TNF-alpha, but significantly increased the levels of IL-4 and IL-10. |
| 2516 | 11999343 | Moreover, MLD-STZ effects on the TGF-beta1 mRNA expression were reversed to the effects on IFN-gamma and TNF-alpha. |
| 2517 | 11999343 | In the nonobese diabetic (NOD) mouse, the T helper (Th)1-type inflammatory cytokines interferon (IFN)-gamma and tumor necrosis factor (TNF)-alpha play a critical role in the development of type 1 diabetes, whereas the Th2-type anti-inflammatory cytokines interleukin (IL)-4 and IL-10 operate counterregulatory. |
| 2518 | 11999343 | Therefore, we used islets to study ex vivo effects of MLD-STZ and in vitro effects of STZ on IFN-gamma, TNF-alpha, IL-4, and IL-10 on both levels of protein-producing cells and the mRNA expression, as well as the mRNA expression of the Th3-type cytokine transforming growth factor TGF-beta1. |
| 2519 | 11999343 | In islets of C57BL/6 mice of both genders MLD-STZ similarly stimulated production of IFN-gamma and TNF-alpha, but significantly reduced IL-4 and IL-10 levels in male mice only. |
| 2520 | 11999343 | Here, MLD-STZ markedly decreased the levels of IFN-gamma and TNF-alpha, but significantly increased the levels of IL-4 and IL-10. |
| 2521 | 11999343 | Moreover, MLD-STZ effects on the TGF-beta1 mRNA expression were reversed to the effects on IFN-gamma and TNF-alpha. |
| 2522 | 12021842 | Female NOD mice were treated orally with ICAM-1, TGF-beta, or control plasmid DNA and received a single injection of cyclophosphamide for synchronization and acceleration of the disease process in the pancreas. |
| 2523 | 12021842 | Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice. |
| 2524 | 12021842 | Treatment with ICAM-1 and TGF-beta DNA resulted in increased levels of IL-10 mRNA in the pancreas, indicating an anti-inflammatory regulatory immune response. |
| 2525 | 12021842 | We conclude that oral vaccination with DNA encoding immunoregulatory molecules such as ICAM-1 and TGF-beta represents an approach for modulating the ongoing inflammatory process in the pancreas of diabetes prone NOD mice. |
| 2526 | 12021842 | Female NOD mice were treated orally with ICAM-1, TGF-beta, or control plasmid DNA and received a single injection of cyclophosphamide for synchronization and acceleration of the disease process in the pancreas. |
| 2527 | 12021842 | Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice. |
| 2528 | 12021842 | Treatment with ICAM-1 and TGF-beta DNA resulted in increased levels of IL-10 mRNA in the pancreas, indicating an anti-inflammatory regulatory immune response. |
| 2529 | 12021842 | We conclude that oral vaccination with DNA encoding immunoregulatory molecules such as ICAM-1 and TGF-beta represents an approach for modulating the ongoing inflammatory process in the pancreas of diabetes prone NOD mice. |
| 2530 | 12021842 | Female NOD mice were treated orally with ICAM-1, TGF-beta, or control plasmid DNA and received a single injection of cyclophosphamide for synchronization and acceleration of the disease process in the pancreas. |
| 2531 | 12021842 | Quantitative RT-PCR analysis of pancreatic mRNA showed that cyclophosphamide induced the expression of Th1 cytokines (IFN-gamma and IL-12p40) in vehicle- or control plasmid-treated mice. |
| 2532 | 12021842 | Treatment with ICAM-1 and TGF-beta DNA resulted in increased levels of IL-10 mRNA in the pancreas, indicating an anti-inflammatory regulatory immune response. |
| 2533 | 12021842 | We conclude that oral vaccination with DNA encoding immunoregulatory molecules such as ICAM-1 and TGF-beta represents an approach for modulating the ongoing inflammatory process in the pancreas of diabetes prone NOD mice. |
| 2534 | 12032117 | Urinary transforming growth factor-beta excretion in patients with hypertension, type 2 diabetes, and elevated albumin excretion rate: effects of angiotensin receptor blockade and sodium restriction. |
| 2535 | 12080814 | [Transforming growth factor beta 1 and interleukin 6 mRNA expression in wound tissues of patients with diabetic ulcers]. |
| 2536 | 12086332 | Effects of the angiotensin II type 1 (AT1) receptor antagonist valsartan and the angiotensin-converting enzyme (ACE) inhibitor enalapril were studied in streptozotocine (STZ)-induced diabetes in rats on the basis of microalbuminuria (Ma) and renal morphology. |
| 2537 | 12086332 | Immunohistochemical staining with an anti-transforming growth factor-beta1 (TGF-beta1) antibody was performed as well. |
| 2538 | 12086332 | Their beneficial effects are related to a blockade of the renin-angiotensin system (RAS) and a decrease in TGF-beta1 expression in glomeruli. |
| 2539 | 12086332 | Effects of the angiotensin II type 1 (AT1) receptor antagonist valsartan and the angiotensin-converting enzyme (ACE) inhibitor enalapril were studied in streptozotocine (STZ)-induced diabetes in rats on the basis of microalbuminuria (Ma) and renal morphology. |
| 2540 | 12086332 | Immunohistochemical staining with an anti-transforming growth factor-beta1 (TGF-beta1) antibody was performed as well. |
| 2541 | 12086332 | Their beneficial effects are related to a blockade of the renin-angiotensin system (RAS) and a decrease in TGF-beta1 expression in glomeruli. |
| 2542 | 12118901 | To address that question, we studied the inheritance patterns for polymorphisms in several cytokine genes (IL-2, IL-6, IL-10, TNF-alpha, TGF-beta, and IFN-gamma) within an ethnically diverse study population comprised of 216 Whites, 58 Blacks, 25 Hispanics, and 31 Asians. |
| 2543 | 12118901 | Blacks, Hispanics and Asians demonstrated marked differences in the inheritance of IL-6 alleles and IL-10 genotypes that result in high expression when compared with Whites. |
| 2544 | 12145178 | The aim of this study was to investigate the effects of glycation of mesangium matrix on MMP-2, the principal MMP secreted by mesangial cells to degrade type IV collagen. |
| 2545 | 12145178 | Also examined were membrane type 1 MMP (MT1-MMP), tissue inhibitors of MMPs (TIMP)-1 and -2, and transforming growth factor-beta (TGF-beta), which together regulate MMP-2 activities in an interacting manner. |
| 2546 | 12145178 | Analogous to the direct effects of high glucose concentrations, glycation of matrix increased the gene expression of MMP-2 and TIMP-1 (control 100 +/- 16.9 vs. glycated 197.3 +/- 30.6% and control 100 +/- 5.3 vs. glycated 152.1 +/- 20.1%, respectively; P < 0.05) and decreased MT1-MMP (control 100 +/- 1.17 vs. glycated 54.1 +/- 15.2%; P < 0.05). |
| 2547 | 12145178 | Our results indicate that glycation of matrix affects the balance between MMP-2 and its activator and inhibitors, but this phenomenon is not due to TGF-beta. |
| 2548 | 12145178 | The aim of this study was to investigate the effects of glycation of mesangium matrix on MMP-2, the principal MMP secreted by mesangial cells to degrade type IV collagen. |
| 2549 | 12145178 | Also examined were membrane type 1 MMP (MT1-MMP), tissue inhibitors of MMPs (TIMP)-1 and -2, and transforming growth factor-beta (TGF-beta), which together regulate MMP-2 activities in an interacting manner. |
| 2550 | 12145178 | Analogous to the direct effects of high glucose concentrations, glycation of matrix increased the gene expression of MMP-2 and TIMP-1 (control 100 +/- 16.9 vs. glycated 197.3 +/- 30.6% and control 100 +/- 5.3 vs. glycated 152.1 +/- 20.1%, respectively; P < 0.05) and decreased MT1-MMP (control 100 +/- 1.17 vs. glycated 54.1 +/- 15.2%; P < 0.05). |
| 2551 | 12145178 | Our results indicate that glycation of matrix affects the balance between MMP-2 and its activator and inhibitors, but this phenomenon is not due to TGF-beta. |
| 2552 | 12164872 | Effects of high glucose and TGF-beta1 on the expression of collagen IV and vascular endothelial growth factor in mouse podocytes. |
| 2553 | 12181650 | In addition, transforming growth factor-beta1 (TGF-beta 1), which can evoke myofibroblast transformation, is detected in interstitial cells in the diabetic kidney, but not in the normal kidney. |
| 2554 | 12193586 | One of them, PDF, was found to have a very high expression level compared to other TGFbeta superfamily members. |
| 2555 | 12193586 | Quantitative reverse transcriptase polymerase chain reaction confirmed these results and demonstrated that the highly expressed PDF was approximately 10-fold down- regulated by glucose while other TGFbeta superfamily members and target genes were up-regulated. |
| 2556 | 12193586 | These results suggest that a highly regulated TGFbeta signaling cascade exists in human islets, and that PDF may play a central role in islet biology. |
| 2557 | 12193586 | One of them, PDF, was found to have a very high expression level compared to other TGFbeta superfamily members. |
| 2558 | 12193586 | Quantitative reverse transcriptase polymerase chain reaction confirmed these results and demonstrated that the highly expressed PDF was approximately 10-fold down- regulated by glucose while other TGFbeta superfamily members and target genes were up-regulated. |
| 2559 | 12193586 | These results suggest that a highly regulated TGFbeta signaling cascade exists in human islets, and that PDF may play a central role in islet biology. |
| 2560 | 12193586 | One of them, PDF, was found to have a very high expression level compared to other TGFbeta superfamily members. |
| 2561 | 12193586 | Quantitative reverse transcriptase polymerase chain reaction confirmed these results and demonstrated that the highly expressed PDF was approximately 10-fold down- regulated by glucose while other TGFbeta superfamily members and target genes were up-regulated. |
| 2562 | 12193586 | These results suggest that a highly regulated TGFbeta signaling cascade exists in human islets, and that PDF may play a central role in islet biology. |
| 2563 | 12196463 | Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes. |
| 2564 | 12196463 | Protein kinase C (PKC) beta isoform activity is increased in myocardium of diabetic rodents and heart failure patients. |
| 2565 | 12196463 | In this study, we characterized the expression of connective tissue growth factor (CTGF) and transforming growth factor beta (TGFbeta) with the development of fibrosis in heart from PKCbeta2Tg mice at 4-16 weeks of age. |
| 2566 | 12196463 | CTGF expression increased in PKCbeta2Tg hearts at all ages, whereas TGFbeta increased only at 8 and 12 weeks. |
| 2567 | 12196463 | In 8-week diabetic mouse heart, CTGF and TGFbeta expression increased two- and fourfold, respectively. |
| 2568 | 12196463 | Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes. |
| 2569 | 12196463 | Protein kinase C (PKC) beta isoform activity is increased in myocardium of diabetic rodents and heart failure patients. |
| 2570 | 12196463 | In this study, we characterized the expression of connective tissue growth factor (CTGF) and transforming growth factor beta (TGFbeta) with the development of fibrosis in heart from PKCbeta2Tg mice at 4-16 weeks of age. |
| 2571 | 12196463 | CTGF expression increased in PKCbeta2Tg hearts at all ages, whereas TGFbeta increased only at 8 and 12 weeks. |
| 2572 | 12196463 | In 8-week diabetic mouse heart, CTGF and TGFbeta expression increased two- and fourfold, respectively. |
| 2573 | 12196463 | Expression of connective tissue growth factor is increased in injured myocardium associated with protein kinase C beta2 activation and diabetes. |
| 2574 | 12196463 | Protein kinase C (PKC) beta isoform activity is increased in myocardium of diabetic rodents and heart failure patients. |
| 2575 | 12196463 | In this study, we characterized the expression of connective tissue growth factor (CTGF) and transforming growth factor beta (TGFbeta) with the development of fibrosis in heart from PKCbeta2Tg mice at 4-16 weeks of age. |
| 2576 | 12196463 | CTGF expression increased in PKCbeta2Tg hearts at all ages, whereas TGFbeta increased only at 8 and 12 weeks. |
| 2577 | 12196463 | In 8-week diabetic mouse heart, CTGF and TGFbeta expression increased two- and fourfold, respectively. |
| 2578 | 12207925 | Smad pathway is activated in the diabetic mouse kidney and Smad3 mediates TGF-beta-induced fibronectin in mesangial cells. |
| 2579 | 12207925 | Streptozotocin-induced diabetic mice were used to examine whether the Smad pathway, which transduces the TGF-beta signal, is activated in the diabetic kidney, employing Southwestern histochemistry with labeled Smad-binding element (SBE) oligonucleotides and immunoblotting of nuclear protein extracts for Smad3. |
| 2580 | 12207925 | In mesangial cells, high glucose potentiated the effect of low-dose TGF-beta1 (0.2ng/ml) on the following TGF-beta-responsive constructs: 3TP-Lux (containing AP-1 sites and PAI-1 promoter), SBE4-Luc (containing four tandem repeats of SBE sequence), and the fibronectin promoter. |
| 2581 | 12207925 | Additionally, Smad3 overexpression increased fibronectin promoter activity, an effect that was enhanced by high ambient glucose or treatment with TGF-beta1 (2ng/ml). |
| 2582 | 12207925 | The TGF-beta-stimulated activity of the fibronectin promoter was prevented by transfection with either a dominant-negative Smad3 or the inhibitory Smad7. |
| 2583 | 12207925 | Smad pathway is activated in the diabetic mouse kidney and Smad3 mediates TGF-beta-induced fibronectin in mesangial cells. |
| 2584 | 12207925 | Streptozotocin-induced diabetic mice were used to examine whether the Smad pathway, which transduces the TGF-beta signal, is activated in the diabetic kidney, employing Southwestern histochemistry with labeled Smad-binding element (SBE) oligonucleotides and immunoblotting of nuclear protein extracts for Smad3. |
| 2585 | 12207925 | In mesangial cells, high glucose potentiated the effect of low-dose TGF-beta1 (0.2ng/ml) on the following TGF-beta-responsive constructs: 3TP-Lux (containing AP-1 sites and PAI-1 promoter), SBE4-Luc (containing four tandem repeats of SBE sequence), and the fibronectin promoter. |
| 2586 | 12207925 | Additionally, Smad3 overexpression increased fibronectin promoter activity, an effect that was enhanced by high ambient glucose or treatment with TGF-beta1 (2ng/ml). |
| 2587 | 12207925 | The TGF-beta-stimulated activity of the fibronectin promoter was prevented by transfection with either a dominant-negative Smad3 or the inhibitory Smad7. |
| 2588 | 12207925 | Smad pathway is activated in the diabetic mouse kidney and Smad3 mediates TGF-beta-induced fibronectin in mesangial cells. |
| 2589 | 12207925 | Streptozotocin-induced diabetic mice were used to examine whether the Smad pathway, which transduces the TGF-beta signal, is activated in the diabetic kidney, employing Southwestern histochemistry with labeled Smad-binding element (SBE) oligonucleotides and immunoblotting of nuclear protein extracts for Smad3. |
| 2590 | 12207925 | In mesangial cells, high glucose potentiated the effect of low-dose TGF-beta1 (0.2ng/ml) on the following TGF-beta-responsive constructs: 3TP-Lux (containing AP-1 sites and PAI-1 promoter), SBE4-Luc (containing four tandem repeats of SBE sequence), and the fibronectin promoter. |
| 2591 | 12207925 | Additionally, Smad3 overexpression increased fibronectin promoter activity, an effect that was enhanced by high ambient glucose or treatment with TGF-beta1 (2ng/ml). |
| 2592 | 12207925 | The TGF-beta-stimulated activity of the fibronectin promoter was prevented by transfection with either a dominant-negative Smad3 or the inhibitory Smad7. |
| 2593 | 12207925 | Smad pathway is activated in the diabetic mouse kidney and Smad3 mediates TGF-beta-induced fibronectin in mesangial cells. |
| 2594 | 12207925 | Streptozotocin-induced diabetic mice were used to examine whether the Smad pathway, which transduces the TGF-beta signal, is activated in the diabetic kidney, employing Southwestern histochemistry with labeled Smad-binding element (SBE) oligonucleotides and immunoblotting of nuclear protein extracts for Smad3. |
| 2595 | 12207925 | In mesangial cells, high glucose potentiated the effect of low-dose TGF-beta1 (0.2ng/ml) on the following TGF-beta-responsive constructs: 3TP-Lux (containing AP-1 sites and PAI-1 promoter), SBE4-Luc (containing four tandem repeats of SBE sequence), and the fibronectin promoter. |
| 2596 | 12207925 | Additionally, Smad3 overexpression increased fibronectin promoter activity, an effect that was enhanced by high ambient glucose or treatment with TGF-beta1 (2ng/ml). |
| 2597 | 12207925 | The TGF-beta-stimulated activity of the fibronectin promoter was prevented by transfection with either a dominant-negative Smad3 or the inhibitory Smad7. |
| 2598 | 12207925 | Smad pathway is activated in the diabetic mouse kidney and Smad3 mediates TGF-beta-induced fibronectin in mesangial cells. |
| 2599 | 12207925 | Streptozotocin-induced diabetic mice were used to examine whether the Smad pathway, which transduces the TGF-beta signal, is activated in the diabetic kidney, employing Southwestern histochemistry with labeled Smad-binding element (SBE) oligonucleotides and immunoblotting of nuclear protein extracts for Smad3. |
| 2600 | 12207925 | In mesangial cells, high glucose potentiated the effect of low-dose TGF-beta1 (0.2ng/ml) on the following TGF-beta-responsive constructs: 3TP-Lux (containing AP-1 sites and PAI-1 promoter), SBE4-Luc (containing four tandem repeats of SBE sequence), and the fibronectin promoter. |
| 2601 | 12207925 | Additionally, Smad3 overexpression increased fibronectin promoter activity, an effect that was enhanced by high ambient glucose or treatment with TGF-beta1 (2ng/ml). |
| 2602 | 12207925 | The TGF-beta-stimulated activity of the fibronectin promoter was prevented by transfection with either a dominant-negative Smad3 or the inhibitory Smad7. |
| 2603 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2604 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2605 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2606 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2607 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2608 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2609 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2610 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2611 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2612 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2613 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2614 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2615 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2616 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2617 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2618 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2619 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2620 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2621 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2622 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2623 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2624 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2625 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2626 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2627 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2628 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2629 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2630 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2631 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2632 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2633 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2634 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2635 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2636 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2637 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2638 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2639 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2640 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2641 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2642 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2643 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2644 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2645 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2646 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2647 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2648 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2649 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2650 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2651 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2652 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2653 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2654 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2655 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2656 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2657 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2658 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2659 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2660 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2661 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2662 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2663 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2664 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2665 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2666 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2667 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2668 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2669 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2670 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2671 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2672 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2673 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2674 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2675 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2676 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2677 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2678 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2679 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2680 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2681 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2682 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2683 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2684 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2685 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2686 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2687 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2688 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2689 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2690 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2691 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2692 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2693 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 2694 | 12213733 | We have previously demonstrated that proximal tubular renal epithelial cell TGF-beta1 synthesis may be modulated by elevated glucose concentration and by cytokines such as platelet-derived growth factor (PDGF). |
| 2695 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 2696 | 12213733 | Addition of either 25 mmol/L of D-glucose or low-dose PDGF increased TGF-beta1 mRNA expression without stimulation of TGF-beta1 protein synthesis. |
| 2697 | 12213733 | In contrast sequential stimulation with 25 mmol/L of D-glucose for 48 hours followed by low-dose (25 ng/ml) PDGF led to a significant increase in TGF-beta1 synthesis. |
| 2698 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 2699 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 2700 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 2701 | 12213733 | In conclusion the data suggests that in diabetic nephropathy, the role of glucose is to lower the threshold at which a stimulus such as PDGF stimulates TGF-beta1 protein synthesis. |
| 2702 | 12213733 | The data also suggest that independent regulation of TGF-beta1 transcription and translation by glucose and PDGF account for their synergistic effect on TGF-beta1 protein synthesis. |
| 2703 | 12217849 | These factors may influence the effects of hyperglycemia and several systems that ultimately control TGF-beta production, including the renin-angiotensin system, cellular redox systems, the polyol pathway, and protein kinase C. |
| 2704 | 12359222 | TGF-beta(1) induces peroxisome proliferator-activated receptor gamma1 and gamma2 expression in human THP-1 monocytes. |
| 2705 | 12359222 | The nuclear hormone receptor peroxisome proliferator-activated gamma (PPARgamma) is expressed as two isoforms (PPARgamma1 and gamma2), and is an important modulator of monocyte gene regulation and function. |
| 2706 | 12359222 | TGF-beta(1) is an essential and potent immune modulator and we therefore examined its effect on PPARgamma expression in human THP-1 monocytes. |
| 2707 | 12359222 | Induction of PPARgamma1 and gamma2 in monocytes by TGF-beta(1) may contribute to the anti-inflammatory effects of this growth factor. |
| 2708 | 12359222 | TGF-beta(1) induces peroxisome proliferator-activated receptor gamma1 and gamma2 expression in human THP-1 monocytes. |
| 2709 | 12359222 | The nuclear hormone receptor peroxisome proliferator-activated gamma (PPARgamma) is expressed as two isoforms (PPARgamma1 and gamma2), and is an important modulator of monocyte gene regulation and function. |
| 2710 | 12359222 | TGF-beta(1) is an essential and potent immune modulator and we therefore examined its effect on PPARgamma expression in human THP-1 monocytes. |
| 2711 | 12359222 | Induction of PPARgamma1 and gamma2 in monocytes by TGF-beta(1) may contribute to the anti-inflammatory effects of this growth factor. |
| 2712 | 12359222 | TGF-beta(1) induces peroxisome proliferator-activated receptor gamma1 and gamma2 expression in human THP-1 monocytes. |
| 2713 | 12359222 | The nuclear hormone receptor peroxisome proliferator-activated gamma (PPARgamma) is expressed as two isoforms (PPARgamma1 and gamma2), and is an important modulator of monocyte gene regulation and function. |
| 2714 | 12359222 | TGF-beta(1) is an essential and potent immune modulator and we therefore examined its effect on PPARgamma expression in human THP-1 monocytes. |
| 2715 | 12359222 | Induction of PPARgamma1 and gamma2 in monocytes by TGF-beta(1) may contribute to the anti-inflammatory effects of this growth factor. |
| 2716 | 12386293 | Evidence will be presented that mesangial cell gremlin expression is up-regulated by high ambient glucose, cyclic mechanical strain and transforming growth factor-beta (TGF-beta) and that gremlin may be an important modulator of mesangial cell proliferation and epithelial-mesenchymal transdifferentiation in a diabetic milieu. |
| 2717 | 12390307 | Protection induced by CTB-insulin was transferred to naive recipients by splenic CD4+ T cells. |
| 2718 | 12390307 | Reverse transcription-polymerase chain reaction analysis of recipients' pancreatic glands revealed an increase of TGF-beta and IL-10 transcripts after donor mice tolerization, while levels of IFN-gamma and IL-4 RNAs were unchanged. |
| 2719 | 12390307 | Higher amounts of IL-4 and IFN-gamma were noticed in pancreatic lymph nodes of tolerized mice upon in vitro stimulation. |
| 2720 | 12397035 | Smad6 and Smad7 are inhibitory SMADs with putative functional roles at the intersection of major intracellular signaling networks, including TGF-beta, receptor tyrosine kinase (RTK), JAK/STAT, and NF-kappaB pathways. |
| 2721 | 12397035 | This study reports differential functional roles and regulation of Smad6 and Smad7 in TGF-beta signaling in renal cells, in murine models of renal disease and in human glomerular diseases. |
| 2722 | 12397035 | Smad7 is upregulated in podocytes in all examined glomerular diseases (focal segmental glomerulosclerosis [FSGS], minimal-change disease [MCD], membranous nephropathy [MNP], lupus nephritis [LN], and diabetic nephropathy [DN]) with a statistically significant upregulation in "classical" podocyte-diseases such as FSGS and MCD. |
| 2723 | 12397035 | TGF-beta induces Smad7 synthesis in cultured podocytes and Smad6 synthesis in cultured mesangial cells. |
| 2724 | 12397035 | Although Smad7 expression inhibited both Smad2- and Smad3-mediated TGF-beta signaling in podocytes, it inhibited only Smad3 but not Smad2 signaling in mesangial cells. |
| 2725 | 12397035 | In contrast, Smad6 had no effect on TGF-beta/Smad signaling in podocytes and enhanced Smad3 signaling in mesangial cells. |
| 2726 | 12397035 | These data suggest that Smad7 is activated in injured podocytes in vitro and in human glomerular disease and participates in negative control of TGF-beta/Smad signaling in addition to its pro-apoptotic activity, whereas Smad6 has no role in TGF-beta response and injury in podocytes. |
| 2727 | 12397035 | These data indicate an important role for Smad6 and Smad7 in glomerular cells in vivo that could be important for the cell homeostasis in physiologic and pathologic conditions. |
| 2728 | 12397035 | Smad6 and Smad7 are inhibitory SMADs with putative functional roles at the intersection of major intracellular signaling networks, including TGF-beta, receptor tyrosine kinase (RTK), JAK/STAT, and NF-kappaB pathways. |
| 2729 | 12397035 | This study reports differential functional roles and regulation of Smad6 and Smad7 in TGF-beta signaling in renal cells, in murine models of renal disease and in human glomerular diseases. |
| 2730 | 12397035 | Smad7 is upregulated in podocytes in all examined glomerular diseases (focal segmental glomerulosclerosis [FSGS], minimal-change disease [MCD], membranous nephropathy [MNP], lupus nephritis [LN], and diabetic nephropathy [DN]) with a statistically significant upregulation in "classical" podocyte-diseases such as FSGS and MCD. |
| 2731 | 12397035 | TGF-beta induces Smad7 synthesis in cultured podocytes and Smad6 synthesis in cultured mesangial cells. |
| 2732 | 12397035 | Although Smad7 expression inhibited both Smad2- and Smad3-mediated TGF-beta signaling in podocytes, it inhibited only Smad3 but not Smad2 signaling in mesangial cells. |
| 2733 | 12397035 | In contrast, Smad6 had no effect on TGF-beta/Smad signaling in podocytes and enhanced Smad3 signaling in mesangial cells. |
| 2734 | 12397035 | These data suggest that Smad7 is activated in injured podocytes in vitro and in human glomerular disease and participates in negative control of TGF-beta/Smad signaling in addition to its pro-apoptotic activity, whereas Smad6 has no role in TGF-beta response and injury in podocytes. |
| 2735 | 12397035 | These data indicate an important role for Smad6 and Smad7 in glomerular cells in vivo that could be important for the cell homeostasis in physiologic and pathologic conditions. |
| 2736 | 12428741 | Gene transfection and expression of transforming growth factor-beta1 in nonobese diabetic mouse islets protects beta-cells in syngeneic islet grafts from autoimmune destruction. |
| 2737 | 12428741 | Because transforming growth factor (TGF)-beta1 downregulates immune responses, we tested whether overexpression of TGF-beta1 by gene transfection of NOD mouse islets could protect beta-cells in islet grafts from autoimmune destruction. |
| 2738 | 12428741 | Immunohistochemical examination of the islet grafts revealed significantly more TGF-beta1+ cells and insulin+ cells and significantly fewer CD45+ leukocytes in Ad TGF-beta1-transfected islet grafts. |
| 2739 | 12428741 | Gene transfection and expression of transforming growth factor-beta1 in nonobese diabetic mouse islets protects beta-cells in syngeneic islet grafts from autoimmune destruction. |
| 2740 | 12428741 | Because transforming growth factor (TGF)-beta1 downregulates immune responses, we tested whether overexpression of TGF-beta1 by gene transfection of NOD mouse islets could protect beta-cells in islet grafts from autoimmune destruction. |
| 2741 | 12428741 | Immunohistochemical examination of the islet grafts revealed significantly more TGF-beta1+ cells and insulin+ cells and significantly fewer CD45+ leukocytes in Ad TGF-beta1-transfected islet grafts. |
| 2742 | 12428741 | Gene transfection and expression of transforming growth factor-beta1 in nonobese diabetic mouse islets protects beta-cells in syngeneic islet grafts from autoimmune destruction. |
| 2743 | 12428741 | Because transforming growth factor (TGF)-beta1 downregulates immune responses, we tested whether overexpression of TGF-beta1 by gene transfection of NOD mouse islets could protect beta-cells in islet grafts from autoimmune destruction. |
| 2744 | 12428741 | Immunohistochemical examination of the islet grafts revealed significantly more TGF-beta1+ cells and insulin+ cells and significantly fewer CD45+ leukocytes in Ad TGF-beta1-transfected islet grafts. |
| 2745 | 12453907 | Inhibition of the Jak/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronectin synthesis in mesangial cells. |
| 2746 | 12453907 | We recently found that exposure of cells to HG also activates the growth-promoting enzyme janus kinase 2 (JAK2) and its latent signal transducers and activators of transcription (STAT) transcription factors (STAT1, STAT3, and STAT5). |
| 2747 | 12453907 | Our purpose was to determine the effect that inhibition of JAK2 and these STAT transcription factors has on the HG-induced increase in TGF-beta and fibronectin synthesis in GMC. |
| 2748 | 12453907 | Exposure of GMC to 25 mmol/l glucose caused the activation of JAK2, STAT1, STAT3, and STAT5 plus an increase in TGF-beta and fibronectin synthesis, as compared with 5.5 mmol/l glucose. |
| 2749 | 12453907 | This HG-induced increase in synthesis of TGF-beta and fibronectin was prevented by concomitant incubation with AG-490, a specific JAK2 inhibitor. |
| 2750 | 12453907 | The HG-induced JAK2, STAT1, and STAT3 tyrosine phosphorylations in GMC were also abolished by AG-490. |
| 2751 | 12453907 | Preincubation of GMC cultured in 25 mmol/l glucose with a specific JAK2 or STAT1 antisense oligonucleotide also prevented both TGF-beta and fibronectin synthesis. |
| 2752 | 12453907 | These results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-beta and fibronectin in GMC. |
| 2753 | 12453907 | Inhibition of the Jak/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronectin synthesis in mesangial cells. |
| 2754 | 12453907 | We recently found that exposure of cells to HG also activates the growth-promoting enzyme janus kinase 2 (JAK2) and its latent signal transducers and activators of transcription (STAT) transcription factors (STAT1, STAT3, and STAT5). |
| 2755 | 12453907 | Our purpose was to determine the effect that inhibition of JAK2 and these STAT transcription factors has on the HG-induced increase in TGF-beta and fibronectin synthesis in GMC. |
| 2756 | 12453907 | Exposure of GMC to 25 mmol/l glucose caused the activation of JAK2, STAT1, STAT3, and STAT5 plus an increase in TGF-beta and fibronectin synthesis, as compared with 5.5 mmol/l glucose. |
| 2757 | 12453907 | This HG-induced increase in synthesis of TGF-beta and fibronectin was prevented by concomitant incubation with AG-490, a specific JAK2 inhibitor. |
| 2758 | 12453907 | The HG-induced JAK2, STAT1, and STAT3 tyrosine phosphorylations in GMC were also abolished by AG-490. |
| 2759 | 12453907 | Preincubation of GMC cultured in 25 mmol/l glucose with a specific JAK2 or STAT1 antisense oligonucleotide also prevented both TGF-beta and fibronectin synthesis. |
| 2760 | 12453907 | These results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-beta and fibronectin in GMC. |
| 2761 | 12453907 | Inhibition of the Jak/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronectin synthesis in mesangial cells. |
| 2762 | 12453907 | We recently found that exposure of cells to HG also activates the growth-promoting enzyme janus kinase 2 (JAK2) and its latent signal transducers and activators of transcription (STAT) transcription factors (STAT1, STAT3, and STAT5). |
| 2763 | 12453907 | Our purpose was to determine the effect that inhibition of JAK2 and these STAT transcription factors has on the HG-induced increase in TGF-beta and fibronectin synthesis in GMC. |
| 2764 | 12453907 | Exposure of GMC to 25 mmol/l glucose caused the activation of JAK2, STAT1, STAT3, and STAT5 plus an increase in TGF-beta and fibronectin synthesis, as compared with 5.5 mmol/l glucose. |
| 2765 | 12453907 | This HG-induced increase in synthesis of TGF-beta and fibronectin was prevented by concomitant incubation with AG-490, a specific JAK2 inhibitor. |
| 2766 | 12453907 | The HG-induced JAK2, STAT1, and STAT3 tyrosine phosphorylations in GMC were also abolished by AG-490. |
| 2767 | 12453907 | Preincubation of GMC cultured in 25 mmol/l glucose with a specific JAK2 or STAT1 antisense oligonucleotide also prevented both TGF-beta and fibronectin synthesis. |
| 2768 | 12453907 | These results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-beta and fibronectin in GMC. |
| 2769 | 12453907 | Inhibition of the Jak/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronectin synthesis in mesangial cells. |
| 2770 | 12453907 | We recently found that exposure of cells to HG also activates the growth-promoting enzyme janus kinase 2 (JAK2) and its latent signal transducers and activators of transcription (STAT) transcription factors (STAT1, STAT3, and STAT5). |
| 2771 | 12453907 | Our purpose was to determine the effect that inhibition of JAK2 and these STAT transcription factors has on the HG-induced increase in TGF-beta and fibronectin synthesis in GMC. |
| 2772 | 12453907 | Exposure of GMC to 25 mmol/l glucose caused the activation of JAK2, STAT1, STAT3, and STAT5 plus an increase in TGF-beta and fibronectin synthesis, as compared with 5.5 mmol/l glucose. |
| 2773 | 12453907 | This HG-induced increase in synthesis of TGF-beta and fibronectin was prevented by concomitant incubation with AG-490, a specific JAK2 inhibitor. |
| 2774 | 12453907 | The HG-induced JAK2, STAT1, and STAT3 tyrosine phosphorylations in GMC were also abolished by AG-490. |
| 2775 | 12453907 | Preincubation of GMC cultured in 25 mmol/l glucose with a specific JAK2 or STAT1 antisense oligonucleotide also prevented both TGF-beta and fibronectin synthesis. |
| 2776 | 12453907 | These results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-beta and fibronectin in GMC. |
| 2777 | 12453907 | Inhibition of the Jak/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronectin synthesis in mesangial cells. |
| 2778 | 12453907 | We recently found that exposure of cells to HG also activates the growth-promoting enzyme janus kinase 2 (JAK2) and its latent signal transducers and activators of transcription (STAT) transcription factors (STAT1, STAT3, and STAT5). |
| 2779 | 12453907 | Our purpose was to determine the effect that inhibition of JAK2 and these STAT transcription factors has on the HG-induced increase in TGF-beta and fibronectin synthesis in GMC. |
| 2780 | 12453907 | Exposure of GMC to 25 mmol/l glucose caused the activation of JAK2, STAT1, STAT3, and STAT5 plus an increase in TGF-beta and fibronectin synthesis, as compared with 5.5 mmol/l glucose. |
| 2781 | 12453907 | This HG-induced increase in synthesis of TGF-beta and fibronectin was prevented by concomitant incubation with AG-490, a specific JAK2 inhibitor. |
| 2782 | 12453907 | The HG-induced JAK2, STAT1, and STAT3 tyrosine phosphorylations in GMC were also abolished by AG-490. |
| 2783 | 12453907 | Preincubation of GMC cultured in 25 mmol/l glucose with a specific JAK2 or STAT1 antisense oligonucleotide also prevented both TGF-beta and fibronectin synthesis. |
| 2784 | 12453907 | These results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-beta and fibronectin in GMC. |
| 2785 | 12453907 | Inhibition of the Jak/STAT signaling pathway prevents the high glucose-induced increase in tgf-beta and fibronectin synthesis in mesangial cells. |
| 2786 | 12453907 | We recently found that exposure of cells to HG also activates the growth-promoting enzyme janus kinase 2 (JAK2) and its latent signal transducers and activators of transcription (STAT) transcription factors (STAT1, STAT3, and STAT5). |
| 2787 | 12453907 | Our purpose was to determine the effect that inhibition of JAK2 and these STAT transcription factors has on the HG-induced increase in TGF-beta and fibronectin synthesis in GMC. |
| 2788 | 12453907 | Exposure of GMC to 25 mmol/l glucose caused the activation of JAK2, STAT1, STAT3, and STAT5 plus an increase in TGF-beta and fibronectin synthesis, as compared with 5.5 mmol/l glucose. |
| 2789 | 12453907 | This HG-induced increase in synthesis of TGF-beta and fibronectin was prevented by concomitant incubation with AG-490, a specific JAK2 inhibitor. |
| 2790 | 12453907 | The HG-induced JAK2, STAT1, and STAT3 tyrosine phosphorylations in GMC were also abolished by AG-490. |
| 2791 | 12453907 | Preincubation of GMC cultured in 25 mmol/l glucose with a specific JAK2 or STAT1 antisense oligonucleotide also prevented both TGF-beta and fibronectin synthesis. |
| 2792 | 12453907 | These results provide direct evidence for linkages between JAK2, STAT1, and the glucose-induced overproduction of TGF-beta and fibronectin in GMC. |
| 2793 | 12453917 | SF mRNA expression levels for TGF-beta1, TGF-beta type II receptor (TGF-beta RII), thrombospondin-1, and latent TGF-beta binding protein-1 (LTBP-1) were measured by real-time RT-PCR. |
| 2794 | 12453917 | LTBP-1 mRNA expression was reduced in slow-track (0.99 +/- 0.38) versus fast-track patients (1.65 +/- 0.52, P = 0.001) and control subjects (1.41 +/- 0.7, P = 0.025). mRNA levels for TGF-beta1, TGF-beta RII, and thrombospondin-1 were similar in the three groups. |
| 2795 | 12453917 | Reduced LTBP-1 mRNA expression in SFs from slow-track patients may reflect genetically determined DN protection and suggests that LTBP-1 may be involved in the pathogenesis of DN through the regulation of TGF-beta activity. |
| 2796 | 12453917 | SF mRNA expression levels for TGF-beta1, TGF-beta type II receptor (TGF-beta RII), thrombospondin-1, and latent TGF-beta binding protein-1 (LTBP-1) were measured by real-time RT-PCR. |
| 2797 | 12453917 | LTBP-1 mRNA expression was reduced in slow-track (0.99 +/- 0.38) versus fast-track patients (1.65 +/- 0.52, P = 0.001) and control subjects (1.41 +/- 0.7, P = 0.025). mRNA levels for TGF-beta1, TGF-beta RII, and thrombospondin-1 were similar in the three groups. |
| 2798 | 12453917 | Reduced LTBP-1 mRNA expression in SFs from slow-track patients may reflect genetically determined DN protection and suggests that LTBP-1 may be involved in the pathogenesis of DN through the regulation of TGF-beta activity. |
| 2799 | 12453917 | SF mRNA expression levels for TGF-beta1, TGF-beta type II receptor (TGF-beta RII), thrombospondin-1, and latent TGF-beta binding protein-1 (LTBP-1) were measured by real-time RT-PCR. |
| 2800 | 12453917 | LTBP-1 mRNA expression was reduced in slow-track (0.99 +/- 0.38) versus fast-track patients (1.65 +/- 0.52, P = 0.001) and control subjects (1.41 +/- 0.7, P = 0.025). mRNA levels for TGF-beta1, TGF-beta RII, and thrombospondin-1 were similar in the three groups. |
| 2801 | 12453917 | Reduced LTBP-1 mRNA expression in SFs from slow-track patients may reflect genetically determined DN protection and suggests that LTBP-1 may be involved in the pathogenesis of DN through the regulation of TGF-beta activity. |
| 2802 | 12453980 | Circulating and urinary transforming growth factor beta1, Amadori albumin, and complications of type 1 diabetes: the EURODIAB prospective complications study. |
| 2803 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2804 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2805 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2806 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2807 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2808 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2809 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2810 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2811 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2812 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2813 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2814 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2815 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2816 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2817 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2818 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2819 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2820 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2821 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2822 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2823 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2824 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2825 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2826 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2827 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2828 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2829 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2830 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2831 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2832 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2833 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2834 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2835 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2836 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2837 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2838 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2839 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2840 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2841 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2842 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2843 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2844 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2845 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2846 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2847 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2848 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2849 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2850 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2851 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2852 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2853 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2854 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2855 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2856 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2857 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2858 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2859 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2860 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2861 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2862 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2863 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2864 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2865 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2866 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2867 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2868 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2869 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2870 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2871 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2872 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2873 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2874 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2875 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2876 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2877 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2878 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2879 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2880 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2881 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2882 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2883 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2884 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2885 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2886 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2887 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2888 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2889 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2890 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2891 | 12456495 | PPARalpha inhibits TGF-beta-induced beta5 integrin transcription in vascular smooth muscle cells by interacting with Smad4. |
| 2892 | 12456495 | We investigated the effects of PPARalpha ligands on TGF-beta-induced beta3 and beta5 integrin expression and potential interaction between PPARalpha and TGF-beta signaling. |
| 2893 | 12456495 | PPARalpha ligands WY-14643 (100 micromol/L) and 5,8,11,14-eicosatetranoic acid (ETYA, 50 micromol/L) inhibited TGF-beta-induced beta5 integrin protein expression by 72+/-6.8% and 73+/-7.1%, respectively (both P<0.05). |
| 2894 | 12456495 | TGF-beta-stimulated beta3 integrin expression was not affected by PPARalpha ligands. |
| 2895 | 12456495 | Both PPARalpha ligands also suppressed TGF-beta-induced beta5 integrin mRNA levels. |
| 2896 | 12456495 | PPARalpha ligands inhibited TGF-beta-inducible transcription of beta5 integrin by an interaction with a TGF-beta response element between nucleotides -63 and -44, which contains a Sp1/Sp3 transcription factor binding site. |
| 2897 | 12456495 | Nuclear complexes binding to the TGF-beta response region contained Sp1/Sp3 and TGF-beta-regulated Smad 2, 3, and 4 transcription factors. |
| 2898 | 12456495 | TGF-beta-stimulated Sp1/Smad4 nuclear complex formation was inhibited by WY-14643 and ETYA with a parallel induction of PPARalpha/Smad4 interactions. |
| 2899 | 12456495 | However, in vitro pull-down experiments failed to demonstrate direct binding between PPARalpha/Smad4. |
| 2900 | 12456495 | Both PPARalpha ligands blocked PDGF-directed migration of TGF-beta-pretreated VSMCs, a process mediated, in part, by beta5 integrins. |
| 2901 | 12456495 | The present study demonstrates that PPARalpha activators inhibit TGF-beta-induced beta5 integrin transcription in VSMCs through a novel indirect interaction between ligand-activated PPARalpha and the TGF-beta-regulated Smad4 transcription factors. |
| 2902 | 12482638 | Role of protein kinase C-angiotensin II pathway for extracellular matrix production in cultured human mesangial cells exposed to high glucose levels. |
| 2903 | 12482638 | This study investigates the mechanisms for glucose-induced increase in angiotensin II (AII) production by human mesangial cells (MCs) in relation to protein kinase C (PKC). |
| 2904 | 12482638 | AII, TGF-beta1, fibronectin and type IV collagen in the culture media were measured by ELISA. |
| 2905 | 12486879 | We review how metzincins, working through unique mechanisms, influence the extracellular milieu of several important cytokines and growth factors including transforming growth factor-beta (TGF-beta), TNF-alpha, IGFs and HB-epidermal growth factor (EGF). |
| 2906 | 12504805 | To study the effects of high glucose on cytokine-induced NGF expression, rat mesangial cells were treated with the cytokines interleukin-1beta and tumor necrosis factor alpha under normal (1.0 g/L) and high (4.5 g/L) glucose concentrations. |
| 2907 | 12504805 | The specific protein kinase C inhibitors Ro31-8220 and CGP41251 suppressed cytokine-induced NGF expression. |
| 2908 | 12504805 | Moreover, blocking the oxidative activation of the protein kinase C pathway by N-acetylcysteine inhibited glucose effects on NGF synthesis. |
| 2909 | 12504805 | Neutralizing antibodies against transforming growth factor-beta inhibited cytokine-induced NGF expression under normal glucose concentrations but not under high glucose conditions. |
| 2910 | 12510848 | Activation of the mitogen-activated protein kinase (MAPK)-transforming growth factor beta1 (TGF beta1)-fibronectin pathway in kidney, responsible for glomerular dysfunction, was markedly blunted by SP treatment in a dose dependent manner. |
| 2911 | 12512830 | These findings revealed that S. mansoni egg deposition which leads to a shift from Th1 (IFN-gamma mainly) to Th2 (IL4, IL5, IL10 and TGF-beta cytokine profiles causes down-regulation of the Th1 cell mediated autoimmune insulin dependant diabetes mellitus (IDDM). |
| 2912 | 12518896 | However, IL-5, IL-12, TGF-beta, and IL-1beta were significantly elevated in NODs receiving encapsulated neonatal porcine ICCs compared with untransplanted controls. |
| 2913 | 12522331 | Failure of angiotensin II and insulin to stimulate transforming growth factor-beta1. |
| 2914 | 12524081 | Effect of glucose on the expression of type I collagen and transforming growth factor-beta1 in cultured human peritoneal fibroblasts. |
| 2915 | 12540629 | Each of these pathogenetic factors may induce changes in cellular function by a common intracellular signaling pathway, the activation of protein kinase C (PKC) beta. |
| 2916 | 12540629 | In vivo inhibition of PKC beta with LY333531 led to a reduction in albuminuria, structural injury, and TGF-beta expression, despite continued hypertension and hyperglycemia. |
| 2917 | 12540631 | We found markedly increased nuclear content in Jun proteins, leading to enhanced DNA-binding activity of activating protein 1 (AP-1). |
| 2918 | 12540631 | AP-1 inhibition reduced fibronectin production in a dosage-dependent manner. |
| 2919 | 12540631 | Moreover, inhibition of classic protein kinase C (PKC) isoforms prevented both the activation of AP-1 and the enhanced fibronectin production. |
| 2920 | 12540631 | In contrast to mesangial cells exposed to high glucose, no activation of the hexosamine biosynthetic, p38, or extracellular signal-related kinase 1 and 2 mitogen-activated protein kinase pathways nor any increase in TGF-beta1 synthesis could be detected, which could be explained by the absence of oxidative stress in cells transfected with the human GLUT1 gene. |
| 2921 | 12540631 | Our data indicate that increased glucose uptake and metabolism induce PKC-dependent AP-1 activation that is sufficient for enhanced fibronectin production, but not for increased TGF-beta1 expression. |
| 2922 | 12540631 | We found markedly increased nuclear content in Jun proteins, leading to enhanced DNA-binding activity of activating protein 1 (AP-1). |
| 2923 | 12540631 | AP-1 inhibition reduced fibronectin production in a dosage-dependent manner. |
| 2924 | 12540631 | Moreover, inhibition of classic protein kinase C (PKC) isoforms prevented both the activation of AP-1 and the enhanced fibronectin production. |
| 2925 | 12540631 | In contrast to mesangial cells exposed to high glucose, no activation of the hexosamine biosynthetic, p38, or extracellular signal-related kinase 1 and 2 mitogen-activated protein kinase pathways nor any increase in TGF-beta1 synthesis could be detected, which could be explained by the absence of oxidative stress in cells transfected with the human GLUT1 gene. |
| 2926 | 12540631 | Our data indicate that increased glucose uptake and metabolism induce PKC-dependent AP-1 activation that is sufficient for enhanced fibronectin production, but not for increased TGF-beta1 expression. |
| 2927 | 12560158 | High glucose potentiates mitogenic responses of cultured ovine coronary smooth muscle cells to platelet derived growth factor and transforming growth factor-beta1. |
| 2928 | 12560158 | Transforming growth factor-beta1 (1 ng/ml) caused a 100% increase of the PDGF-bb response in both normal and high glucose media. |
| 2929 | 12560158 | In conclusion, high glucose, per se, only very weakly stimulates smooth muscle cell growth but it interacts positively to potentiate the responses to the vascular derived growth factors PDGF and TGF-beta1. |
| 2930 | 12560158 | High glucose potentiates mitogenic responses of cultured ovine coronary smooth muscle cells to platelet derived growth factor and transforming growth factor-beta1. |
| 2931 | 12560158 | Transforming growth factor-beta1 (1 ng/ml) caused a 100% increase of the PDGF-bb response in both normal and high glucose media. |
| 2932 | 12560158 | In conclusion, high glucose, per se, only very weakly stimulates smooth muscle cell growth but it interacts positively to potentiate the responses to the vascular derived growth factors PDGF and TGF-beta1. |
| 2933 | 12560158 | High glucose potentiates mitogenic responses of cultured ovine coronary smooth muscle cells to platelet derived growth factor and transforming growth factor-beta1. |
| 2934 | 12560158 | Transforming growth factor-beta1 (1 ng/ml) caused a 100% increase of the PDGF-bb response in both normal and high glucose media. |
| 2935 | 12560158 | In conclusion, high glucose, per se, only very weakly stimulates smooth muscle cell growth but it interacts positively to potentiate the responses to the vascular derived growth factors PDGF and TGF-beta1. |
| 2936 | 12563296 | Recent data indicate that transforming growth factor-beta-dependent CD4+CD25+ regulatory T cells might have a central role in this effect. |
| 2937 | 12569274 | The effect of ramipril on albumin excretion in diabetes and hypertension: the role of increased lysosomal activity and decreased transforming growth factor-beta expression. |
| 2938 | 12570678 | In particular, we have successfully used this approach to deliver neutralizing cytokine receptors such as interferon gamma (IFNgamma)-receptor-Ig fusion proteins or anti-inflammatory cytokines such as transforming growth factor beta-1 (TGF-beta1) and interleukin 4 (IL-4). |
| 2939 | 12570678 | Intramuscular gene therapy is effective in protecting against several experimental autoimmune diseases including insulin-dependent diabetes mellitus (IDDM), experimental allergic encephalomyelitis (EAE), and systemic lupus erythematosus (SLE). |
| 2940 | 12577314 | Glomerular mesangial cells both synthesize and respond to insulin-like growth factor-1 (IGF-1). |
| 2941 | 12577314 | We have reported that primary glomerular mesangial cells derived from SPARC-null mice exhibit an accelerated rate of proliferation and produce substantially decreased levels of transforming growth factor beta1 (TGF-beta1) in comparison to their wild-type counterparts (Francki et al. [1999] J. |
| 2942 | 12577314 | SPARC-null mesangial cells produce increased amounts of IGF-1 and -2, as well as IGF-1 receptor (IGF-1R) in comparison to wild-type cells. |
| 2943 | 12577314 | Addition of recombinant SPARC to SPARC-null cells inhibited IGF-1-stimulated mitogen activated protein kinase (MAPK) activation and DNA synthesis. |
| 2944 | 12577314 | We also show that the observed accelerated rate of basal and IGF-1-stimulated proliferation in mesangial cells derived from SPARC-null animals is due, at least in part, to markedly diminished levels of cyclin D1 and the cyclin-dependent kinase (cdk) inhibitors p21 and p27. |
| 2945 | 12594852 | The imbalance of Th1/Th2 subsets is an important pathogenic mechanism for insulin-dependent diabetes mellitus (IDDM). |
| 2946 | 12594852 | We hypothesize that exogenous CGRP administration during insulitis may modulate the balance of Th lymphocytes, thereby providing a therapeutic intervention for IDDM. |
| 2947 | 12594852 | The effect of CGRP gene transfer on pathogenesis of IDDM was observedin autoimmune diabetic C57BL mice induced by multiple low-dose streptozotocin (MLDS) administration. |
| 2948 | 12594852 | CGRP gene transfer significantly inhibited T cell proliferation and secretion of the Th1 cytokine IFN-gamma, increased the level of the Th2 cytokine IL-10, but had no effect on IL-4 and TGF-beta1 secretion. |
| 2949 | 12594852 | CGRP gene transfer also decreased IL-12 and IFN-gamma levels in peritoneal effusion. |
| 2950 | 12594852 | Our results demonstrate that CGRP gene transfer selectively suppresses the pro-inflammatory Th1 subsets and promote anti-inflammatory Th2 subsets, resulting in amelioration of beta cell destruction and reduction of IDDM occurrence in mice with MLDS-induced diabetes. |
| 2951 | 12595507 | While transforming growth factor-beta1 (TGF-beta1) is the final mediator of ECM accumulation, reactive oxygen species (ROS) and protein kinase C (PKC) are the upstream signaling molecules that mediate hyperglycemia-induced ECM expansion. |
| 2952 | 12595507 | It significantly suppressed renal malondialdehyde (MDA), microalbuminuria, glomerular hypertrophy, mesangial expansion, and the upregulation of renal TGF-beta1, fibronectin, and collagen in STZR without significantly affecting plasma glucose. |
| 2953 | 12595507 | While transforming growth factor-beta1 (TGF-beta1) is the final mediator of ECM accumulation, reactive oxygen species (ROS) and protein kinase C (PKC) are the upstream signaling molecules that mediate hyperglycemia-induced ECM expansion. |
| 2954 | 12595507 | It significantly suppressed renal malondialdehyde (MDA), microalbuminuria, glomerular hypertrophy, mesangial expansion, and the upregulation of renal TGF-beta1, fibronectin, and collagen in STZR without significantly affecting plasma glucose. |
| 2955 | 12606526 | Latent transforming growth factor-beta binding protein-1, a component of latent transforming growth factor-beta complex, accelerates the migration of aortic smooth muscle cells in diabetic rats through integrin-beta3. |
| 2956 | 12606526 | Aortic smooth muscle cells (SMCs) of diabetic animals have unique properties, including the overexpression of transforming growth factor-beta (TGF-beta) type II receptor, fibronectin, and platelet-derived growth factor beta-receptor. |
| 2957 | 12606526 | TGF-beta1 is produced and secreted as latent high-molecular weight complex consisting of mature TGF-beta1, latency-associated peptide (LAP), and a latent TGF-beta1 binding protein (LTBP-1). |
| 2958 | 12606526 | LAP has an important function in the latency of TGF-beta complex, but the role of LTBP-1 is not known in diabetic angiopathy. |
| 2959 | 12606526 | Furthermore, cross-linking experiments show that LTBP-1 binds integrin-beta(3) in diabetic SMCs much more than in control SMCs in coincidence with the increase of integrin-beta(3) in diabetic aorta by immunohistochemistry. |
| 2960 | 12606526 | Taken together, these observations suggest that LTBP-1 plays a critical role in intimal thickening of diabetic artery through the acceleration of SMC migration via integrin-beta(3). |
| 2961 | 12606526 | Latent transforming growth factor-beta binding protein-1, a component of latent transforming growth factor-beta complex, accelerates the migration of aortic smooth muscle cells in diabetic rats through integrin-beta3. |
| 2962 | 12606526 | Aortic smooth muscle cells (SMCs) of diabetic animals have unique properties, including the overexpression of transforming growth factor-beta (TGF-beta) type II receptor, fibronectin, and platelet-derived growth factor beta-receptor. |
| 2963 | 12606526 | TGF-beta1 is produced and secreted as latent high-molecular weight complex consisting of mature TGF-beta1, latency-associated peptide (LAP), and a latent TGF-beta1 binding protein (LTBP-1). |
| 2964 | 12606526 | LAP has an important function in the latency of TGF-beta complex, but the role of LTBP-1 is not known in diabetic angiopathy. |
| 2965 | 12606526 | Furthermore, cross-linking experiments show that LTBP-1 binds integrin-beta(3) in diabetic SMCs much more than in control SMCs in coincidence with the increase of integrin-beta(3) in diabetic aorta by immunohistochemistry. |
| 2966 | 12606526 | Taken together, these observations suggest that LTBP-1 plays a critical role in intimal thickening of diabetic artery through the acceleration of SMC migration via integrin-beta(3). |
| 2967 | 12606526 | Latent transforming growth factor-beta binding protein-1, a component of latent transforming growth factor-beta complex, accelerates the migration of aortic smooth muscle cells in diabetic rats through integrin-beta3. |
| 2968 | 12606526 | Aortic smooth muscle cells (SMCs) of diabetic animals have unique properties, including the overexpression of transforming growth factor-beta (TGF-beta) type II receptor, fibronectin, and platelet-derived growth factor beta-receptor. |
| 2969 | 12606526 | TGF-beta1 is produced and secreted as latent high-molecular weight complex consisting of mature TGF-beta1, latency-associated peptide (LAP), and a latent TGF-beta1 binding protein (LTBP-1). |
| 2970 | 12606526 | LAP has an important function in the latency of TGF-beta complex, but the role of LTBP-1 is not known in diabetic angiopathy. |
| 2971 | 12606526 | Furthermore, cross-linking experiments show that LTBP-1 binds integrin-beta(3) in diabetic SMCs much more than in control SMCs in coincidence with the increase of integrin-beta(3) in diabetic aorta by immunohistochemistry. |
| 2972 | 12606526 | Taken together, these observations suggest that LTBP-1 plays a critical role in intimal thickening of diabetic artery through the acceleration of SMC migration via integrin-beta(3). |
| 2973 | 12612942 | Angiotensin II production upregulates the expression of transforming growth factor-beta1, tumor necrosis factor-alpha, nuclear factor-kappaB, and several adhesion molecules and chemoattractants. |
| 2974 | 12612942 | Treatment with one of several growth factors may ameliorate the progression of kidney disease: insulin-like growth factor-1, hepatocyte growth factor, and bone morphogenetic protein-7. |
| 2975 | 12634871 | The primary mechanisms that contribute to these endothelial dysfunctions in diabetes appear to involve the activation of protein kinase C (PKC) pathways, increased non-enzymatic glycation, increased oxidant stress, and reduced endothelial insulin action. |
| 2976 | 12634871 | In addition, many of the adverse effects of these abnormalities associated with hyperglycemia and insulin resistance are mediated and amplified by potent vasoactive hormones including angiotensin II, transforming growth factor-beta, and vascular endothelial growth factor. |
| 2977 | 12634871 | Multiple interventions have been shown to improve endothelial dysfunction in diabetes, including PKC inhibition, infusion of soluble receptors for advanced glycation end-products, antioxidant and insulin supplementation, and angiotensin-converting enzyme inhibition. |
| 2978 | 12643211 | ROS mimic the stimulatory effects of HG and upregulate transforming growth factor-beta 1, plasminogen activator inhibitor-1, and extracellular matrix (ECM) proteins by glomerular mesangial cells, thus leading to mesangial expansion. |
| 2979 | 12643211 | ROS activate other signaling molecules, such as protein kinase C and mitogen-activated protein kinases and transcription factors, such as nuclear factor-kappa B, activator protein-1, and specificity protein 1 leading to transcription of genes encoding cytokines, growth factors, and ECM proteins. |
| 2980 | 12644443 | When rat mesangial cells were cultured with an amino acid mixture designed to replicate the composition in plasma after protein feeding, production of mRNA (Northern blot analysis) and/or protein (ELISA or Western blot analysis) for transforming growth factor-beta1 (TGF-beta1), fibronectin, thrombospondin-1 (TSP-1), and collagen IV were enhanced in a manner comparable to a culture with high glucose (30.5 mM). |
| 2981 | 12644443 | The bioactive portion of total TGF-beta (NRK assay) increased in response to amino acids. |
| 2982 | 12644443 | The TSP-1 antagonist LSKL peptide reduced bioactive TGF-beta and fibronectin, indicating the dependence of TGF-beta1 activation on TSP-1. |
| 2983 | 12644443 | When rat mesangial cells were cultured with an amino acid mixture designed to replicate the composition in plasma after protein feeding, production of mRNA (Northern blot analysis) and/or protein (ELISA or Western blot analysis) for transforming growth factor-beta1 (TGF-beta1), fibronectin, thrombospondin-1 (TSP-1), and collagen IV were enhanced in a manner comparable to a culture with high glucose (30.5 mM). |
| 2984 | 12644443 | The bioactive portion of total TGF-beta (NRK assay) increased in response to amino acids. |
| 2985 | 12644443 | The TSP-1 antagonist LSKL peptide reduced bioactive TGF-beta and fibronectin, indicating the dependence of TGF-beta1 activation on TSP-1. |
| 2986 | 12644443 | When rat mesangial cells were cultured with an amino acid mixture designed to replicate the composition in plasma after protein feeding, production of mRNA (Northern blot analysis) and/or protein (ELISA or Western blot analysis) for transforming growth factor-beta1 (TGF-beta1), fibronectin, thrombospondin-1 (TSP-1), and collagen IV were enhanced in a manner comparable to a culture with high glucose (30.5 mM). |
| 2987 | 12644443 | The bioactive portion of total TGF-beta (NRK assay) increased in response to amino acids. |
| 2988 | 12644443 | The TSP-1 antagonist LSKL peptide reduced bioactive TGF-beta and fibronectin, indicating the dependence of TGF-beta1 activation on TSP-1. |
| 2989 | 12648610 | Impact of renal denervation on renal content of GLUT1, albuminuria and urinary TGF-beta1 in streptozotocin-induced diabetic rats. |
| 2990 | 12648610 | This study was designed to evaluate the effects of bilateral denervation of the kidneys of streptozotocin-diabetic rats, an experimental model that presents diabetic nephropathy with increased abundance of cortical GLUT1 in the kidney and increased urinary excretion of albumin and transforming growth factor-beta1 (TGF-beta1). |
| 2991 | 12648610 | Twenty-four-hour urinary TGF-beta1 (ELISA), urinary albumin (electroimmunoassay) and GLUT1 protein levels (Western blotting) in the renal cortex and medulla were evaluated in diabetic (n=13) and control (n=13) rats 45 days after streptozotocin injection, submitted or not to surgical renal denervation. |
| 2992 | 12648610 | However, renal denervation did not determine any changes in urinary albumin and urinary TGF-beta1 in both diabetic (127.3+/-12 microg/24 h and 111.8+/-24 ng mg(-1) creatinine, respectively) and control rats (45.9+/-3 microg/24 h and 13.4+/-4 ng mg(-1) creatinine, respectively). |
| 2993 | 12648610 | In conclusion, early-phase renal denervation in streptozotocin-diabetic rats produces a normalisation of previously elevated cortical GLUT1 protein content, but is not enough for reverting the increased urinary TGF-beta1 and albuminuria of diabetes. |
| 2994 | 12648610 | Impact of renal denervation on renal content of GLUT1, albuminuria and urinary TGF-beta1 in streptozotocin-induced diabetic rats. |
| 2995 | 12648610 | This study was designed to evaluate the effects of bilateral denervation of the kidneys of streptozotocin-diabetic rats, an experimental model that presents diabetic nephropathy with increased abundance of cortical GLUT1 in the kidney and increased urinary excretion of albumin and transforming growth factor-beta1 (TGF-beta1). |
| 2996 | 12648610 | Twenty-four-hour urinary TGF-beta1 (ELISA), urinary albumin (electroimmunoassay) and GLUT1 protein levels (Western blotting) in the renal cortex and medulla were evaluated in diabetic (n=13) and control (n=13) rats 45 days after streptozotocin injection, submitted or not to surgical renal denervation. |
| 2997 | 12648610 | However, renal denervation did not determine any changes in urinary albumin and urinary TGF-beta1 in both diabetic (127.3+/-12 microg/24 h and 111.8+/-24 ng mg(-1) creatinine, respectively) and control rats (45.9+/-3 microg/24 h and 13.4+/-4 ng mg(-1) creatinine, respectively). |
| 2998 | 12648610 | In conclusion, early-phase renal denervation in streptozotocin-diabetic rats produces a normalisation of previously elevated cortical GLUT1 protein content, but is not enough for reverting the increased urinary TGF-beta1 and albuminuria of diabetes. |
| 2999 | 12648610 | Impact of renal denervation on renal content of GLUT1, albuminuria and urinary TGF-beta1 in streptozotocin-induced diabetic rats. |
| 3000 | 12648610 | This study was designed to evaluate the effects of bilateral denervation of the kidneys of streptozotocin-diabetic rats, an experimental model that presents diabetic nephropathy with increased abundance of cortical GLUT1 in the kidney and increased urinary excretion of albumin and transforming growth factor-beta1 (TGF-beta1). |
| 3001 | 12648610 | Twenty-four-hour urinary TGF-beta1 (ELISA), urinary albumin (electroimmunoassay) and GLUT1 protein levels (Western blotting) in the renal cortex and medulla were evaluated in diabetic (n=13) and control (n=13) rats 45 days after streptozotocin injection, submitted or not to surgical renal denervation. |
| 3002 | 12648610 | However, renal denervation did not determine any changes in urinary albumin and urinary TGF-beta1 in both diabetic (127.3+/-12 microg/24 h and 111.8+/-24 ng mg(-1) creatinine, respectively) and control rats (45.9+/-3 microg/24 h and 13.4+/-4 ng mg(-1) creatinine, respectively). |
| 3003 | 12648610 | In conclusion, early-phase renal denervation in streptozotocin-diabetic rats produces a normalisation of previously elevated cortical GLUT1 protein content, but is not enough for reverting the increased urinary TGF-beta1 and albuminuria of diabetes. |
| 3004 | 12648610 | Impact of renal denervation on renal content of GLUT1, albuminuria and urinary TGF-beta1 in streptozotocin-induced diabetic rats. |
| 3005 | 12648610 | This study was designed to evaluate the effects of bilateral denervation of the kidneys of streptozotocin-diabetic rats, an experimental model that presents diabetic nephropathy with increased abundance of cortical GLUT1 in the kidney and increased urinary excretion of albumin and transforming growth factor-beta1 (TGF-beta1). |
| 3006 | 12648610 | Twenty-four-hour urinary TGF-beta1 (ELISA), urinary albumin (electroimmunoassay) and GLUT1 protein levels (Western blotting) in the renal cortex and medulla were evaluated in diabetic (n=13) and control (n=13) rats 45 days after streptozotocin injection, submitted or not to surgical renal denervation. |
| 3007 | 12648610 | However, renal denervation did not determine any changes in urinary albumin and urinary TGF-beta1 in both diabetic (127.3+/-12 microg/24 h and 111.8+/-24 ng mg(-1) creatinine, respectively) and control rats (45.9+/-3 microg/24 h and 13.4+/-4 ng mg(-1) creatinine, respectively). |
| 3008 | 12648610 | In conclusion, early-phase renal denervation in streptozotocin-diabetic rats produces a normalisation of previously elevated cortical GLUT1 protein content, but is not enough for reverting the increased urinary TGF-beta1 and albuminuria of diabetes. |
| 3009 | 12648610 | Impact of renal denervation on renal content of GLUT1, albuminuria and urinary TGF-beta1 in streptozotocin-induced diabetic rats. |
| 3010 | 12648610 | This study was designed to evaluate the effects of bilateral denervation of the kidneys of streptozotocin-diabetic rats, an experimental model that presents diabetic nephropathy with increased abundance of cortical GLUT1 in the kidney and increased urinary excretion of albumin and transforming growth factor-beta1 (TGF-beta1). |
| 3011 | 12648610 | Twenty-four-hour urinary TGF-beta1 (ELISA), urinary albumin (electroimmunoassay) and GLUT1 protein levels (Western blotting) in the renal cortex and medulla were evaluated in diabetic (n=13) and control (n=13) rats 45 days after streptozotocin injection, submitted or not to surgical renal denervation. |
| 3012 | 12648610 | However, renal denervation did not determine any changes in urinary albumin and urinary TGF-beta1 in both diabetic (127.3+/-12 microg/24 h and 111.8+/-24 ng mg(-1) creatinine, respectively) and control rats (45.9+/-3 microg/24 h and 13.4+/-4 ng mg(-1) creatinine, respectively). |
| 3013 | 12648610 | In conclusion, early-phase renal denervation in streptozotocin-diabetic rats produces a normalisation of previously elevated cortical GLUT1 protein content, but is not enough for reverting the increased urinary TGF-beta1 and albuminuria of diabetes. |
| 3014 | 12649573 | Increased abdominal obesity, insulin and glucose levels in nondiabetic subjects with a T29C polymorphism of the transforming growth factor-beta1 gene. |
| 3015 | 12651605 | Postulated mechanisms include roles for vascular endothelial growth factor (VEGF), produced by podocytes and contributing to enhanced excretion of urinary albumin and recruitment/activation of inflammatory cells, and transforming growth factor-beta (TGF-beta), elicited largely from mesangial cells and driving production of extracellular matrix. |
| 3016 | 12651605 | We propose that activation of RAGE contributes to expression of VEGF and enhanced attraction/activation of inflammatory cells in the diabetic glomerulus, thereby setting the stage for mesangial activation and TGF-beta production; processes which converge to cause albuminuria and glomerulosclerosis. |
| 3017 | 12651605 | Postulated mechanisms include roles for vascular endothelial growth factor (VEGF), produced by podocytes and contributing to enhanced excretion of urinary albumin and recruitment/activation of inflammatory cells, and transforming growth factor-beta (TGF-beta), elicited largely from mesangial cells and driving production of extracellular matrix. |
| 3018 | 12651605 | We propose that activation of RAGE contributes to expression of VEGF and enhanced attraction/activation of inflammatory cells in the diabetic glomerulus, thereby setting the stage for mesangial activation and TGF-beta production; processes which converge to cause albuminuria and glomerulosclerosis. |
| 3019 | 12653847 | Anti-cytokine autoantibodies in autoimmunity: preponderance of neutralizing autoantibodies against interferon-alpha, interferon-omega and interleukin-12 in patients with thymoma and/or myasthenia gravis. |
| 3020 | 12653847 | We tested for both binding and neutralizing autoantibodies to a range of human cytokines, including interleukin-1alpha (IL-1alpha), IL-1beta, IL-2, IL-4, IL-6, IL-8, IL-10, IL-12, IL-18, interferon-alpha2 (IFN-alpha2), IFN-omega, IFN-beta, IFN-gamma, tumour necrosis factor alpha (TNF-alpha), transforming growth factor beta-1 (TGF-beta1) and granulocyte-macrophage colony stimulating factor (GM-CSF), in plasmas or sera. |
| 3021 | 12653847 | With two notable exceptions described below, we found only occasional, mostly low-titre, non-neutralizing antibodies, mainly to GM-CSF; also to IL-10 in pemphigoid. |
| 3022 | 12653847 | Strikingly, however, high-titre, mainly IgG, autoantibodies to IFN-alpha2, IFN-omega and IL-12 were common at diagnosis in patients with late-onset myasthenia gravis (LOMG+), thymoma (T) but no MG (TMG-) and especially with both thymoma and MG together (TMG+). |
| 3023 | 12653847 | The antibodies recognized other closely related type I IFN-alpha subtypes, but rarely the distantly related type I IFN-beta, and never (detectably) the unrelated type II IFN-gamma. |
| 3024 | 12653847 | Antibodies to IL-12 showed a similar distribution to those against IFN-alpha2, although prevalences were slightly lower; correlations between individual titres against each were so modest that they appear to be entirely different specificities. |
| 3025 | 12657834 | A short-term administration of antibodies against ICAM-1/LFA-1 or CD8 molecules during a critical period of younger age resulted in complete protection of autoimmune diabetes in NOD mice. |
| 3026 | 12657834 | Furthermore, semiquantitative RT-PCR analysis of cytokines showed that T cells from anti-CD8-treated mice could express IFN-gamma, IL-4, IL-10 and TGF-beta1 in response to islet antigen. |
| 3027 | 12657834 | In contrast, T cells from anti-ICAM-1/LFA-1-treated mice expressed IFN-gamma, IL-10 and TGF-beta1 but not IL-4. |
| 3028 | 12657834 | A short-term administration of antibodies against ICAM-1/LFA-1 or CD8 molecules during a critical period of younger age resulted in complete protection of autoimmune diabetes in NOD mice. |
| 3029 | 12657834 | Furthermore, semiquantitative RT-PCR analysis of cytokines showed that T cells from anti-CD8-treated mice could express IFN-gamma, IL-4, IL-10 and TGF-beta1 in response to islet antigen. |
| 3030 | 12657834 | In contrast, T cells from anti-ICAM-1/LFA-1-treated mice expressed IFN-gamma, IL-10 and TGF-beta1 but not IL-4. |
| 3031 | 12660331 | SPARC (Secreted Protein, Acidic and Rich in Cysteine) is a matricellular protein that inhibits mesangial cell proliferation and also affects production of extracellular matrix (ECM) by regulating transforming growth factor-beta1 (TGF-beta1) and type I collagen in mesangial cells. |
| 3032 | 12660331 | Deposition of type I and IV collagen and laminin was evaluated by IHC, and TGF-beta 1 mRNA was assessed by ISH. |
| 3033 | 12660331 | Further characterization of diabetic SPARC-null mice revealed diminished glomerular deposition of type IV collagen and laminin, and diminished interstitial deposition of type I and type IV collagen correlated with decreases in TGF-beta 1 mRNA compared with WT diabetic mice. |
| 3034 | 12660331 | These observations suggest that SPARC contributes to glomerulosclerosis and tubulointerstitial damage in response to hyperglycemia through increasing TGF-beta 1 expression in this model of chronic DN. |
| 3035 | 12660331 | SPARC (Secreted Protein, Acidic and Rich in Cysteine) is a matricellular protein that inhibits mesangial cell proliferation and also affects production of extracellular matrix (ECM) by regulating transforming growth factor-beta1 (TGF-beta1) and type I collagen in mesangial cells. |
| 3036 | 12660331 | Deposition of type I and IV collagen and laminin was evaluated by IHC, and TGF-beta 1 mRNA was assessed by ISH. |
| 3037 | 12660331 | Further characterization of diabetic SPARC-null mice revealed diminished glomerular deposition of type IV collagen and laminin, and diminished interstitial deposition of type I and type IV collagen correlated with decreases in TGF-beta 1 mRNA compared with WT diabetic mice. |
| 3038 | 12660331 | These observations suggest that SPARC contributes to glomerulosclerosis and tubulointerstitial damage in response to hyperglycemia through increasing TGF-beta 1 expression in this model of chronic DN. |
| 3039 | 12660331 | SPARC (Secreted Protein, Acidic and Rich in Cysteine) is a matricellular protein that inhibits mesangial cell proliferation and also affects production of extracellular matrix (ECM) by regulating transforming growth factor-beta1 (TGF-beta1) and type I collagen in mesangial cells. |
| 3040 | 12660331 | Deposition of type I and IV collagen and laminin was evaluated by IHC, and TGF-beta 1 mRNA was assessed by ISH. |
| 3041 | 12660331 | Further characterization of diabetic SPARC-null mice revealed diminished glomerular deposition of type IV collagen and laminin, and diminished interstitial deposition of type I and type IV collagen correlated with decreases in TGF-beta 1 mRNA compared with WT diabetic mice. |
| 3042 | 12660331 | These observations suggest that SPARC contributes to glomerulosclerosis and tubulointerstitial damage in response to hyperglycemia through increasing TGF-beta 1 expression in this model of chronic DN. |
| 3043 | 12660331 | SPARC (Secreted Protein, Acidic and Rich in Cysteine) is a matricellular protein that inhibits mesangial cell proliferation and also affects production of extracellular matrix (ECM) by regulating transforming growth factor-beta1 (TGF-beta1) and type I collagen in mesangial cells. |
| 3044 | 12660331 | Deposition of type I and IV collagen and laminin was evaluated by IHC, and TGF-beta 1 mRNA was assessed by ISH. |
| 3045 | 12660331 | Further characterization of diabetic SPARC-null mice revealed diminished glomerular deposition of type IV collagen and laminin, and diminished interstitial deposition of type I and type IV collagen correlated with decreases in TGF-beta 1 mRNA compared with WT diabetic mice. |
| 3046 | 12660331 | These observations suggest that SPARC contributes to glomerulosclerosis and tubulointerstitial damage in response to hyperglycemia through increasing TGF-beta 1 expression in this model of chronic DN. |
| 3047 | 12669952 | Intradermal injection of transforming growth factor-beta1 gene enhances wound healing in genetically diabetic mice. |
| 3048 | 12677169 | Glycated albumin increases oxidative stress, activates NF-kappa B and extracellular signal-regulated kinase (ERK), and stimulates ERK-dependent transforming growth factor-beta 1 production in macrophage RAW cells. |
| 3049 | 12677169 | RAW cells were cultured in medium containing 5.5 mmol/L glucose and glycated or nonglycated albumin, with and without the addition of PD98059, a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK), followed by analysis of phosphorylated ERK and the nuclear translocation of nuclear factor (NF)-kappa B and measurement of cellular content of thiobarbituric acid-reactive substances and the concentration of transforming growth factor (TGF)-beta(1) in the spent medium. |
| 3050 | 12677169 | We demonstrate, for the first time, that glycated albumin activates RAW cell ERK and promotes ERK-dependent increases in TGF-beta(1) production, oxidative stress, and NF-kappa B activation. |
| 3051 | 12677169 | Preincubation with the antioxidant alpha-lipoic acid partially prevented the glycated albumin-induced increase in NF-kappa B activation. |
| 3052 | 12677169 | Glycated albumin increases oxidative stress, activates NF-kappa B and extracellular signal-regulated kinase (ERK), and stimulates ERK-dependent transforming growth factor-beta 1 production in macrophage RAW cells. |
| 3053 | 12677169 | RAW cells were cultured in medium containing 5.5 mmol/L glucose and glycated or nonglycated albumin, with and without the addition of PD98059, a specific inhibitor of mitogen-activated protein kinase/extracellular signal-regulated kinase (ERK), followed by analysis of phosphorylated ERK and the nuclear translocation of nuclear factor (NF)-kappa B and measurement of cellular content of thiobarbituric acid-reactive substances and the concentration of transforming growth factor (TGF)-beta(1) in the spent medium. |
| 3054 | 12677169 | We demonstrate, for the first time, that glycated albumin activates RAW cell ERK and promotes ERK-dependent increases in TGF-beta(1) production, oxidative stress, and NF-kappa B activation. |
| 3055 | 12677169 | Preincubation with the antioxidant alpha-lipoic acid partially prevented the glycated albumin-induced increase in NF-kappa B activation. |
| 3056 | 12682618 | The accumulation of advanced glycosilation end products (AGEPs), the activation of isoforms of protein kinase C (PKC) and the acceleration of the aldose reductase pathway may explain how hyperglycaemia damages vessels. |
| 3057 | 12682618 | TGF-b, IGF-1, VEGF) may also play an important role in the pathogenesis. |
| 3058 | 12682618 | The two main treatment strategies for prevention of diabetic nephropathy are improved glycaemic control and blood pressure lowering, particularly using drugs such angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists. |
| 3059 | 12697153 | The mRNA levels of IFN-gamma, IL-10, TNF-alpha, TGF-beta, and inducible NO synthase in the small intestine and the Peyer's patches were determined by semi-quantitative RT-PCR. |
| 3060 | 12697153 | Mice fed on the cereal-based NTP-2000 diet expressed higher levels of the Th1-type and pro-inflammatory markers IFN-gamma, TNF-alpha, and inducible NO synthase mRNA compared to the Prosobee-fed animals. |
| 3061 | 12697153 | The expression of the counterregulatory cytokines IL-10 and TGF-beta was unaffected. |
| 3062 | 12697153 | The mRNA levels of IFN-gamma, IL-10, TNF-alpha, TGF-beta, and inducible NO synthase in the small intestine and the Peyer's patches were determined by semi-quantitative RT-PCR. |
| 3063 | 12697153 | Mice fed on the cereal-based NTP-2000 diet expressed higher levels of the Th1-type and pro-inflammatory markers IFN-gamma, TNF-alpha, and inducible NO synthase mRNA compared to the Prosobee-fed animals. |
| 3064 | 12697153 | The expression of the counterregulatory cytokines IL-10 and TGF-beta was unaffected. |
| 3065 | 12709399 | While it is thought that advanced glycation end products (AGEs) act by stimulating transforming growth factor (TGF)-beta to mediate diabetic injury, we report that AGEs can activate TGF-beta signaling, Smads, and mediate diabetic scarring directly and independently of TGF-beta. |
| 3066 | 12709399 | AGEs activate Smad2/3 in renal and vascular cells at 5 min, peaking over 15-30 min before TGF-beta synthesis at 24 h and occurs in TGF-beta receptor I and II mutant cells. |
| 3067 | 12709399 | A substantial inhibition of AGE-induced Smad activation and collagen synthesis by ERK/p38 MAPK inhibitors, but not by TGF-beta blockade, suggests that the MAPK-Smad signaling crosstalk pathway is a key mechanism in diabetic scarring. |
| 3068 | 12709399 | Prevention of AGE-induced Smad activation and collagen synthesis by overexpression of Smad7 indicates that Smad signaling may play a critical role in diabetic complications. |
| 3069 | 12709399 | While it is thought that advanced glycation end products (AGEs) act by stimulating transforming growth factor (TGF)-beta to mediate diabetic injury, we report that AGEs can activate TGF-beta signaling, Smads, and mediate diabetic scarring directly and independently of TGF-beta. |
| 3070 | 12709399 | AGEs activate Smad2/3 in renal and vascular cells at 5 min, peaking over 15-30 min before TGF-beta synthesis at 24 h and occurs in TGF-beta receptor I and II mutant cells. |
| 3071 | 12709399 | A substantial inhibition of AGE-induced Smad activation and collagen synthesis by ERK/p38 MAPK inhibitors, but not by TGF-beta blockade, suggests that the MAPK-Smad signaling crosstalk pathway is a key mechanism in diabetic scarring. |
| 3072 | 12709399 | Prevention of AGE-induced Smad activation and collagen synthesis by overexpression of Smad7 indicates that Smad signaling may play a critical role in diabetic complications. |
| 3073 | 12709399 | While it is thought that advanced glycation end products (AGEs) act by stimulating transforming growth factor (TGF)-beta to mediate diabetic injury, we report that AGEs can activate TGF-beta signaling, Smads, and mediate diabetic scarring directly and independently of TGF-beta. |
| 3074 | 12709399 | AGEs activate Smad2/3 in renal and vascular cells at 5 min, peaking over 15-30 min before TGF-beta synthesis at 24 h and occurs in TGF-beta receptor I and II mutant cells. |
| 3075 | 12709399 | A substantial inhibition of AGE-induced Smad activation and collagen synthesis by ERK/p38 MAPK inhibitors, but not by TGF-beta blockade, suggests that the MAPK-Smad signaling crosstalk pathway is a key mechanism in diabetic scarring. |
| 3076 | 12709399 | Prevention of AGE-induced Smad activation and collagen synthesis by overexpression of Smad7 indicates that Smad signaling may play a critical role in diabetic complications. |
| 3077 | 12711314 | c-Fos-driven transcriptional activation of transforming growth factor beta-1: inhibition of high glucose-induced promoter activity by thiazolidinediones. |
| 3078 | 12711314 | The peroxisome proliferator-activated receptor gamma activating compounds thiazolidinedione (TZD) have been shown to inhibit diabetes-induced glomerular transforming growth factor-beta1 (TGF-beta1) expression, thereby ameliorating diabetic nephropathy. |
| 3079 | 12711314 | Here we examined the hypothesis that TZDs block high glucose-induced TGF-beta1 gene activation by interaction with the activated protein kinase C-c-Fos-TGF-beta1 promoter cascade in mesangial cells. |
| 3080 | 12711314 | The TZD compounds troglitazone and rosiglitazone completely prevented the high glucose induction of both TGF-beta1 promoter activity and elevation in nuclear c-Fos protein levels. |
| 3081 | 12711314 | TZD-treatment did not interfere with the transcriptional activity of c-Fos responsible for stimulation of the TGF-beta1 promoter. |
| 3082 | 12711314 | The findings suggest a molecular mechanism by which TZD-treatment reduces specifically high glucose-induced, c-Fos-mediated gene activation, since phorbol ester-induced c-Fos mRNA and protein expression and subsequent elevation of TGF-beta1 mRNA expression were not prevented by TZDs. |
| 3083 | 12711314 | c-Fos-driven transcriptional activation of transforming growth factor beta-1: inhibition of high glucose-induced promoter activity by thiazolidinediones. |
| 3084 | 12711314 | The peroxisome proliferator-activated receptor gamma activating compounds thiazolidinedione (TZD) have been shown to inhibit diabetes-induced glomerular transforming growth factor-beta1 (TGF-beta1) expression, thereby ameliorating diabetic nephropathy. |
| 3085 | 12711314 | Here we examined the hypothesis that TZDs block high glucose-induced TGF-beta1 gene activation by interaction with the activated protein kinase C-c-Fos-TGF-beta1 promoter cascade in mesangial cells. |
| 3086 | 12711314 | The TZD compounds troglitazone and rosiglitazone completely prevented the high glucose induction of both TGF-beta1 promoter activity and elevation in nuclear c-Fos protein levels. |
| 3087 | 12711314 | TZD-treatment did not interfere with the transcriptional activity of c-Fos responsible for stimulation of the TGF-beta1 promoter. |
| 3088 | 12711314 | The findings suggest a molecular mechanism by which TZD-treatment reduces specifically high glucose-induced, c-Fos-mediated gene activation, since phorbol ester-induced c-Fos mRNA and protein expression and subsequent elevation of TGF-beta1 mRNA expression were not prevented by TZDs. |
| 3089 | 12711314 | c-Fos-driven transcriptional activation of transforming growth factor beta-1: inhibition of high glucose-induced promoter activity by thiazolidinediones. |
| 3090 | 12711314 | The peroxisome proliferator-activated receptor gamma activating compounds thiazolidinedione (TZD) have been shown to inhibit diabetes-induced glomerular transforming growth factor-beta1 (TGF-beta1) expression, thereby ameliorating diabetic nephropathy. |
| 3091 | 12711314 | Here we examined the hypothesis that TZDs block high glucose-induced TGF-beta1 gene activation by interaction with the activated protein kinase C-c-Fos-TGF-beta1 promoter cascade in mesangial cells. |
| 3092 | 12711314 | The TZD compounds troglitazone and rosiglitazone completely prevented the high glucose induction of both TGF-beta1 promoter activity and elevation in nuclear c-Fos protein levels. |
| 3093 | 12711314 | TZD-treatment did not interfere with the transcriptional activity of c-Fos responsible for stimulation of the TGF-beta1 promoter. |
| 3094 | 12711314 | The findings suggest a molecular mechanism by which TZD-treatment reduces specifically high glucose-induced, c-Fos-mediated gene activation, since phorbol ester-induced c-Fos mRNA and protein expression and subsequent elevation of TGF-beta1 mRNA expression were not prevented by TZDs. |
| 3095 | 12711314 | c-Fos-driven transcriptional activation of transforming growth factor beta-1: inhibition of high glucose-induced promoter activity by thiazolidinediones. |
| 3096 | 12711314 | The peroxisome proliferator-activated receptor gamma activating compounds thiazolidinedione (TZD) have been shown to inhibit diabetes-induced glomerular transforming growth factor-beta1 (TGF-beta1) expression, thereby ameliorating diabetic nephropathy. |
| 3097 | 12711314 | Here we examined the hypothesis that TZDs block high glucose-induced TGF-beta1 gene activation by interaction with the activated protein kinase C-c-Fos-TGF-beta1 promoter cascade in mesangial cells. |
| 3098 | 12711314 | The TZD compounds troglitazone and rosiglitazone completely prevented the high glucose induction of both TGF-beta1 promoter activity and elevation in nuclear c-Fos protein levels. |
| 3099 | 12711314 | TZD-treatment did not interfere with the transcriptional activity of c-Fos responsible for stimulation of the TGF-beta1 promoter. |
| 3100 | 12711314 | The findings suggest a molecular mechanism by which TZD-treatment reduces specifically high glucose-induced, c-Fos-mediated gene activation, since phorbol ester-induced c-Fos mRNA and protein expression and subsequent elevation of TGF-beta1 mRNA expression were not prevented by TZDs. |
| 3101 | 12711314 | c-Fos-driven transcriptional activation of transforming growth factor beta-1: inhibition of high glucose-induced promoter activity by thiazolidinediones. |
| 3102 | 12711314 | The peroxisome proliferator-activated receptor gamma activating compounds thiazolidinedione (TZD) have been shown to inhibit diabetes-induced glomerular transforming growth factor-beta1 (TGF-beta1) expression, thereby ameliorating diabetic nephropathy. |
| 3103 | 12711314 | Here we examined the hypothesis that TZDs block high glucose-induced TGF-beta1 gene activation by interaction with the activated protein kinase C-c-Fos-TGF-beta1 promoter cascade in mesangial cells. |
| 3104 | 12711314 | The TZD compounds troglitazone and rosiglitazone completely prevented the high glucose induction of both TGF-beta1 promoter activity and elevation in nuclear c-Fos protein levels. |
| 3105 | 12711314 | TZD-treatment did not interfere with the transcriptional activity of c-Fos responsible for stimulation of the TGF-beta1 promoter. |
| 3106 | 12711314 | The findings suggest a molecular mechanism by which TZD-treatment reduces specifically high glucose-induced, c-Fos-mediated gene activation, since phorbol ester-induced c-Fos mRNA and protein expression and subsequent elevation of TGF-beta1 mRNA expression were not prevented by TZDs. |
| 3107 | 12711314 | c-Fos-driven transcriptional activation of transforming growth factor beta-1: inhibition of high glucose-induced promoter activity by thiazolidinediones. |
| 3108 | 12711314 | The peroxisome proliferator-activated receptor gamma activating compounds thiazolidinedione (TZD) have been shown to inhibit diabetes-induced glomerular transforming growth factor-beta1 (TGF-beta1) expression, thereby ameliorating diabetic nephropathy. |
| 3109 | 12711314 | Here we examined the hypothesis that TZDs block high glucose-induced TGF-beta1 gene activation by interaction with the activated protein kinase C-c-Fos-TGF-beta1 promoter cascade in mesangial cells. |
| 3110 | 12711314 | The TZD compounds troglitazone and rosiglitazone completely prevented the high glucose induction of both TGF-beta1 promoter activity and elevation in nuclear c-Fos protein levels. |
| 3111 | 12711314 | TZD-treatment did not interfere with the transcriptional activity of c-Fos responsible for stimulation of the TGF-beta1 promoter. |
| 3112 | 12711314 | The findings suggest a molecular mechanism by which TZD-treatment reduces specifically high glucose-induced, c-Fos-mediated gene activation, since phorbol ester-induced c-Fos mRNA and protein expression and subsequent elevation of TGF-beta1 mRNA expression were not prevented by TZDs. |
| 3113 | 12728786 | Hyperglycaemia activates the renin-angiotensin system and induces transforming growth factor-beta expression. |
| 3114 | 12728786 | Angiotensinogen and type 1 angiotensin-II-receptor gene mutations may be also predisposing factors for diabetic nephropathy. |
| 3115 | 12728786 | Angiotensin-II-receptor blockers exert the same effect in type 2 diabetic patients, and presumably angiotensin-I-converting-enzyme inhibitors have similar activity in this group of patients. |
| 3116 | 12728786 | Combination therapy of angiotensin-I-converting-enzyme inhibitors with angiotensin-II-receptor blockers can be the choice of treatment in the future. |
| 3117 | 12733703 | Hypertension accelerates diabetic nephropathy in Wistar fatty rats, a model of type 2 diabetes mellitus, via mitogen-activated protein kinase cascades and transforming growth factor-beta1. |
| 3118 | 12733703 | At the end of the study, the expressions of mitogen-activated protein kinases (MAPK) and transforming growth factor-beta1 (TGF-beta1) were examined in the isolated glomeruli by Western blot analysis, and the number of glomerular lesions was determined by conventional histology. |
| 3119 | 12733703 | There was no difference among the four groups in the expression of c-Jun-NH2-terminal kinase (JNK). |
| 3120 | 12733703 | In contrast, the expressions of extracellular signal-regulated kinase 1/2 (ERK1/2) and its upstream regulator, MAPK/ERK kinase 1 (MEK1), were augmented in the hypertensive WFR. |
| 3121 | 12733703 | Hypertension accelerates diabetic nephropathy in Wistar fatty rats, a model of type 2 diabetes mellitus, via mitogen-activated protein kinase cascades and transforming growth factor-beta1. |
| 3122 | 12733703 | At the end of the study, the expressions of mitogen-activated protein kinases (MAPK) and transforming growth factor-beta1 (TGF-beta1) were examined in the isolated glomeruli by Western blot analysis, and the number of glomerular lesions was determined by conventional histology. |
| 3123 | 12733703 | There was no difference among the four groups in the expression of c-Jun-NH2-terminal kinase (JNK). |
| 3124 | 12733703 | In contrast, the expressions of extracellular signal-regulated kinase 1/2 (ERK1/2) and its upstream regulator, MAPK/ERK kinase 1 (MEK1), were augmented in the hypertensive WFR. |
| 3125 | 12767930 | In order to evaluate a role of Smad3, one of the major signaling molecules downstream of TGF-beta, in the pathogenesis of diabetic glomerulopathy, Smad3-null mice were made diabetic with streptozotocin injection and analyzed 4 weeks after induction of diabetes. |
| 3126 | 12767930 | Urinary albumin excretion was dramatically increased in wild-type diabetic mice, whereas Smad3-null diabetic mice did not show any overt albuminuria. |
| 3127 | 12767930 | Northern blotting revealed that mRNA levels of fibronectin and alpha 3 chain of type IV collagen (alpha 3Col4) in renal cortex of wild-type diabetic mice were approximately twice as much as those of non-diabetic mice, whereas their mRNA levels were not increased in Smad3-null diabetic mice. |
| 3128 | 12767930 | Glomerular expression of TGF-beta 1, as assessed by real-time PCR, was enhanced to a similar degree in wild-type and smad3-null diabetic mice, indicating that the observed differences between wild-type and Smad3-null mice are not attributable to difference in the expression of TGF-beta 1. |
| 3129 | 12767930 | In order to evaluate a role of Smad3, one of the major signaling molecules downstream of TGF-beta, in the pathogenesis of diabetic glomerulopathy, Smad3-null mice were made diabetic with streptozotocin injection and analyzed 4 weeks after induction of diabetes. |
| 3130 | 12767930 | Urinary albumin excretion was dramatically increased in wild-type diabetic mice, whereas Smad3-null diabetic mice did not show any overt albuminuria. |
| 3131 | 12767930 | Northern blotting revealed that mRNA levels of fibronectin and alpha 3 chain of type IV collagen (alpha 3Col4) in renal cortex of wild-type diabetic mice were approximately twice as much as those of non-diabetic mice, whereas their mRNA levels were not increased in Smad3-null diabetic mice. |
| 3132 | 12767930 | Glomerular expression of TGF-beta 1, as assessed by real-time PCR, was enhanced to a similar degree in wild-type and smad3-null diabetic mice, indicating that the observed differences between wild-type and Smad3-null mice are not attributable to difference in the expression of TGF-beta 1. |
| 3133 | 12771048 | At similar levels of systemic hypertension, Dahl salt-sensitive but not spontaneously hypertensive rats (SHR) develop glomerular hypertension, which is accompanied by upregulation of transforming growth factor beta1 (TGF-beta1), mesangial matrix expansion, and sclerosis. |
| 3134 | 12771048 | In mesangial cells in vitro, GLUT-1 overexpression increases basal glucose transport, resulting in excess fibronectin and collagen production. |
| 3135 | 12771048 | TGF-beta1 has been shown to upregulate GLUT-1 expression. |
| 3136 | 12771048 | This was accompanied by a 2.7-fold upregulation of TGF-beta1 protein expression in glomeruli of DSH compared with DSN rats (P=0.02). |
| 3137 | 12771048 | At similar levels of systemic hypertension, Dahl salt-sensitive but not spontaneously hypertensive rats (SHR) develop glomerular hypertension, which is accompanied by upregulation of transforming growth factor beta1 (TGF-beta1), mesangial matrix expansion, and sclerosis. |
| 3138 | 12771048 | In mesangial cells in vitro, GLUT-1 overexpression increases basal glucose transport, resulting in excess fibronectin and collagen production. |
| 3139 | 12771048 | TGF-beta1 has been shown to upregulate GLUT-1 expression. |
| 3140 | 12771048 | This was accompanied by a 2.7-fold upregulation of TGF-beta1 protein expression in glomeruli of DSH compared with DSN rats (P=0.02). |
| 3141 | 12771048 | At similar levels of systemic hypertension, Dahl salt-sensitive but not spontaneously hypertensive rats (SHR) develop glomerular hypertension, which is accompanied by upregulation of transforming growth factor beta1 (TGF-beta1), mesangial matrix expansion, and sclerosis. |
| 3142 | 12771048 | In mesangial cells in vitro, GLUT-1 overexpression increases basal glucose transport, resulting in excess fibronectin and collagen production. |
| 3143 | 12771048 | TGF-beta1 has been shown to upregulate GLUT-1 expression. |
| 3144 | 12771048 | This was accompanied by a 2.7-fold upregulation of TGF-beta1 protein expression in glomeruli of DSH compared with DSN rats (P=0.02). |
| 3145 | 12783777 | High glucose-mediated effects on endothelial cell proliferation occur via p38 MAP kinase. |
| 3146 | 12783777 | The roles of p38 and p42/44 MAP kinases in the high glucose-induced growth effects were determined by assessment of phosphorylated MAP kinases and their downstream activators by Western blot and by pharmacological inhibition of these MAP kinases. |
| 3147 | 12783777 | High glucose increased the activity of total and phosphorylated p38 MAP kinase (P < 0.001) and p42/44 MAP kinase (P < 0.001). |
| 3148 | 12783777 | Coexposure of p38 MAP kinase blocker with high glucose reversed the antiproliferative but not the hypertrophic effects associated with high-glucose conditions. |
| 3149 | 12783777 | Transforming growth factor (TGF)-beta1 increased the levels of phosphorylated p38 MAP kinase, and p38 MAP kinase blockade reversed the antiproliferative effects of this cytokine. |
| 3150 | 12783777 | The high glucose-induced increase in phosphorylated p38 MAP kinase was reversed in the presence of TGF-beta1 neutralizing antibody. |
| 3151 | 12783777 | Although hyperosmolarity also induced antiproliferation (P < 0.0001) and cell hypertrophy (P < 0.05), there was no change in p38 activity, and therefore inhibition of p38 MAP kinase had no influence on these growth responses. |
| 3152 | 12783777 | Blockade of p42/44 MAP kinase had no effect on the changes in endothelial cell growth induced by either high glucose or hyperosmolarity. |
| 3153 | 12783777 | High glucose increased p42/44 and p38 MAP kinase activity in human endothelial cells, but only p38 MAP kinase mediated the antiproliferative growth response through the effects of autocrine TGF-beta1. |
| 3154 | 12783777 | High glucose-mediated effects on endothelial cell proliferation occur via p38 MAP kinase. |
| 3155 | 12783777 | The roles of p38 and p42/44 MAP kinases in the high glucose-induced growth effects were determined by assessment of phosphorylated MAP kinases and their downstream activators by Western blot and by pharmacological inhibition of these MAP kinases. |
| 3156 | 12783777 | High glucose increased the activity of total and phosphorylated p38 MAP kinase (P < 0.001) and p42/44 MAP kinase (P < 0.001). |
| 3157 | 12783777 | Coexposure of p38 MAP kinase blocker with high glucose reversed the antiproliferative but not the hypertrophic effects associated with high-glucose conditions. |
| 3158 | 12783777 | Transforming growth factor (TGF)-beta1 increased the levels of phosphorylated p38 MAP kinase, and p38 MAP kinase blockade reversed the antiproliferative effects of this cytokine. |
| 3159 | 12783777 | The high glucose-induced increase in phosphorylated p38 MAP kinase was reversed in the presence of TGF-beta1 neutralizing antibody. |
| 3160 | 12783777 | Although hyperosmolarity also induced antiproliferation (P < 0.0001) and cell hypertrophy (P < 0.05), there was no change in p38 activity, and therefore inhibition of p38 MAP kinase had no influence on these growth responses. |
| 3161 | 12783777 | Blockade of p42/44 MAP kinase had no effect on the changes in endothelial cell growth induced by either high glucose or hyperosmolarity. |
| 3162 | 12783777 | High glucose increased p42/44 and p38 MAP kinase activity in human endothelial cells, but only p38 MAP kinase mediated the antiproliferative growth response through the effects of autocrine TGF-beta1. |
| 3163 | 12819241 | Due to the pivotal role of transforming growth factor-beta (TGF-beta) in the pathogenesis of diabetic kidney disease, this study tested the effect of simultaneously interrupting TGF-beta and angiotensin II on disease progression in diabetic rats with overt nephropathy. |
| 3164 | 12841849 | Regulation of type II transforming-growth-factor-beta receptors by protein kinase C iota. |
| 3165 | 12874439 | High glucose-induced ROS in mesangial cells can be effectively blocked by inhibition of protein kinase C (PKC), NADPH oxidase, and mitochondrial electron transfer chain complex I, suggesting that PKC, NADPH oxidase, and mitochondrial metabolism all play a role in high glucose-induced ROS generation. |
| 3166 | 12874439 | Both high glucose and ROS activate signal transduction cascade (PKC, mitogen-activated protein kinases, and janus kinase/signal transducers and activators of transcription) and transcription factors (nuclear factor-kappaB, activated protein-1, and specificity protein 1) and upregulate TGF-beta1 and ECM genes and proteins. |
| 3167 | 12874442 | AGE also interact with specific receptors and binding proteins to influence the expression of growth factors and cytokines, including TGF-beta1 and CTGF, thereby regulating the growth and proliferation of the various renal cell types. |
| 3168 | 12876066 | We postulated that diabetes-induced transforming growth factor (TGF)-beta production contributes to impaired ANG II response of vascular smooth muscle cells in macrovessels and microvessels. |
| 3169 | 12876066 | The impact of diabetes on [Ca2+] transients was replicated by addition of TGF-beta1 and -beta2 isoforms to aortic smooth muscle cells in culture and diabetic cells had enhanced production of TGF-beta2. |
| 3170 | 12876066 | In the in vivo condition, TGF-beta1 was increased in diabetic glomeruli, whereas TGF-beta2 was increased in diabetic aorta. |
| 3171 | 12876066 | Impaired vascular dysfunction may be partly due to decreased inositol 1,4,5-trisphosphate receptor (IP3R), as reduced type I IP3R expression was found in diabetic aorta and restored by anti-TGF-beta antibodies. |
| 3172 | 12876066 | We postulated that diabetes-induced transforming growth factor (TGF)-beta production contributes to impaired ANG II response of vascular smooth muscle cells in macrovessels and microvessels. |
| 3173 | 12876066 | The impact of diabetes on [Ca2+] transients was replicated by addition of TGF-beta1 and -beta2 isoforms to aortic smooth muscle cells in culture and diabetic cells had enhanced production of TGF-beta2. |
| 3174 | 12876066 | In the in vivo condition, TGF-beta1 was increased in diabetic glomeruli, whereas TGF-beta2 was increased in diabetic aorta. |
| 3175 | 12876066 | Impaired vascular dysfunction may be partly due to decreased inositol 1,4,5-trisphosphate receptor (IP3R), as reduced type I IP3R expression was found in diabetic aorta and restored by anti-TGF-beta antibodies. |
| 3176 | 12882934 | Expression of constitutively active cGMP-dependent protein kinase prevents glucose stimulation of thrombospondin 1 expression and TGF-beta activity. |
| 3177 | 12882934 | We previously showed that high glucose upregulates thrombospondin 1 (TSP1)-dependent transforming growth factor (TGF)-beta activation by altering cGMP-dependent protein kinase (PKG) activity as a result of decreased nitric oxide signaling. |
| 3178 | 12882934 | To further examine the mechanisms by which PKG regulates TSP1 expression and TSP1-dependent TGF-beta activation, we generated stably transfected rat mesangial cells (RMCs) with inducible expression tetracycline-induced gene expression of the catalytic domain of PKG. |
| 3179 | 12882934 | Glucose stimulation of TSP1 protein expression and TGF-beta bioactivity were also downregulated. |
| 3180 | 12882934 | TGF-beta-dependent fibronectin and type IV collagen expression under high glucose conditions were significantly reduced upon catalytic domain expression in transfected RMCs. |
| 3181 | 12882934 | These results show that constitutively active PKG inhibits the fibrogenic potential of high glucose through repression of TSP1-dependent TGF-beta bioactivity, suggesting that gene transfer of the catalytic domain of PKG might provide a new strategy for treatment of diabetic renal fibrosis. |
| 3182 | 12882934 | Expression of constitutively active cGMP-dependent protein kinase prevents glucose stimulation of thrombospondin 1 expression and TGF-beta activity. |
| 3183 | 12882934 | We previously showed that high glucose upregulates thrombospondin 1 (TSP1)-dependent transforming growth factor (TGF)-beta activation by altering cGMP-dependent protein kinase (PKG) activity as a result of decreased nitric oxide signaling. |
| 3184 | 12882934 | To further examine the mechanisms by which PKG regulates TSP1 expression and TSP1-dependent TGF-beta activation, we generated stably transfected rat mesangial cells (RMCs) with inducible expression tetracycline-induced gene expression of the catalytic domain of PKG. |
| 3185 | 12882934 | Glucose stimulation of TSP1 protein expression and TGF-beta bioactivity were also downregulated. |
| 3186 | 12882934 | TGF-beta-dependent fibronectin and type IV collagen expression under high glucose conditions were significantly reduced upon catalytic domain expression in transfected RMCs. |
| 3187 | 12882934 | These results show that constitutively active PKG inhibits the fibrogenic potential of high glucose through repression of TSP1-dependent TGF-beta bioactivity, suggesting that gene transfer of the catalytic domain of PKG might provide a new strategy for treatment of diabetic renal fibrosis. |
| 3188 | 12882934 | Expression of constitutively active cGMP-dependent protein kinase prevents glucose stimulation of thrombospondin 1 expression and TGF-beta activity. |
| 3189 | 12882934 | We previously showed that high glucose upregulates thrombospondin 1 (TSP1)-dependent transforming growth factor (TGF)-beta activation by altering cGMP-dependent protein kinase (PKG) activity as a result of decreased nitric oxide signaling. |
| 3190 | 12882934 | To further examine the mechanisms by which PKG regulates TSP1 expression and TSP1-dependent TGF-beta activation, we generated stably transfected rat mesangial cells (RMCs) with inducible expression tetracycline-induced gene expression of the catalytic domain of PKG. |
| 3191 | 12882934 | Glucose stimulation of TSP1 protein expression and TGF-beta bioactivity were also downregulated. |
| 3192 | 12882934 | TGF-beta-dependent fibronectin and type IV collagen expression under high glucose conditions were significantly reduced upon catalytic domain expression in transfected RMCs. |
| 3193 | 12882934 | These results show that constitutively active PKG inhibits the fibrogenic potential of high glucose through repression of TSP1-dependent TGF-beta bioactivity, suggesting that gene transfer of the catalytic domain of PKG might provide a new strategy for treatment of diabetic renal fibrosis. |
| 3194 | 12882934 | Expression of constitutively active cGMP-dependent protein kinase prevents glucose stimulation of thrombospondin 1 expression and TGF-beta activity. |
| 3195 | 12882934 | We previously showed that high glucose upregulates thrombospondin 1 (TSP1)-dependent transforming growth factor (TGF)-beta activation by altering cGMP-dependent protein kinase (PKG) activity as a result of decreased nitric oxide signaling. |
| 3196 | 12882934 | To further examine the mechanisms by which PKG regulates TSP1 expression and TSP1-dependent TGF-beta activation, we generated stably transfected rat mesangial cells (RMCs) with inducible expression tetracycline-induced gene expression of the catalytic domain of PKG. |
| 3197 | 12882934 | Glucose stimulation of TSP1 protein expression and TGF-beta bioactivity were also downregulated. |
| 3198 | 12882934 | TGF-beta-dependent fibronectin and type IV collagen expression under high glucose conditions were significantly reduced upon catalytic domain expression in transfected RMCs. |
| 3199 | 12882934 | These results show that constitutively active PKG inhibits the fibrogenic potential of high glucose through repression of TSP1-dependent TGF-beta bioactivity, suggesting that gene transfer of the catalytic domain of PKG might provide a new strategy for treatment of diabetic renal fibrosis. |
| 3200 | 12882934 | Expression of constitutively active cGMP-dependent protein kinase prevents glucose stimulation of thrombospondin 1 expression and TGF-beta activity. |
| 3201 | 12882934 | We previously showed that high glucose upregulates thrombospondin 1 (TSP1)-dependent transforming growth factor (TGF)-beta activation by altering cGMP-dependent protein kinase (PKG) activity as a result of decreased nitric oxide signaling. |
| 3202 | 12882934 | To further examine the mechanisms by which PKG regulates TSP1 expression and TSP1-dependent TGF-beta activation, we generated stably transfected rat mesangial cells (RMCs) with inducible expression tetracycline-induced gene expression of the catalytic domain of PKG. |
| 3203 | 12882934 | Glucose stimulation of TSP1 protein expression and TGF-beta bioactivity were also downregulated. |
| 3204 | 12882934 | TGF-beta-dependent fibronectin and type IV collagen expression under high glucose conditions were significantly reduced upon catalytic domain expression in transfected RMCs. |
| 3205 | 12882934 | These results show that constitutively active PKG inhibits the fibrogenic potential of high glucose through repression of TSP1-dependent TGF-beta bioactivity, suggesting that gene transfer of the catalytic domain of PKG might provide a new strategy for treatment of diabetic renal fibrosis. |
| 3206 | 12882935 | The majority of these genes fall into four signaling pathways: insulin, transforming growth factor-beta, tumor necrosis factor-alpha, and peroxisome proliferator-activated receptor. |
| 3207 | 12887099 | I-A.Y secreted IL-4, TGF-beta and IL-10 while I-A.D T cell line secreted IL-10 and IFN-gamma. |
| 3208 | 12896967 | Using a Cre-loxP approach to overcome early embryonic lethality, we have studied functions of TGF-beta/Smad4 signals in the central nervous system (CNS). |
| 3209 | 12896967 | In contrast, deletion of Smad4 resulted in a marked decrease in the number of cerebellar Purkinje cells and parvalbumin-positive interneurons. |
| 3210 | 12911563 | Transforming growth factor beta1 genotype polymorphisms determine AV fistula patency in hemodialysis patients. |
| 3211 | 12921671 | [Expression and significance of transforming growth factor-beta1, matrix metalloproteinase-2 and its inhibitor in lens epithelial cells of diabetic cataract]. |
| 3212 | 12937416 | Here we report that treatment with CD3epsilon-specific antibodies induces transferable T-cell-mediated tolerance involving CD4+CD25+ cells. |
| 3213 | 12937416 | However, these CD4+CD25+ T cells are distinct from naturally occurring regulatory T cells that control physiological autoreactivity. |
| 3214 | 12937416 | The central role of TGF-beta was further suggested by its increased, long-lasting production by CD4+ T cells from tolerant mice. |
| 3215 | 12939231 | Glucose-induced TGF-beta1 and TGF-beta receptor-1 expression in vascular smooth muscle cells is mediated by protein kinase C-alpha. |
| 3216 | 12939231 | We now investigated the hypothesis that glucose-induced expression of TGF-beta1 and its receptors (TGF-beta-R1 and -R2) are mediated by activation of this PKC isoform. |
| 3217 | 12939231 | High glucose (20 mmol/L) increased VSMC TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3218 | 12939231 | PKC inhibitors and specific PKC-alpha downregulation by antisense treatment prevented this effect, whereas antisense treatment against PKC-beta, -epsilon, and -zeta had no influence. |
| 3219 | 12939231 | PKC-alpha overexpression increased TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3220 | 12939231 | PKC-alpha microinjection into individual VSMCs also increased TGF-beta1 and TGF-beta-R immunofluorescence. |
| 3221 | 12939231 | We propose that high glucose-induced TGF-beta1 and TGF-beta-R1 expression is mediated by PKC-alpha. |
| 3222 | 12939231 | Glucose-induced TGF-beta1 and TGF-beta receptor-1 expression in vascular smooth muscle cells is mediated by protein kinase C-alpha. |
| 3223 | 12939231 | We now investigated the hypothesis that glucose-induced expression of TGF-beta1 and its receptors (TGF-beta-R1 and -R2) are mediated by activation of this PKC isoform. |
| 3224 | 12939231 | High glucose (20 mmol/L) increased VSMC TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3225 | 12939231 | PKC inhibitors and specific PKC-alpha downregulation by antisense treatment prevented this effect, whereas antisense treatment against PKC-beta, -epsilon, and -zeta had no influence. |
| 3226 | 12939231 | PKC-alpha overexpression increased TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3227 | 12939231 | PKC-alpha microinjection into individual VSMCs also increased TGF-beta1 and TGF-beta-R immunofluorescence. |
| 3228 | 12939231 | We propose that high glucose-induced TGF-beta1 and TGF-beta-R1 expression is mediated by PKC-alpha. |
| 3229 | 12939231 | Glucose-induced TGF-beta1 and TGF-beta receptor-1 expression in vascular smooth muscle cells is mediated by protein kinase C-alpha. |
| 3230 | 12939231 | We now investigated the hypothesis that glucose-induced expression of TGF-beta1 and its receptors (TGF-beta-R1 and -R2) are mediated by activation of this PKC isoform. |
| 3231 | 12939231 | High glucose (20 mmol/L) increased VSMC TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3232 | 12939231 | PKC inhibitors and specific PKC-alpha downregulation by antisense treatment prevented this effect, whereas antisense treatment against PKC-beta, -epsilon, and -zeta had no influence. |
| 3233 | 12939231 | PKC-alpha overexpression increased TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3234 | 12939231 | PKC-alpha microinjection into individual VSMCs also increased TGF-beta1 and TGF-beta-R immunofluorescence. |
| 3235 | 12939231 | We propose that high glucose-induced TGF-beta1 and TGF-beta-R1 expression is mediated by PKC-alpha. |
| 3236 | 12939231 | Glucose-induced TGF-beta1 and TGF-beta receptor-1 expression in vascular smooth muscle cells is mediated by protein kinase C-alpha. |
| 3237 | 12939231 | We now investigated the hypothesis that glucose-induced expression of TGF-beta1 and its receptors (TGF-beta-R1 and -R2) are mediated by activation of this PKC isoform. |
| 3238 | 12939231 | High glucose (20 mmol/L) increased VSMC TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3239 | 12939231 | PKC inhibitors and specific PKC-alpha downregulation by antisense treatment prevented this effect, whereas antisense treatment against PKC-beta, -epsilon, and -zeta had no influence. |
| 3240 | 12939231 | PKC-alpha overexpression increased TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3241 | 12939231 | PKC-alpha microinjection into individual VSMCs also increased TGF-beta1 and TGF-beta-R immunofluorescence. |
| 3242 | 12939231 | We propose that high glucose-induced TGF-beta1 and TGF-beta-R1 expression is mediated by PKC-alpha. |
| 3243 | 12939231 | Glucose-induced TGF-beta1 and TGF-beta receptor-1 expression in vascular smooth muscle cells is mediated by protein kinase C-alpha. |
| 3244 | 12939231 | We now investigated the hypothesis that glucose-induced expression of TGF-beta1 and its receptors (TGF-beta-R1 and -R2) are mediated by activation of this PKC isoform. |
| 3245 | 12939231 | High glucose (20 mmol/L) increased VSMC TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3246 | 12939231 | PKC inhibitors and specific PKC-alpha downregulation by antisense treatment prevented this effect, whereas antisense treatment against PKC-beta, -epsilon, and -zeta had no influence. |
| 3247 | 12939231 | PKC-alpha overexpression increased TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3248 | 12939231 | PKC-alpha microinjection into individual VSMCs also increased TGF-beta1 and TGF-beta-R immunofluorescence. |
| 3249 | 12939231 | We propose that high glucose-induced TGF-beta1 and TGF-beta-R1 expression is mediated by PKC-alpha. |
| 3250 | 12939231 | Glucose-induced TGF-beta1 and TGF-beta receptor-1 expression in vascular smooth muscle cells is mediated by protein kinase C-alpha. |
| 3251 | 12939231 | We now investigated the hypothesis that glucose-induced expression of TGF-beta1 and its receptors (TGF-beta-R1 and -R2) are mediated by activation of this PKC isoform. |
| 3252 | 12939231 | High glucose (20 mmol/L) increased VSMC TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3253 | 12939231 | PKC inhibitors and specific PKC-alpha downregulation by antisense treatment prevented this effect, whereas antisense treatment against PKC-beta, -epsilon, and -zeta had no influence. |
| 3254 | 12939231 | PKC-alpha overexpression increased TGF-beta1 and TGF-beta-R1 expression but not TGF-beta-R2 expression. |
| 3255 | 12939231 | PKC-alpha microinjection into individual VSMCs also increased TGF-beta1 and TGF-beta-R immunofluorescence. |
| 3256 | 12939231 | We propose that high glucose-induced TGF-beta1 and TGF-beta-R1 expression is mediated by PKC-alpha. |
| 3257 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3258 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3259 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3260 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3261 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3262 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3263 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3264 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3265 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3266 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3267 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3268 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3269 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3270 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3271 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3272 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3273 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3274 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3275 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3276 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3277 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3278 | 12949259 | CD4+CD25+ T regulatory cells control anti-islet CD8+ T cells through TGF-beta-TGF-beta receptor interactions in type 1 diabetes. |
| 3279 | 12949259 | Pancreatic lymph node-derived CD4+CD25+ T regulatory (Treg) cells inhibit in situ differentiation of islet-reactive CD8+ T cells into cytotoxic T lymphocytes, thereby preventing diabetes progression. |
| 3280 | 12949259 | Here, we show by using a CD8+ T cell-mediated model of type 1 diabetes that transforming growth factor (TGF)-beta-TGF-beta receptor signals are critical for CD4+CD25+ Treg cell regulation of autoreactive islet-specific cytotoxic T lymphocytes. |
| 3281 | 12949259 | Transgenic expression of tumor necrosis factor alpha from birth to 25 days of age in the islets of B6 mice that constitutively express CD80 on their beta cells results in accumulation of CD4+CD25+TGF-beta+ cells exclusively in the islets and pancreatic lymph nodes, which delays diabetes progression. |
| 3282 | 12949259 | In contrast, expression of tumor necrosis factor alpha until 28 days of age prevents islet accumulation of CD4+CD25+TGF-beta+ Treg cells, resulting in acceleration to diabetes. |
| 3283 | 12949259 | Furthermore, adoptive transfer experiments demonstrated that CD4+CD25+ Treg cells could not control naïve or activated islet-reactive CD8+ T cells bearing a dominant negative TGF-beta receptor type II. |
| 3284 | 12949259 | Our data demonstrate that, in vivo, TGF-beta signaling in CD8+ T cells is critical for CD4+CD25+ Treg cell suppression of islet-reactive CD8+ T cells in type 1 diabetes. |
| 3285 | 12952860 | ERK and p38 mediate high-glucose-induced hypertrophy and TGF-beta expression in renal tubular cells. |
| 3286 | 12952860 | We investigated the expression of ERK, p38 mitogen-activated protein kinase (p38), and JNK in renal tubules of diabetic rats following 3 wk after streptozotocin injection (DM). |
| 3287 | 12952860 | Although the expression of ERK was not different between controls and DM, phosphorylated ERK was expressed more intensely in DM. p38 And phosphorylated p38 were detected only in the diabetic kidney and were localized in all tubular segments. |
| 3288 | 12952860 | Transforming growth factor (TGF)-beta was expressed in all tubular segments of DM, coinciding with the localization of p38. |
| 3289 | 12952860 | In LLC-PK1 cells, phosphorylation of ERK and p38 increased after 24- to 72-h exposure to high glucose (HG). |
| 3290 | 12952860 | These results demonstrate that ERK and p38 are activated in renal tubular cells of DM and may mediate HG-induced cellular hypertrophy and TGF-beta expression. |
| 3291 | 12952860 | ERK and p38 mediate high-glucose-induced hypertrophy and TGF-beta expression in renal tubular cells. |
| 3292 | 12952860 | We investigated the expression of ERK, p38 mitogen-activated protein kinase (p38), and JNK in renal tubules of diabetic rats following 3 wk after streptozotocin injection (DM). |
| 3293 | 12952860 | Although the expression of ERK was not different between controls and DM, phosphorylated ERK was expressed more intensely in DM. p38 And phosphorylated p38 were detected only in the diabetic kidney and were localized in all tubular segments. |
| 3294 | 12952860 | Transforming growth factor (TGF)-beta was expressed in all tubular segments of DM, coinciding with the localization of p38. |
| 3295 | 12952860 | In LLC-PK1 cells, phosphorylation of ERK and p38 increased after 24- to 72-h exposure to high glucose (HG). |
| 3296 | 12952860 | These results demonstrate that ERK and p38 are activated in renal tubular cells of DM and may mediate HG-induced cellular hypertrophy and TGF-beta expression. |
| 3297 | 12955673 | Ruboxistaurin (LY333531) mesylate is a bisindolylmaleimide that shows a high degree of specificity within the protein kinase C (PKC) gene family for inhibiting PKC beta isoforms. |
| 3298 | 12955673 | In animal models of diabetes, including the streptozotocin (STZ) rat, Lepr(db)/Lepr(db) mouse, and STZ-Ren 2 rat models, ruboxistaurin normalized glomerular hyperfiltration, decreased urinary albumin excretion, and reduced glomerular transforming growth factor-beta1 and extracellular matrix protein production. |
| 3299 | 12958202 | It also reduced diabetes-induced increases in gene expression of transforming growth factor beta1 (TGF-beta1), connective tissue growth factor (CTGF), and collagen IV. |
| 3300 | 12958202 | However, glomerulosclerotic index, tubulointerstitial area, total renal collagen, nitrotyrosine, protein expression of collagen IV, and TGF-beta1 only showed improvement with early ALT treatment alone. |
| 3301 | 12958202 | It also reduced diabetes-induced increases in gene expression of transforming growth factor beta1 (TGF-beta1), connective tissue growth factor (CTGF), and collagen IV. |
| 3302 | 12958202 | However, glomerulosclerotic index, tubulointerstitial area, total renal collagen, nitrotyrosine, protein expression of collagen IV, and TGF-beta1 only showed improvement with early ALT treatment alone. |
| 3303 | 13679655 | TNF pathway and TGFb play an important role in the regulation of PAI-1 synthesis in the adipose tissue and the liver with steatosis. |
| 3304 | 14514644 | Several mechanisms, including activation of protein kinase C, advanced glycation end products, and overexpression of transforming growth factor (TGF)-beta, are believed to be involved in the pathogenesis of diabetic nephropathy. |
| 3305 | 14514644 | Urinary albumin excretion, glomerular hypertrophy, and mesangial matrix expansion were significantly lower in diabetic ICAM-1(-/-) mice than in diabetic ICAM-1(+/+) mice. |
| 3306 | 14514644 | Moreover, expressions of TGF-beta and type IV collagen in glomeruli were also suppressed in diabetic ICAM-1(-/-) mice. |
| 3307 | 14519594 | Suppressions of chronic glomerular injuries and TGF-beta 1 production by HGF in attenuation of murine diabetic nephropathy. |
| 3308 | 14519594 | Herein, we provide evidence that hepatocyte growth factor (HGF) targets mesangial cells, suppresses TGF-beta 1 production, and minimizes glomerular sclerotic changes, using streptozotocin-induced diabetic mice. |
| 3309 | 14519594 | Even more important, HGF repressed TGF-beta 1 production in glomerular mesangial cells even under hyperglycemic conditions both in vitro and in vivo. |
| 3310 | 14519594 | Suppressions of chronic glomerular injuries and TGF-beta 1 production by HGF in attenuation of murine diabetic nephropathy. |
| 3311 | 14519594 | Herein, we provide evidence that hepatocyte growth factor (HGF) targets mesangial cells, suppresses TGF-beta 1 production, and minimizes glomerular sclerotic changes, using streptozotocin-induced diabetic mice. |
| 3312 | 14519594 | Even more important, HGF repressed TGF-beta 1 production in glomerular mesangial cells even under hyperglycemic conditions both in vitro and in vivo. |
| 3313 | 14519594 | Suppressions of chronic glomerular injuries and TGF-beta 1 production by HGF in attenuation of murine diabetic nephropathy. |
| 3314 | 14519594 | Herein, we provide evidence that hepatocyte growth factor (HGF) targets mesangial cells, suppresses TGF-beta 1 production, and minimizes glomerular sclerotic changes, using streptozotocin-induced diabetic mice. |
| 3315 | 14519594 | Even more important, HGF repressed TGF-beta 1 production in glomerular mesangial cells even under hyperglycemic conditions both in vitro and in vivo. |
| 3316 | 14521940 | DNA sequencing revealed that CDK4 represents the rat beta defensin-1 gene (rBD-1). rBD-1 mRNA was detected in rat kidney, heart, lung, and skeletal muscle using RT-PCR. |
| 3317 | 14521940 | Biglycan and TGF-beta1 mRNAs were significantly up-regulated in kidneys of GK rats at 26 weeks compared to 16 and 6 weeks, showing that the kidneys of GK rats mimic the gene expression pattern described for human and experimental DN. |
| 3318 | 14530509 | However, which of the two plasminogen activators (PAs) present in renal tissue, tissue plasminogen activator (tPA) or urokinase-type plasminogen activator (uPA), is responsible for plasmin generation and those factors that modulate the activity of this system remain unclear. |
| 3319 | 14530509 | This study utilized mesangial cells isolated from mice with gene deletions for tPA, uPA, and plasminogen activator inhibitor 1 (PAI-1) to further delineate the role of the PA/plasminogen/plasmin system in ECM accumulation. |
| 3320 | 14530509 | In contrast, ECM degradation by tPA-null mesangial cells was markedly reduced (-78 +/- 1%, n = 12, P < 0.05) compared with controls, whereas tPA/uPA double-null mesangial cells degraded virtually no ECM. |
| 3321 | 14530509 | Previous studies from this laboratory have established that transforming growth factor-beta1 (TGFbeta1) inhibits ECM degradation by cultured mesangial cells by increasing the production of PAI-1, the major physiological PA inhibitor. |
| 3322 | 14530509 | Taken together, these results document the importance of tPA versus uPA in renal plasmin production and indicate that in contrast to elevated glucose, glycated albumin may contribute to ECM accumulation in diabetic nephropathy. |
| 3323 | 14550911 | We analyzed the expression pattern of transforming growth factor-beta isoforms (TGF-beta1, TGF-beta2 and TGF-beta3) in the developing brain of embryos derived from the normal and diabetic mice exposed to cyclophosphamide (CP), a cytotoxic teratogen. |
| 3324 | 14550911 | The CP-treated diabetic embryos showed significantly more TGF-beta1 and TGF-beta2 immunoreactive cells in the regions of telencephalon and diencephalon in comparison to that of CP-treated non-diabetic embryos. |
| 3325 | 14550911 | We analyzed the expression pattern of transforming growth factor-beta isoforms (TGF-beta1, TGF-beta2 and TGF-beta3) in the developing brain of embryos derived from the normal and diabetic mice exposed to cyclophosphamide (CP), a cytotoxic teratogen. |
| 3326 | 14550911 | The CP-treated diabetic embryos showed significantly more TGF-beta1 and TGF-beta2 immunoreactive cells in the regions of telencephalon and diencephalon in comparison to that of CP-treated non-diabetic embryos. |
| 3327 | 14561205 | These regulatory T cells produce down-regulatory cytokines such as IL4, IL10 and TGFbeta, a Th2 / Th3 cytokine pattern. |
| 3328 | 14568009 | It also demonstrates similar effects of aminoguanidine and ramipril (an angiotensin converting enzyme inhibitor) on fluorescent and immunoassayable AGE levels, renal protein kinase C activity, nitrotyrosine expression, lysosomal function, and protein handling in experimental diabetes. |
| 3329 | 14568009 | We postulate that the chemical pathways leading to advanced glycation endproduct formation and the renin angiotensin systems may interact through the generation of free radicals, induced both by glucose and angiotensin II. |
| 3330 | 14568009 | This effect is mediated through RAGE and is TGF-beta and CTGF-dependent. |
| 3331 | 14583181 | The development of diabetic nephropathy is considered to be dependent on profibrotic cytokine, transforming growth factor-beta1 (TGFbeta1). |
| 3332 | 14583181 | We investigated the response of human skin fibroblasts to elevated glucose level (11.0 and 30.0 mM) in terms of: (1) the expression and secretion of fibronectin (FN) and plasminogen activator inhibitor-1 (PAI-1); (2) the accumulation of hyaluronic acid (HA) in pericellular matrix and in the conditioned medium; (3) TGFbeta1 expression, secretion and activation; (4) TSP-1 expression and secretion. |
| 3333 | 14585103 | Peripheral monocytes from diabetic patients with coronary artery disease display increased bFGF and VEGF mRNA expression. |
| 3334 | 14585103 | BACKGROUND: Macrophages can produce vascular endothelial growth factor (VEGF) in response to hypoxia, transforming growth factor beta1 (TGF-beta1), angiotensin II, basic fibroblast growth factor (bFGF), and interleukin-1. |
| 3335 | 14585103 | The aim of the present study was to test the hypothesis that the expression of VEGF, TGF-beta1 and bFGF in peripheral monocytes and lymphocytes is related to CAD. |
| 3336 | 14585103 | RESULTS: The statistical analysis revealed a significant increase of the basal level expression for macrophage VEGF and bFGF in the CAD SA (stable angina) patient group compared to the noCAD (control) (p = 0.041 and p = 0.022 respectively) and CAD UA (unstable angina) (p = 0.024 and p = 0.005 respectively) groups, which was highly dependent on the diabetic status of the population. |
| 3337 | 14585103 | Furthermore, we demonstrated with an in vitro cell culture model that the levels of VEGF and bFGF in monocytes of healthy donors are not affected by short term exposure to increased glucose levels (usually observed in the diabetic patients) and/or statin. |
| 3338 | 14585103 | CONCLUSION: Our findings display a statistically significant association of the increased VEGF and bFGF levels in peripheral monocytes, with stable angina and diabetes in coronary artery disease. |
| 3339 | 14585103 | Peripheral monocytes from diabetic patients with coronary artery disease display increased bFGF and VEGF mRNA expression. |
| 3340 | 14585103 | BACKGROUND: Macrophages can produce vascular endothelial growth factor (VEGF) in response to hypoxia, transforming growth factor beta1 (TGF-beta1), angiotensin II, basic fibroblast growth factor (bFGF), and interleukin-1. |
| 3341 | 14585103 | The aim of the present study was to test the hypothesis that the expression of VEGF, TGF-beta1 and bFGF in peripheral monocytes and lymphocytes is related to CAD. |
| 3342 | 14585103 | RESULTS: The statistical analysis revealed a significant increase of the basal level expression for macrophage VEGF and bFGF in the CAD SA (stable angina) patient group compared to the noCAD (control) (p = 0.041 and p = 0.022 respectively) and CAD UA (unstable angina) (p = 0.024 and p = 0.005 respectively) groups, which was highly dependent on the diabetic status of the population. |
| 3343 | 14585103 | Furthermore, we demonstrated with an in vitro cell culture model that the levels of VEGF and bFGF in monocytes of healthy donors are not affected by short term exposure to increased glucose levels (usually observed in the diabetic patients) and/or statin. |
| 3344 | 14585103 | CONCLUSION: Our findings display a statistically significant association of the increased VEGF and bFGF levels in peripheral monocytes, with stable angina and diabetes in coronary artery disease. |
| 3345 | 14599847 | CD4+CD25+ regulatory T cells generated in response to insulin B:9-23 peptide prevent adoptive transfer of diabetes by diabetogenic T cells. |
| 3346 | 14599847 | NOD mice have a relative deficiency of CD4+CD25+ regulatory T cells that could result in an inability to maintain peripheral tolerance. |
| 3347 | 14599847 | The aim of this study was to induce the generation of CD4+CD25+ regulatory T cells in response to autoantigens to prevent type 1 diabetes (T1D). |
| 3348 | 14599847 | We found that immunization of NOD mice with insulin B-chain peptide B:9-23 followed by 72 h in vitro culture with B:9-23 peptide induces generation of CD4+CD25+ regulatory T cells. |
| 3349 | 14599847 | Non-autoimmune mice BALB/c, C57BL/6 and NOR did not show up regulation of CD4+CD25+ regulatory T cells. |
| 3350 | 14599847 | These cells secreted large amounts of TGF-beta and TNF-alpha with little or no IFN-gamma and IL-10. |
| 3351 | 14599847 | Adoptive transfer of these CD4+CD25+ regulatory T cells into NOD-SCID mice completely prevented the adoptive transfer of disease by diabetogenic T cells. |
| 3352 | 14599847 | Although, non-self antigenic OVA (323-339) peptide immunization and in vitro culture with OVA (323-339) peptide does result in up regulation of CD4+CD25+ T cells, these cells did not prevent transfer of diabetes. |
| 3353 | 14599847 | Our study for the first time identified the generation of antigen-specific CD4+CD25+ regulatory T cells specifically in response to immunization with B:9-23 peptide in NOD mice that are capable of blocking adoptive transfer of diabetes. |
| 3354 | 14609225 | In the thymus these regulatory cells are CD25+-like CD4+ cells shown to control physiologic organ-specific autoimmunity. |
| 3355 | 14609225 | In contrast, in the periphery, both CD4+CD25+ and CD4+CD25- cells exhibit regulatory capacities. |
| 3356 | 14609225 | Additionally, onset of autoimmune diabetes was preceded by a functional abnormality of CD4+CD25+ regulatory T cells as assessed by their inability to suppress in vitro the proliferation of polyclonally activated CD25- T cells. |
| 3357 | 14609225 | Furthermore, we also obtained evidence in CD3-treated NOD for a significant increase (in the pancreatic and mesenteric lymph nodes but not in the spleen) in the proportion of CD4+CD25+CTLA4+ T cells which produce TGFbeta. |
| 3358 | 14617289 | HoxD3 expression and collagen synthesis in diabetic fibroblasts. |
| 3359 | 14617289 | We have observed that expression of homeobox D3 (HoxD3), a collagen-inducing transcription factor, and expression of collagen are reduced in an established animal model of diabetic wound repair, the leptin-deficient diabetic (db/db) mouse. |
| 3360 | 14617289 | We sought to evaluate whether the diminished expression of collagen and HoxD3 would be maintained once fibroblasts were removed from the diabetic wound environment. |
| 3361 | 14617289 | Fibroblasts were isolated from both wild-type and diabetic animals and expression of HoxD3 and collagen assessed. |
| 3362 | 14617289 | We found that when removed from the diabetic wound environment, HoxD3 and type I collagen expression are increased in diabetic fibroblasts when compared to wild-type fibroblasts. |
| 3363 | 14617289 | The increase in type I collagen is not related to increased production or activation of transforming growth factor-beta1. |
| 3364 | 14617289 | However, when the diabetic fibroblasts are cultured in a 3D collagen matrix, expression of type I collagen and HoxD3 is markedly reduced and reflects the pattern of gene expression observed in the in vivo diabetic wound environment. |
| 3365 | 14617289 | Thus, although diabetic fibroblasts can regain the capacity to express high levels of collagen and HoxD3 once removed from the diabetic wound environment, culturing cells in the presence of a 3D collagen matrix is sufficient to revert these fibroblasts to their previous nonsynthetic state. |
| 3366 | 14631561 | In experimental diabetes mellitus, several reports describe overexpression of TGF-beta or TGF-beta type II receptor in the glomerular and tubulointerstitial compartments. |
| 3367 | 14631561 | In concert with TGF-beta, other metabolic mediators such as connective tissue growth factor and reactive oxygen species promote the accumulation of excess matrix. |
| 3368 | 14631561 | In experimental diabetes mellitus, several reports describe overexpression of TGF-beta or TGF-beta type II receptor in the glomerular and tubulointerstitial compartments. |
| 3369 | 14631561 | In concert with TGF-beta, other metabolic mediators such as connective tissue growth factor and reactive oxygen species promote the accumulation of excess matrix. |
| 3370 | 14633126 | Beta-hydroxybutyrate-induced growth inhibition and collagen production in HK-2 cells are dependent on TGF-beta and Smad3. |
| 3371 | 14633859 | Connective tissue growth factor and igf-I are produced by human renal fibroblasts and cooperate in the induction of collagen production by high glucose. |
| 3372 | 14633859 | Here we examined the effects of connective tissue growth factor (CTGF) and IGF-I on collagen type I and III production by human renal fibroblasts and their involvement in glucose-induced matrix accumulation. |
| 3373 | 14633859 | We have demonstrated that both CTGF and IGF-I expressions were increased in renal fibroblasts under hyperglycemic conditions, also in the absence of TGF-beta signaling. |
| 3374 | 14633859 | Although CTGF alone had no effect on collagen secretion, combined stimulation with IGF-I enhanced collagen accumulation. |
| 3375 | 14633859 | Moreover, we observed a partial inhibition in glucose-induced collagen secretion with neutralizing anti-CTGF antibodies, thereby demonstrating for the first time the involvement of endogenous CTGF in glucose-induced effects in human renal fibroblasts. |
| 3376 | 14633859 | Therefore, the cooperation between CTGF and IGF-I might be involved in glucose-induced matrix accumulation in tubulointerstitial fibrosis and might contribute to the pathogenesis of diabetic nephropathy. |
| 3377 | 14640237 | The effects of dual blockade of the renin-angiotensin system on urinary protein and transforming growth factor-beta excretion in 2 groups of patients with IgA and diabetic nephropathy. |
| 3378 | 14668046 | Therefore, attention is limited to factors that may be important in the development of early diabetic glomerulopathy, including transforming growth factor-beta (TGF-beta), insulin-like growth factor (IGF)-I, vascular endothelial growth factor (VEGF)-A, and connective tissue growth factor (CTGF). |
| 3379 | 14668051 | Neuropoietic cytokines, including interleukin-1 (IL-1), interleukin-6 (IL-6), leukemia inhibitory factor (LIF), ciliary neurotrophic factor (CNTF), tumor necrosis factor alpha (TNF-alpha), and transforming growth factor beta (TGF-beta), exhibit pleiotrophic effects on homeostasis of glia and neurons in central, peripheral, and autonomic nervous system. |
| 3380 | 14683523 | Our previous studies have found that high glucose does not induce cellular hypertrophy or expression of TGF-beta1 (transforming growth factor-beta1) in distal renal tubule cells [Yang, Guh, Yang, Lai, Tsai, Hung, Chang and Chuang (1998) J. |
| 3381 | 14683523 | Since TSP-1 (thrombospondin-1) has been demonstrated to activate latent TGF-beta1 in a variety of systems, the following experiments were performed. |
| 3382 | 14683523 | In addition, we observed several putative transcription factor binding sites in the TSP-1 promoter, including those for AP-1 (activator protein-1), CREB (cAMP response element binding protein), NF-kappaB (nuclear factor-kappaB), SRF (serum response factor) and HSF (heat-shock factor), by sequence mapping. |
| 3383 | 14683523 | We showed that AP-1 and CREB were specifically induced by AGEs; furthermore, TFD (transcription factor decoy) for AP-1 could attenuate the AGE-induced increases in TSP-1 levels and cellular hypertrophy. |
| 3384 | 14683523 | Our previous studies have found that high glucose does not induce cellular hypertrophy or expression of TGF-beta1 (transforming growth factor-beta1) in distal renal tubule cells [Yang, Guh, Yang, Lai, Tsai, Hung, Chang and Chuang (1998) J. |
| 3385 | 14683523 | Since TSP-1 (thrombospondin-1) has been demonstrated to activate latent TGF-beta1 in a variety of systems, the following experiments were performed. |
| 3386 | 14683523 | In addition, we observed several putative transcription factor binding sites in the TSP-1 promoter, including those for AP-1 (activator protein-1), CREB (cAMP response element binding protein), NF-kappaB (nuclear factor-kappaB), SRF (serum response factor) and HSF (heat-shock factor), by sequence mapping. |
| 3387 | 14683523 | We showed that AP-1 and CREB were specifically induced by AGEs; furthermore, TFD (transcription factor decoy) for AP-1 could attenuate the AGE-induced increases in TSP-1 levels and cellular hypertrophy. |
| 3388 | 14684674 | The TGF-beta receptor signaling system is also triggered, as evidenced by upregulation of the TGF-beta type II receptor and activation of the downstream Smad signaling pathway. |
| 3389 | 14693716 | Peroxisome proliferator-activated receptor-gamma ligands inhibit TGF-beta 1-induced fibronectin expression in glomerular mesangial cells. |
| 3390 | 14693716 | The thiazolidinedione (TZD) class of antidiabetic drugs, which are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, has been shown to possess potent anti-inflammatory and antineoplastic actions. |
| 3391 | 14693716 | Here, we show in mesangial cells that PPAR-gamma agonists inhibit fibronectin expression by transforming growth factor (TGF)-beta 1. |
| 3392 | 14693716 | Electrophoretic mobility shift assay identified that pioglitazone inhibited TGF-beta 1-induced DNA binding of activator protein-1 (AP-1). |
| 3393 | 14693716 | Pioglitazone inhibited AP-1 reporter activity but not Smad binding elements reporter activity without affecting TGF-beta 1-induced activation of mitogen-activated protein kinases (MAPKs) or Smad2. |
| 3394 | 14693716 | PPAR-gamma overexpression inhibited TGF-beta 1-induced fibronectin expression as well as the activation of AP-1. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, also inhibited TGF-beta1-induced fibronectin expression by suppressing AP-1 activation by TGF-beta 1. 15d-PGJ(2) inhibited the TGF-beta 1-induced MAPK activation. |
| 3395 | 14693716 | Dominant-negative PPAR-gamma (Delta PPAR-gamma) completely abrogated the inhibitory effect of pioglitazone and incompletely blocked its effect of 15d-PGJ(2) on TGF-beta 1-induced AP-1 reporter activity. |
| 3396 | 14693716 | Delta PPAR-gamma overexpression did not affect the inhibitory effect of 15d-PGJ(2) on TGF-beta 1-induced MAPK activation. |
| 3397 | 14693716 | In conclusion, pioglitazone inhibits TGF-beta 1-induced fibronectin expression by inhibiting AP-1 activation dependent on PPAR-gamma, while 15d-PGJ(2) acts through a dual mechanism independent of and dependent on PPAR-gamma activation in mouse mesangial cells. |
| 3398 | 14693716 | Peroxisome proliferator-activated receptor-gamma ligands inhibit TGF-beta 1-induced fibronectin expression in glomerular mesangial cells. |
| 3399 | 14693716 | The thiazolidinedione (TZD) class of antidiabetic drugs, which are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, has been shown to possess potent anti-inflammatory and antineoplastic actions. |
| 3400 | 14693716 | Here, we show in mesangial cells that PPAR-gamma agonists inhibit fibronectin expression by transforming growth factor (TGF)-beta 1. |
| 3401 | 14693716 | Electrophoretic mobility shift assay identified that pioglitazone inhibited TGF-beta 1-induced DNA binding of activator protein-1 (AP-1). |
| 3402 | 14693716 | Pioglitazone inhibited AP-1 reporter activity but not Smad binding elements reporter activity without affecting TGF-beta 1-induced activation of mitogen-activated protein kinases (MAPKs) or Smad2. |
| 3403 | 14693716 | PPAR-gamma overexpression inhibited TGF-beta 1-induced fibronectin expression as well as the activation of AP-1. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, also inhibited TGF-beta1-induced fibronectin expression by suppressing AP-1 activation by TGF-beta 1. 15d-PGJ(2) inhibited the TGF-beta 1-induced MAPK activation. |
| 3404 | 14693716 | Dominant-negative PPAR-gamma (Delta PPAR-gamma) completely abrogated the inhibitory effect of pioglitazone and incompletely blocked its effect of 15d-PGJ(2) on TGF-beta 1-induced AP-1 reporter activity. |
| 3405 | 14693716 | Delta PPAR-gamma overexpression did not affect the inhibitory effect of 15d-PGJ(2) on TGF-beta 1-induced MAPK activation. |
| 3406 | 14693716 | In conclusion, pioglitazone inhibits TGF-beta 1-induced fibronectin expression by inhibiting AP-1 activation dependent on PPAR-gamma, while 15d-PGJ(2) acts through a dual mechanism independent of and dependent on PPAR-gamma activation in mouse mesangial cells. |
| 3407 | 14693716 | Peroxisome proliferator-activated receptor-gamma ligands inhibit TGF-beta 1-induced fibronectin expression in glomerular mesangial cells. |
| 3408 | 14693716 | The thiazolidinedione (TZD) class of antidiabetic drugs, which are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, has been shown to possess potent anti-inflammatory and antineoplastic actions. |
| 3409 | 14693716 | Here, we show in mesangial cells that PPAR-gamma agonists inhibit fibronectin expression by transforming growth factor (TGF)-beta 1. |
| 3410 | 14693716 | Electrophoretic mobility shift assay identified that pioglitazone inhibited TGF-beta 1-induced DNA binding of activator protein-1 (AP-1). |
| 3411 | 14693716 | Pioglitazone inhibited AP-1 reporter activity but not Smad binding elements reporter activity without affecting TGF-beta 1-induced activation of mitogen-activated protein kinases (MAPKs) or Smad2. |
| 3412 | 14693716 | PPAR-gamma overexpression inhibited TGF-beta 1-induced fibronectin expression as well as the activation of AP-1. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, also inhibited TGF-beta1-induced fibronectin expression by suppressing AP-1 activation by TGF-beta 1. 15d-PGJ(2) inhibited the TGF-beta 1-induced MAPK activation. |
| 3413 | 14693716 | Dominant-negative PPAR-gamma (Delta PPAR-gamma) completely abrogated the inhibitory effect of pioglitazone and incompletely blocked its effect of 15d-PGJ(2) on TGF-beta 1-induced AP-1 reporter activity. |
| 3414 | 14693716 | Delta PPAR-gamma overexpression did not affect the inhibitory effect of 15d-PGJ(2) on TGF-beta 1-induced MAPK activation. |
| 3415 | 14693716 | In conclusion, pioglitazone inhibits TGF-beta 1-induced fibronectin expression by inhibiting AP-1 activation dependent on PPAR-gamma, while 15d-PGJ(2) acts through a dual mechanism independent of and dependent on PPAR-gamma activation in mouse mesangial cells. |
| 3416 | 14693716 | Peroxisome proliferator-activated receptor-gamma ligands inhibit TGF-beta 1-induced fibronectin expression in glomerular mesangial cells. |
| 3417 | 14693716 | The thiazolidinedione (TZD) class of antidiabetic drugs, which are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, has been shown to possess potent anti-inflammatory and antineoplastic actions. |
| 3418 | 14693716 | Here, we show in mesangial cells that PPAR-gamma agonists inhibit fibronectin expression by transforming growth factor (TGF)-beta 1. |
| 3419 | 14693716 | Electrophoretic mobility shift assay identified that pioglitazone inhibited TGF-beta 1-induced DNA binding of activator protein-1 (AP-1). |
| 3420 | 14693716 | Pioglitazone inhibited AP-1 reporter activity but not Smad binding elements reporter activity without affecting TGF-beta 1-induced activation of mitogen-activated protein kinases (MAPKs) or Smad2. |
| 3421 | 14693716 | PPAR-gamma overexpression inhibited TGF-beta 1-induced fibronectin expression as well as the activation of AP-1. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, also inhibited TGF-beta1-induced fibronectin expression by suppressing AP-1 activation by TGF-beta 1. 15d-PGJ(2) inhibited the TGF-beta 1-induced MAPK activation. |
| 3422 | 14693716 | Dominant-negative PPAR-gamma (Delta PPAR-gamma) completely abrogated the inhibitory effect of pioglitazone and incompletely blocked its effect of 15d-PGJ(2) on TGF-beta 1-induced AP-1 reporter activity. |
| 3423 | 14693716 | Delta PPAR-gamma overexpression did not affect the inhibitory effect of 15d-PGJ(2) on TGF-beta 1-induced MAPK activation. |
| 3424 | 14693716 | In conclusion, pioglitazone inhibits TGF-beta 1-induced fibronectin expression by inhibiting AP-1 activation dependent on PPAR-gamma, while 15d-PGJ(2) acts through a dual mechanism independent of and dependent on PPAR-gamma activation in mouse mesangial cells. |
| 3425 | 14693716 | Peroxisome proliferator-activated receptor-gamma ligands inhibit TGF-beta 1-induced fibronectin expression in glomerular mesangial cells. |
| 3426 | 14693716 | The thiazolidinedione (TZD) class of antidiabetic drugs, which are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, has been shown to possess potent anti-inflammatory and antineoplastic actions. |
| 3427 | 14693716 | Here, we show in mesangial cells that PPAR-gamma agonists inhibit fibronectin expression by transforming growth factor (TGF)-beta 1. |
| 3428 | 14693716 | Electrophoretic mobility shift assay identified that pioglitazone inhibited TGF-beta 1-induced DNA binding of activator protein-1 (AP-1). |
| 3429 | 14693716 | Pioglitazone inhibited AP-1 reporter activity but not Smad binding elements reporter activity without affecting TGF-beta 1-induced activation of mitogen-activated protein kinases (MAPKs) or Smad2. |
| 3430 | 14693716 | PPAR-gamma overexpression inhibited TGF-beta 1-induced fibronectin expression as well as the activation of AP-1. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, also inhibited TGF-beta1-induced fibronectin expression by suppressing AP-1 activation by TGF-beta 1. 15d-PGJ(2) inhibited the TGF-beta 1-induced MAPK activation. |
| 3431 | 14693716 | Dominant-negative PPAR-gamma (Delta PPAR-gamma) completely abrogated the inhibitory effect of pioglitazone and incompletely blocked its effect of 15d-PGJ(2) on TGF-beta 1-induced AP-1 reporter activity. |
| 3432 | 14693716 | Delta PPAR-gamma overexpression did not affect the inhibitory effect of 15d-PGJ(2) on TGF-beta 1-induced MAPK activation. |
| 3433 | 14693716 | In conclusion, pioglitazone inhibits TGF-beta 1-induced fibronectin expression by inhibiting AP-1 activation dependent on PPAR-gamma, while 15d-PGJ(2) acts through a dual mechanism independent of and dependent on PPAR-gamma activation in mouse mesangial cells. |
| 3434 | 14693716 | Peroxisome proliferator-activated receptor-gamma ligands inhibit TGF-beta 1-induced fibronectin expression in glomerular mesangial cells. |
| 3435 | 14693716 | The thiazolidinedione (TZD) class of antidiabetic drugs, which are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, has been shown to possess potent anti-inflammatory and antineoplastic actions. |
| 3436 | 14693716 | Here, we show in mesangial cells that PPAR-gamma agonists inhibit fibronectin expression by transforming growth factor (TGF)-beta 1. |
| 3437 | 14693716 | Electrophoretic mobility shift assay identified that pioglitazone inhibited TGF-beta 1-induced DNA binding of activator protein-1 (AP-1). |
| 3438 | 14693716 | Pioglitazone inhibited AP-1 reporter activity but not Smad binding elements reporter activity without affecting TGF-beta 1-induced activation of mitogen-activated protein kinases (MAPKs) or Smad2. |
| 3439 | 14693716 | PPAR-gamma overexpression inhibited TGF-beta 1-induced fibronectin expression as well as the activation of AP-1. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, also inhibited TGF-beta1-induced fibronectin expression by suppressing AP-1 activation by TGF-beta 1. 15d-PGJ(2) inhibited the TGF-beta 1-induced MAPK activation. |
| 3440 | 14693716 | Dominant-negative PPAR-gamma (Delta PPAR-gamma) completely abrogated the inhibitory effect of pioglitazone and incompletely blocked its effect of 15d-PGJ(2) on TGF-beta 1-induced AP-1 reporter activity. |
| 3441 | 14693716 | Delta PPAR-gamma overexpression did not affect the inhibitory effect of 15d-PGJ(2) on TGF-beta 1-induced MAPK activation. |
| 3442 | 14693716 | In conclusion, pioglitazone inhibits TGF-beta 1-induced fibronectin expression by inhibiting AP-1 activation dependent on PPAR-gamma, while 15d-PGJ(2) acts through a dual mechanism independent of and dependent on PPAR-gamma activation in mouse mesangial cells. |
| 3443 | 14693716 | Peroxisome proliferator-activated receptor-gamma ligands inhibit TGF-beta 1-induced fibronectin expression in glomerular mesangial cells. |
| 3444 | 14693716 | The thiazolidinedione (TZD) class of antidiabetic drugs, which are ligands for peroxisome proliferator-activated receptor (PPAR)-gamma, has been shown to possess potent anti-inflammatory and antineoplastic actions. |
| 3445 | 14693716 | Here, we show in mesangial cells that PPAR-gamma agonists inhibit fibronectin expression by transforming growth factor (TGF)-beta 1. |
| 3446 | 14693716 | Electrophoretic mobility shift assay identified that pioglitazone inhibited TGF-beta 1-induced DNA binding of activator protein-1 (AP-1). |
| 3447 | 14693716 | Pioglitazone inhibited AP-1 reporter activity but not Smad binding elements reporter activity without affecting TGF-beta 1-induced activation of mitogen-activated protein kinases (MAPKs) or Smad2. |
| 3448 | 14693716 | PPAR-gamma overexpression inhibited TGF-beta 1-induced fibronectin expression as well as the activation of AP-1. 15-Deoxy-Delta(12,14)-prostaglandin J(2) (15d-PGJ(2)), a natural PPAR-gamma ligand, also inhibited TGF-beta1-induced fibronectin expression by suppressing AP-1 activation by TGF-beta 1. 15d-PGJ(2) inhibited the TGF-beta 1-induced MAPK activation. |
| 3449 | 14693716 | Dominant-negative PPAR-gamma (Delta PPAR-gamma) completely abrogated the inhibitory effect of pioglitazone and incompletely blocked its effect of 15d-PGJ(2) on TGF-beta 1-induced AP-1 reporter activity. |
| 3450 | 14693716 | Delta PPAR-gamma overexpression did not affect the inhibitory effect of 15d-PGJ(2) on TGF-beta 1-induced MAPK activation. |
| 3451 | 14693716 | In conclusion, pioglitazone inhibits TGF-beta 1-induced fibronectin expression by inhibiting AP-1 activation dependent on PPAR-gamma, while 15d-PGJ(2) acts through a dual mechanism independent of and dependent on PPAR-gamma activation in mouse mesangial cells. |
| 3452 | 14726227 | Transforming growth factor-beta1 (TGF-beta1) is a potent multifunctional polypeptide that is involved in normal renal function and in the development of glomerular sclerosis. |
| 3453 | 14726227 | TGF-beta1 was also measured in 38 patients with type 1 (insulin-dependent) diabetes mellitus (12 with newly diagnosed diabetes, 26 long-standing diabetes) and 31 healthy controls. |
| 3454 | 14726227 | Urinary TGF-beta1 levels did not correlate with indices of renal function (serum creatinine, glomerular filtration rate (GFR), albumin excretion rate [AER]). |
| 3455 | 14726227 | Transforming growth factor-beta1 (TGF-beta1) is a potent multifunctional polypeptide that is involved in normal renal function and in the development of glomerular sclerosis. |
| 3456 | 14726227 | TGF-beta1 was also measured in 38 patients with type 1 (insulin-dependent) diabetes mellitus (12 with newly diagnosed diabetes, 26 long-standing diabetes) and 31 healthy controls. |
| 3457 | 14726227 | Urinary TGF-beta1 levels did not correlate with indices of renal function (serum creatinine, glomerular filtration rate (GFR), albumin excretion rate [AER]). |
| 3458 | 14726227 | Transforming growth factor-beta1 (TGF-beta1) is a potent multifunctional polypeptide that is involved in normal renal function and in the development of glomerular sclerosis. |
| 3459 | 14726227 | TGF-beta1 was also measured in 38 patients with type 1 (insulin-dependent) diabetes mellitus (12 with newly diagnosed diabetes, 26 long-standing diabetes) and 31 healthy controls. |
| 3460 | 14726227 | Urinary TGF-beta1 levels did not correlate with indices of renal function (serum creatinine, glomerular filtration rate (GFR), albumin excretion rate [AER]). |
| 3461 | 14732718 | Type IV collagen is transcriptionally regulated by Smad1 under advanced glycation end product (AGE) stimulation. |
| 3462 | 14732718 | To elucidate the interaction between transforming growth factor-beta and Smad1, we investigated whether activin receptor-liked kinase1 (ALK1) was involved in this regulation. |
| 3463 | 14732718 | We also demonstrated that Smad1 and ALK1 were highly expressed in human diabetic nephropathy. |
| 3464 | 14743439 | The expression of cytokines such as tumor necrosis factor-alpha (TNF-alpha) and transforming growth factor-beta1 (TGF-beta1) in the fetal brain of normal and diabetic embryos was induced in the neural tubes after CP treatment. |
| 3465 | 14767489 | In parallel glomerular PCNA+cells were significantly more frequent and expression of TGF-beta and PDGF by immunohistochemistry in glomeruli and in the tubulointerstitial space was more pronounced in SHR/N-cp compared to STZ rats. |
| 3466 | 14768049 | However, in vivo neutralization of IL-4, IL-10 or TGF-beta using monoclonal antibodies did not prevent the inhibition whereas treatment with an antibody against the glucocorticoid-induced TNF receptor abrogated the protection from disease. |
| 3467 | 14965305 | Some studies have suggested that the stimulation of host immunoregulatory networks with parasite molecules leading to the synthesis of anti-inflammatory cytokines (interleukin10, transforming growth factor-beta (TGF-beta and others) can provide new therapy for immunological disorders. |
| 3468 | 14965305 | It is known that parasites produce some types of molecule that mimic host molecules such as CD40 ligand, TGF-beta and macrophage migration inhibitory factor. |
| 3469 | 14965305 | Some studies have suggested that the stimulation of host immunoregulatory networks with parasite molecules leading to the synthesis of anti-inflammatory cytokines (interleukin10, transforming growth factor-beta (TGF-beta and others) can provide new therapy for immunological disorders. |
| 3470 | 14965305 | It is known that parasites produce some types of molecule that mimic host molecules such as CD40 ligand, TGF-beta and macrophage migration inhibitory factor. |
| 3471 | 14969747 | Transforming growth factor beta receptor family ligands inhibit hepatocyte growth factor synthesis and secretion from astrocytoma cells. |
| 3472 | 14969747 | Transforming growth factor beta (TGFbeta) and hepatocyte growth factor (HGF) promote glioma progression. |
| 3473 | 14969747 | Using U87human astrocytoma cells, which express TGFbeta receptors (TbetaRs), we show (1) mRNA expression of Smads (2, 3, 4), bone morphogenetic protein (BMP)- and activin-A receptors; (2) TGFbeta1 inhibits and HGF induces proliferation; (3) TGFbeta1 and activin-A equipotently inhibit HGF secretion more than BMP-2, but none alters c-Met expression. |
| 3474 | 14969747 | Transforming growth factor beta receptor family ligands inhibit hepatocyte growth factor synthesis and secretion from astrocytoma cells. |
| 3475 | 14969747 | Transforming growth factor beta (TGFbeta) and hepatocyte growth factor (HGF) promote glioma progression. |
| 3476 | 14969747 | Using U87human astrocytoma cells, which express TGFbeta receptors (TbetaRs), we show (1) mRNA expression of Smads (2, 3, 4), bone morphogenetic protein (BMP)- and activin-A receptors; (2) TGFbeta1 inhibits and HGF induces proliferation; (3) TGFbeta1 and activin-A equipotently inhibit HGF secretion more than BMP-2, but none alters c-Met expression. |
| 3477 | 14969747 | Transforming growth factor beta receptor family ligands inhibit hepatocyte growth factor synthesis and secretion from astrocytoma cells. |
| 3478 | 14969747 | Transforming growth factor beta (TGFbeta) and hepatocyte growth factor (HGF) promote glioma progression. |
| 3479 | 14969747 | Using U87human astrocytoma cells, which express TGFbeta receptors (TbetaRs), we show (1) mRNA expression of Smads (2, 3, 4), bone morphogenetic protein (BMP)- and activin-A receptors; (2) TGFbeta1 inhibits and HGF induces proliferation; (3) TGFbeta1 and activin-A equipotently inhibit HGF secretion more than BMP-2, but none alters c-Met expression. |
| 3480 | 14974969 | Active transforming growth factor-beta 1 (TGF-beta 1) was measured in the serum using the plasminogen activator inhibitor-1/luciferase assay and serum total TGF-beta was measured using an enzyme-linked immunosorbent assay. |
| 3481 | 14974969 | Both active and total TGF-beta was measured in tissue sections using the plasminogen activator inhibitor-1/luciferase assay. |
| 3482 | 14974969 | Active transforming growth factor-beta 1 (TGF-beta 1) was measured in the serum using the plasminogen activator inhibitor-1/luciferase assay and serum total TGF-beta was measured using an enzyme-linked immunosorbent assay. |
| 3483 | 14974969 | Both active and total TGF-beta was measured in tissue sections using the plasminogen activator inhibitor-1/luciferase assay. |
| 3484 | 14976204 | Syndecan-2 regulates transforming growth factor-beta signaling. |
| 3485 | 14976204 | We report here that a transmembrane heparan sulfate proteoglycan, syndecan-2 (S2), can regulate TGF-beta signaling. |
| 3486 | 14976204 | In contrast, S2DeltaS dramatically increased the level of type III TGF-beta receptor (TbetaRIII), betaglycan, whereas S2 resulted in a decrease. |
| 3487 | 14976204 | Syndecan-2 specifically co-immunoprecipitated with betaglycan but not with TbetaRI or TbetaRII. |
| 3488 | 14976204 | Syndecan-2 regulates transforming growth factor-beta signaling. |
| 3489 | 14976204 | We report here that a transmembrane heparan sulfate proteoglycan, syndecan-2 (S2), can regulate TGF-beta signaling. |
| 3490 | 14976204 | In contrast, S2DeltaS dramatically increased the level of type III TGF-beta receptor (TbetaRIII), betaglycan, whereas S2 resulted in a decrease. |
| 3491 | 14976204 | Syndecan-2 specifically co-immunoprecipitated with betaglycan but not with TbetaRI or TbetaRII. |
| 3492 | 14976204 | Syndecan-2 regulates transforming growth factor-beta signaling. |
| 3493 | 14976204 | We report here that a transmembrane heparan sulfate proteoglycan, syndecan-2 (S2), can regulate TGF-beta signaling. |
| 3494 | 14976204 | In contrast, S2DeltaS dramatically increased the level of type III TGF-beta receptor (TbetaRIII), betaglycan, whereas S2 resulted in a decrease. |
| 3495 | 14976204 | Syndecan-2 specifically co-immunoprecipitated with betaglycan but not with TbetaRI or TbetaRII. |
| 3496 | 14988262 | However, in NTg-db/db mice, albuminuria, glomerular accumulation of immunoreactive transforming growth factor-beta, collagen alpha1(IV), nitrotyrosine, and mesangial matrix were all significantly increased compared with either nondiabetic mice or SOD-Tg-db/db. |
| 3497 | 15004023 | This study reports the inhibitory effect of OPB-9195 (OPB), an inhibitor of AGEs formation, and the role of a collagen-specific molecular chaperone, a 47-kDa heat shock protein (HSP47) in diabetic nephropathy. |
| 3498 | 15004023 | Transgenic mice carrying nitric-oxide synthase cDNA fused with insulin promoter (iNOSTg) leads to diabetes mellitus. |
| 3499 | 15004023 | AGEs significantly increased the expression of HSP47, type IV collagen, and TGF-beta mRNA. |
| 3500 | 15004023 | Neutralizing antibody for TGF-beta inhibited the overexpression of both HSP47 and type IV collagen in vitro. |
| 3501 | 15004023 | This study reports the inhibitory effect of OPB-9195 (OPB), an inhibitor of AGEs formation, and the role of a collagen-specific molecular chaperone, a 47-kDa heat shock protein (HSP47) in diabetic nephropathy. |
| 3502 | 15004023 | Transgenic mice carrying nitric-oxide synthase cDNA fused with insulin promoter (iNOSTg) leads to diabetes mellitus. |
| 3503 | 15004023 | AGEs significantly increased the expression of HSP47, type IV collagen, and TGF-beta mRNA. |
| 3504 | 15004023 | Neutralizing antibody for TGF-beta inhibited the overexpression of both HSP47 and type IV collagen in vitro. |
| 3505 | 15047614 | Gene expression of transforming growth factor-beta1 was increased in the ZDF pancreas (ZL, 1.0 +/- 0.1; ZDF, 2.0 +/- 0.3; P < 0.05) and reduced after blockade of the RAS (ZDF + P, 1.3 +/- 0.2; ZDF + I, 1.5 +/- 0.1; vs. |
| 3506 | 15047629 | Transforming growth factor-beta 1 production is correlated with genetically determined ACE expression in congenic rats: a possible link between ACE genotype and diabetic nephropathy. |
| 3507 | 15047629 | The aim of this study was to determine whether the ACE genotype could modify factors, such as transforming growth factor (TGF)-beta 1, involved in the complications of diabetes. |
| 3508 | 15047629 | Diabetes was induced in rats of both strains, and its effects on ACE and TGF-beta 1 expressions were evaluated in lungs and kidneys. |
| 3509 | 15047629 | Furthermore, a strong correlation was found between TGF-beta 1 and ACE expressions. |
| 3510 | 15047629 | In renal arterioles, ACE and TGF-beta mRNA expressions were higher in L.BNAce10 rats than LOU rats (both diabetic and nondiabetic). |
| 3511 | 15047629 | In these vessels, there was also a correlation between ACE and TGF-beta 1 expressions. |
| 3512 | 15047629 | These results show that TGF-beta 1 expression is correlated with ACE expression and suggest that this growth factor could be a link between ACE gene polymorphism and diabetic vascular complications. |
| 3513 | 15047629 | Transforming growth factor-beta 1 production is correlated with genetically determined ACE expression in congenic rats: a possible link between ACE genotype and diabetic nephropathy. |
| 3514 | 15047629 | The aim of this study was to determine whether the ACE genotype could modify factors, such as transforming growth factor (TGF)-beta 1, involved in the complications of diabetes. |
| 3515 | 15047629 | Diabetes was induced in rats of both strains, and its effects on ACE and TGF-beta 1 expressions were evaluated in lungs and kidneys. |
| 3516 | 15047629 | Furthermore, a strong correlation was found between TGF-beta 1 and ACE expressions. |
| 3517 | 15047629 | In renal arterioles, ACE and TGF-beta mRNA expressions were higher in L.BNAce10 rats than LOU rats (both diabetic and nondiabetic). |
| 3518 | 15047629 | In these vessels, there was also a correlation between ACE and TGF-beta 1 expressions. |
| 3519 | 15047629 | These results show that TGF-beta 1 expression is correlated with ACE expression and suggest that this growth factor could be a link between ACE gene polymorphism and diabetic vascular complications. |
| 3520 | 15047629 | Transforming growth factor-beta 1 production is correlated with genetically determined ACE expression in congenic rats: a possible link between ACE genotype and diabetic nephropathy. |
| 3521 | 15047629 | The aim of this study was to determine whether the ACE genotype could modify factors, such as transforming growth factor (TGF)-beta 1, involved in the complications of diabetes. |
| 3522 | 15047629 | Diabetes was induced in rats of both strains, and its effects on ACE and TGF-beta 1 expressions were evaluated in lungs and kidneys. |
| 3523 | 15047629 | Furthermore, a strong correlation was found between TGF-beta 1 and ACE expressions. |
| 3524 | 15047629 | In renal arterioles, ACE and TGF-beta mRNA expressions were higher in L.BNAce10 rats than LOU rats (both diabetic and nondiabetic). |
| 3525 | 15047629 | In these vessels, there was also a correlation between ACE and TGF-beta 1 expressions. |
| 3526 | 15047629 | These results show that TGF-beta 1 expression is correlated with ACE expression and suggest that this growth factor could be a link between ACE gene polymorphism and diabetic vascular complications. |
| 3527 | 15047629 | Transforming growth factor-beta 1 production is correlated with genetically determined ACE expression in congenic rats: a possible link between ACE genotype and diabetic nephropathy. |
| 3528 | 15047629 | The aim of this study was to determine whether the ACE genotype could modify factors, such as transforming growth factor (TGF)-beta 1, involved in the complications of diabetes. |
| 3529 | 15047629 | Diabetes was induced in rats of both strains, and its effects on ACE and TGF-beta 1 expressions were evaluated in lungs and kidneys. |
| 3530 | 15047629 | Furthermore, a strong correlation was found between TGF-beta 1 and ACE expressions. |
| 3531 | 15047629 | In renal arterioles, ACE and TGF-beta mRNA expressions were higher in L.BNAce10 rats than LOU rats (both diabetic and nondiabetic). |
| 3532 | 15047629 | In these vessels, there was also a correlation between ACE and TGF-beta 1 expressions. |
| 3533 | 15047629 | These results show that TGF-beta 1 expression is correlated with ACE expression and suggest that this growth factor could be a link between ACE gene polymorphism and diabetic vascular complications. |
| 3534 | 15047629 | Transforming growth factor-beta 1 production is correlated with genetically determined ACE expression in congenic rats: a possible link between ACE genotype and diabetic nephropathy. |
| 3535 | 15047629 | The aim of this study was to determine whether the ACE genotype could modify factors, such as transforming growth factor (TGF)-beta 1, involved in the complications of diabetes. |
| 3536 | 15047629 | Diabetes was induced in rats of both strains, and its effects on ACE and TGF-beta 1 expressions were evaluated in lungs and kidneys. |
| 3537 | 15047629 | Furthermore, a strong correlation was found between TGF-beta 1 and ACE expressions. |
| 3538 | 15047629 | In renal arterioles, ACE and TGF-beta mRNA expressions were higher in L.BNAce10 rats than LOU rats (both diabetic and nondiabetic). |
| 3539 | 15047629 | In these vessels, there was also a correlation between ACE and TGF-beta 1 expressions. |
| 3540 | 15047629 | These results show that TGF-beta 1 expression is correlated with ACE expression and suggest that this growth factor could be a link between ACE gene polymorphism and diabetic vascular complications. |
| 3541 | 15047629 | Transforming growth factor-beta 1 production is correlated with genetically determined ACE expression in congenic rats: a possible link between ACE genotype and diabetic nephropathy. |
| 3542 | 15047629 | The aim of this study was to determine whether the ACE genotype could modify factors, such as transforming growth factor (TGF)-beta 1, involved in the complications of diabetes. |
| 3543 | 15047629 | Diabetes was induced in rats of both strains, and its effects on ACE and TGF-beta 1 expressions were evaluated in lungs and kidneys. |
| 3544 | 15047629 | Furthermore, a strong correlation was found between TGF-beta 1 and ACE expressions. |
| 3545 | 15047629 | In renal arterioles, ACE and TGF-beta mRNA expressions were higher in L.BNAce10 rats than LOU rats (both diabetic and nondiabetic). |
| 3546 | 15047629 | In these vessels, there was also a correlation between ACE and TGF-beta 1 expressions. |
| 3547 | 15047629 | These results show that TGF-beta 1 expression is correlated with ACE expression and suggest that this growth factor could be a link between ACE gene polymorphism and diabetic vascular complications. |
| 3548 | 15047630 | These findings were associated with suppression of renal TGF-beta1 and mesangial connective tissue growth factor (CTGF) upregulation, inhibition of renal tissue inhibitor of metalloproteinase (TIMP)-1 expression, and reduction of renal interstitial myofibroblasts. |
| 3549 | 15070169 | Exposure of the GMCs to 20 mM glucose caused both ECM (collagen and fibronectin) accumulation and TGF-beta secretion, and these changes were significantly diminished by treatment of GMCs with Phytolaccaceae (10 microg/ml). |
| 3550 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3551 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3552 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3553 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3554 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3555 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3556 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3557 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3558 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3559 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3560 | 15070759 | TGF-beta regulates in vivo expansion of Foxp3-expressing CD4+CD25+ regulatory T cells responsible for protection against diabetes. |
| 3561 | 15070759 | CD4+CD25+ regulatory T cells are essential in the protection from organ-specific autoimmune diseases. |
| 3562 | 15070759 | Here we show that a transient pulse of transforming growth factor beta (TGF-beta) in the islets during the priming phase of diabetes is sufficient to inhibit disease onset by promoting the expansion of intraislet CD4+CD25+ T cell pool. |
| 3563 | 15070759 | Approximately 40-50% of intraislet CD4+ T cells expressed the CD25 marker and exhibited characteristics of regulatory T cells including small size, high level of intracellular CTLA-4, expression of Foxp3, and transfer of protection against diabetes. |
| 3564 | 15070759 | Thus, these findings demonstrate a previously uncharacterized mechanism by which TGF-beta inhibits autoimmune diseases via regulation of the size of the CD4+CD25+ regulatory T cell pool in vivo. |
| 3565 | 15111500 | Interleukin-4 but not interleukin-10 protects against spontaneous and recurrent type 1 diabetes by activated CD1d-restricted invariant natural killer T-cells. |
| 3566 | 15111500 | Although interleukin (IL)-4 and IL-10 have been implicated in alpha-GalCer-induced protection from type 1 diabetes, a precise role for these cytokines in iNKT cell regulation of susceptibility to type 1 diabetes has not been identified. |
| 3567 | 15111500 | Here we use NOD.IL-4(-/-) and NOD.IL-10(-/-) knockout mice to further evaluate the roles of IL-4 and IL-10 in alpha-GalCer-induced protection from type 1 diabetes. |
| 3568 | 15111500 | We found that IL-4 but not IL-10 expression mediates protection against spontaneous type 1 diabetes, recurrent type 1 diabetes, and prolonged syngeneic islet graft function. |
| 3569 | 15111500 | Increased transforming growth factor-beta gene expression in pancreatic lymph nodes may be involved in alpha-GalCer-mediated protection in NOD.IL-10(-/-) knockout mice. |
| 3570 | 15111500 | Unlike the requirement of IL-7 and IL-15 to maintain iNKT cell homeostasis, IL-4 and IL-10 are not required for alpha-GalCer-induced iNKT cell expansion and/or survival. |
| 3571 | 15130897 | However, concurrent treatment with spironolactone did block the increase in TGF-beta, indicating that the effect depends on the mineralocorticoid receptor. |
| 3572 | 15131119 | White adipose tissue of FIRKO mice is also characterized by a polarization into two major populations of adipocytes, one small (<50 microm) and one large (>100 microm), which differ with regard to basal triglyceride synthesis and lipolysis, as well as in the expression of fatty acid synthase, sterol regulatory element-binding protein 1c, and CCAAT/enhancer-binding protein alpha (C/EBP-alpha). |
| 3573 | 15131119 | These alterations exhibited 10 defined patterns and occurred in response to two distinct regulatory effects. 63 genes were identified as changed in expression depending primarily upon adipocyte size, including C/EBP-alpha, C/EBP-delta, superoxide dismutase 3, and the platelet-derived growth factor receptor. 48 genes were regulated primarily by impairment of insulin signaling, including transforming growth factor beta, interferon gamma, insulin-like growth factor I receptor, activating transcription factor 3, aldehyde dehydrogenase 2, and protein kinase Cdelta. |
| 3574 | 15131119 | These data suggest an intrinsic heterogeneity of adipocytes with differences in gene expression related to adipocyte size and insulin signaling. |
| 3575 | 15149972 | Body weight, kidney weight, glucose, insulin, renal transforming growth factor-beta(1), and glomerular area were examined for effects of sex, genotype, and diabetes. |
| 3576 | 15154911 | The use of mice with a targeted deletion of Smad3, one of the two homologous proteins which signals from TGF-beta/activin, shows that most of the pro-fibrotic activities of TGF-beta are mediated by Smad3. |
| 3577 | 15154911 | Smad3 null inflammatory cells and fibroblasts do not respond to the chemotactic effects of TGF-beta and do not autoinduce TGF-beta. |
| 3578 | 15154911 | The loss of Smad3 also interferes with TGF-beta-mediated induction of EMT and genes for collagens, plasminogen activator inhibitor-1 and the tissue inhibitor of metalloprotease-1. |
| 3579 | 15154911 | Additionally, inhibition of Smad3 by overexpression of the inhibitory Smad7 protein or by treatment with the small molecule, halofuginone, dramatically reduces responses in animal models of kidney, lung, liver and radiation-induced fibrosis. |
| 3580 | 15154911 | The use of mice with a targeted deletion of Smad3, one of the two homologous proteins which signals from TGF-beta/activin, shows that most of the pro-fibrotic activities of TGF-beta are mediated by Smad3. |
| 3581 | 15154911 | Smad3 null inflammatory cells and fibroblasts do not respond to the chemotactic effects of TGF-beta and do not autoinduce TGF-beta. |
| 3582 | 15154911 | The loss of Smad3 also interferes with TGF-beta-mediated induction of EMT and genes for collagens, plasminogen activator inhibitor-1 and the tissue inhibitor of metalloprotease-1. |
| 3583 | 15154911 | Additionally, inhibition of Smad3 by overexpression of the inhibitory Smad7 protein or by treatment with the small molecule, halofuginone, dramatically reduces responses in animal models of kidney, lung, liver and radiation-induced fibrosis. |
| 3584 | 15154911 | The use of mice with a targeted deletion of Smad3, one of the two homologous proteins which signals from TGF-beta/activin, shows that most of the pro-fibrotic activities of TGF-beta are mediated by Smad3. |
| 3585 | 15154911 | Smad3 null inflammatory cells and fibroblasts do not respond to the chemotactic effects of TGF-beta and do not autoinduce TGF-beta. |
| 3586 | 15154911 | The loss of Smad3 also interferes with TGF-beta-mediated induction of EMT and genes for collagens, plasminogen activator inhibitor-1 and the tissue inhibitor of metalloprotease-1. |
| 3587 | 15154911 | Additionally, inhibition of Smad3 by overexpression of the inhibitory Smad7 protein or by treatment with the small molecule, halofuginone, dramatically reduces responses in animal models of kidney, lung, liver and radiation-induced fibrosis. |
| 3588 | 15158370 | Furthermore, since the protein kinase C (PKC) pathway appears to be a key factor for the enhanced production of TGFbeta(1), we also analyzed the effect of the selective PKCbeta inhibitor LY379196 on TGFbeta(1) response to CSC. |
| 3589 | 15158370 | These data suggest that smoking could increase TGFbeta(1) production, probably due to oxidative stress and PKCbeta activation. |
| 3590 | 15158370 | Furthermore, since the protein kinase C (PKC) pathway appears to be a key factor for the enhanced production of TGFbeta(1), we also analyzed the effect of the selective PKCbeta inhibitor LY379196 on TGFbeta(1) response to CSC. |
| 3591 | 15158370 | These data suggest that smoking could increase TGFbeta(1) production, probably due to oxidative stress and PKCbeta activation. |
| 3592 | 15161601 | Both glucose and anisomycin attenuated CCP-cAMP, but not PMA, angiotensin II, or transforming growth factor-beta. |
| 3593 | 15178441 | We have generated a phosphorothioated double-stranded Sp1-decoy oligodeoxynucleotide that effectively blocks Sp1 binding to the promoter region for transcriptional regulation of transforming growth factor-beta1 and plasminogen activator inhibitor-1. |
| 3594 | 15178645 | Here we report expressions of PTTG and its interacting protein, PTTG-binding factor in human astrocytic cells. |
| 3595 | 15178645 | PTTG expression was higher in malignant cells than in primary astrocytes, whereas PTTG-binding factor was not. |
| 3596 | 15178645 | Furthermore, in U87 cells PTTG expression was up-regulated by promalignant ligands epithelial growth factor (EGF) and TGFalpha, both at the protein and mRNA levels. |
| 3597 | 15178645 | PTTG induction by EGF receptor (EGFR) ligands could be blocked by the specific EGFR inhibitor, AG1478. |
| 3598 | 15178645 | Hepatocyte growth factor (HGF) also induced PTTG but to a lesser extent than EGF. |
| 3599 | 15178645 | Although EGF stimulates HGF secretion in U87 cells, the effect of EGF on PTTG mRNA expression is independent of HGF as neutralizing antibody against HGF failed to abolish EGF-induced up-regulation of PTTG mRNA. |
| 3600 | 15178645 | PTTG mRNA was unchanged by incubating U87 cells with the promalignant growth factor TGFbeta, apoptosis inducing TNFalpha and ligands for nuclear receptors, such as retinoic acid and retinoid X receptors and peroxisome proliferator-activated receptor-gamma, known for their growth-inhibitory and apoptosis-inducing effects on gliomas. |
| 3601 | 15178645 | Finally, regulation of its expression has glioma-specific features and is selectively regulated by promalignant cytokines including EGFR ligands and HGF. |
| 3602 | 15180456 | Activins, myostatin and related TGF-beta family members as novel therapeutic targets for endocrine, metabolic and immune disorders. |
| 3603 | 15180456 | Recent studies have revealed that activins and myostatin signal through activin type II receptors (ActRIIA and ActRIIB) and their activities are regulated by extracellular binding proteins, follistatins and follistatin-related gene (FLRG). |
| 3604 | 15180953 | RAGE- and TGF-beta receptor-mediated signals converge on STAT5 and p21waf to control cell-cycle progression of mesangial cells: a possible role in the development and progression of diabetic nephropathy. |
| 3605 | 15180953 | TGF-beta1 blockade inhibited AGE-mediated collagen production but only partially affected AGE-induced p21waf expression and cell-cycle events, indicating that AGE by binding to AGE receptor (RAGE) per se could control MC growth. |
| 3606 | 15180953 | Moreover, AGE and TGF-beta treatment led to the activation of the signal transduction and activators of transcription (STAT)5 and the formation of a STAT5/p21SIE2 complex. |
| 3607 | 15180953 | The role of STAT5 in AGE- and TGF-beta-mediated p21waf expression and growth arrest, but not collagen production, was confirmed by the expression of the dominant negative STAT5 (DeltaSTAT5) or the constitutively activated STAT5 (1*6-STAT5) constructs. |
| 3608 | 15180953 | A potential in vivo role of these mechanisms was sustained by the increasing immunoreactivity for the activated STAT5 and p21(waf) in kidney biopsies from early to advanced stage of diabetic nephropathy. |
| 3609 | 15180953 | Our data indicate that AGE- and TGF-beta-mediated signals, by converging on STAT5 activation and p21waf expression, may regulate MC growth. |
| 3610 | 15180953 | RAGE- and TGF-beta receptor-mediated signals converge on STAT5 and p21waf to control cell-cycle progression of mesangial cells: a possible role in the development and progression of diabetic nephropathy. |
| 3611 | 15180953 | TGF-beta1 blockade inhibited AGE-mediated collagen production but only partially affected AGE-induced p21waf expression and cell-cycle events, indicating that AGE by binding to AGE receptor (RAGE) per se could control MC growth. |
| 3612 | 15180953 | Moreover, AGE and TGF-beta treatment led to the activation of the signal transduction and activators of transcription (STAT)5 and the formation of a STAT5/p21SIE2 complex. |
| 3613 | 15180953 | The role of STAT5 in AGE- and TGF-beta-mediated p21waf expression and growth arrest, but not collagen production, was confirmed by the expression of the dominant negative STAT5 (DeltaSTAT5) or the constitutively activated STAT5 (1*6-STAT5) constructs. |
| 3614 | 15180953 | A potential in vivo role of these mechanisms was sustained by the increasing immunoreactivity for the activated STAT5 and p21(waf) in kidney biopsies from early to advanced stage of diabetic nephropathy. |
| 3615 | 15180953 | Our data indicate that AGE- and TGF-beta-mediated signals, by converging on STAT5 activation and p21waf expression, may regulate MC growth. |
| 3616 | 15180953 | RAGE- and TGF-beta receptor-mediated signals converge on STAT5 and p21waf to control cell-cycle progression of mesangial cells: a possible role in the development and progression of diabetic nephropathy. |
| 3617 | 15180953 | TGF-beta1 blockade inhibited AGE-mediated collagen production but only partially affected AGE-induced p21waf expression and cell-cycle events, indicating that AGE by binding to AGE receptor (RAGE) per se could control MC growth. |
| 3618 | 15180953 | Moreover, AGE and TGF-beta treatment led to the activation of the signal transduction and activators of transcription (STAT)5 and the formation of a STAT5/p21SIE2 complex. |
| 3619 | 15180953 | The role of STAT5 in AGE- and TGF-beta-mediated p21waf expression and growth arrest, but not collagen production, was confirmed by the expression of the dominant negative STAT5 (DeltaSTAT5) or the constitutively activated STAT5 (1*6-STAT5) constructs. |
| 3620 | 15180953 | A potential in vivo role of these mechanisms was sustained by the increasing immunoreactivity for the activated STAT5 and p21(waf) in kidney biopsies from early to advanced stage of diabetic nephropathy. |
| 3621 | 15180953 | Our data indicate that AGE- and TGF-beta-mediated signals, by converging on STAT5 activation and p21waf expression, may regulate MC growth. |
| 3622 | 15180953 | RAGE- and TGF-beta receptor-mediated signals converge on STAT5 and p21waf to control cell-cycle progression of mesangial cells: a possible role in the development and progression of diabetic nephropathy. |
| 3623 | 15180953 | TGF-beta1 blockade inhibited AGE-mediated collagen production but only partially affected AGE-induced p21waf expression and cell-cycle events, indicating that AGE by binding to AGE receptor (RAGE) per se could control MC growth. |
| 3624 | 15180953 | Moreover, AGE and TGF-beta treatment led to the activation of the signal transduction and activators of transcription (STAT)5 and the formation of a STAT5/p21SIE2 complex. |
| 3625 | 15180953 | The role of STAT5 in AGE- and TGF-beta-mediated p21waf expression and growth arrest, but not collagen production, was confirmed by the expression of the dominant negative STAT5 (DeltaSTAT5) or the constitutively activated STAT5 (1*6-STAT5) constructs. |
| 3626 | 15180953 | A potential in vivo role of these mechanisms was sustained by the increasing immunoreactivity for the activated STAT5 and p21(waf) in kidney biopsies from early to advanced stage of diabetic nephropathy. |
| 3627 | 15180953 | Our data indicate that AGE- and TGF-beta-mediated signals, by converging on STAT5 activation and p21waf expression, may regulate MC growth. |
| 3628 | 15180953 | RAGE- and TGF-beta receptor-mediated signals converge on STAT5 and p21waf to control cell-cycle progression of mesangial cells: a possible role in the development and progression of diabetic nephropathy. |
| 3629 | 15180953 | TGF-beta1 blockade inhibited AGE-mediated collagen production but only partially affected AGE-induced p21waf expression and cell-cycle events, indicating that AGE by binding to AGE receptor (RAGE) per se could control MC growth. |
| 3630 | 15180953 | Moreover, AGE and TGF-beta treatment led to the activation of the signal transduction and activators of transcription (STAT)5 and the formation of a STAT5/p21SIE2 complex. |
| 3631 | 15180953 | The role of STAT5 in AGE- and TGF-beta-mediated p21waf expression and growth arrest, but not collagen production, was confirmed by the expression of the dominant negative STAT5 (DeltaSTAT5) or the constitutively activated STAT5 (1*6-STAT5) constructs. |
| 3632 | 15180953 | A potential in vivo role of these mechanisms was sustained by the increasing immunoreactivity for the activated STAT5 and p21(waf) in kidney biopsies from early to advanced stage of diabetic nephropathy. |
| 3633 | 15180953 | Our data indicate that AGE- and TGF-beta-mediated signals, by converging on STAT5 activation and p21waf expression, may regulate MC growth. |
| 3634 | 15198374 | The authors' previous studies of cultured endothelial cells demonstrated that oncofetal FN synthesis is, at least in part, mediated via transforming growth factor-beta (TGF-beta) and endothelin-1 (ET-1). |
| 3635 | 15198374 | Diabetes caused significant increase in mRNA expression of ET-1 and TGF-beta, which was not prevented by C-peptide treatment. |
| 3636 | 15198374 | Hence it appears that C-peptide is effective in preventing diabetes-induced oncofetal FN expression and that these effects are not mediated via ET-1 or TGF-beta. |
| 3637 | 15198374 | The authors' previous studies of cultured endothelial cells demonstrated that oncofetal FN synthesis is, at least in part, mediated via transforming growth factor-beta (TGF-beta) and endothelin-1 (ET-1). |
| 3638 | 15198374 | Diabetes caused significant increase in mRNA expression of ET-1 and TGF-beta, which was not prevented by C-peptide treatment. |
| 3639 | 15198374 | Hence it appears that C-peptide is effective in preventing diabetes-induced oncofetal FN expression and that these effects are not mediated via ET-1 or TGF-beta. |
| 3640 | 15198374 | The authors' previous studies of cultured endothelial cells demonstrated that oncofetal FN synthesis is, at least in part, mediated via transforming growth factor-beta (TGF-beta) and endothelin-1 (ET-1). |
| 3641 | 15198374 | Diabetes caused significant increase in mRNA expression of ET-1 and TGF-beta, which was not prevented by C-peptide treatment. |
| 3642 | 15198374 | Hence it appears that C-peptide is effective in preventing diabetes-induced oncofetal FN expression and that these effects are not mediated via ET-1 or TGF-beta. |
| 3643 | 15198928 | Glycated albumin activates PAI-1 transcription through Smad DNA binding sites in mesangial cells. |
| 3644 | 15198928 | Amadori-modified glycated albumin stimulates extracellular matrix and transforming growth factor-beta (TGF-beta) expression in cultured mesangial cells. |
| 3645 | 15198928 | Smad proteins transduce the TGF-beta-mediated signal, and Smad-binding CAGA sequences are present in the plasminogen activator inhibitor-1 (PAI-1) promoter. |
| 3646 | 15198928 | This study examined whether glycated albumin induces PAI-1 transcription in human mesangial cells (HMC) through Smad-binding sites in the PAI-1 promoter. |
| 3647 | 15198928 | At 24 h, Gly-BSA stimulated TGF-beta1 and PAI-1 mRNA expression in HMC to 1.8 and 3.2 times that in the BSA-treated control cells. |
| 3648 | 15198928 | Gly-BSA-treated cells enhanced Smad2 and Smad3 protein levels 2.5 times the control levels in the nuclei. |
| 3649 | 15198928 | Transfection of phosphorothioate CAGA oligonucleotide, a CAGA antisense analog, inhibited Gly-BSA-induced PAI-1 mRNA expression. |
| 3650 | 15198928 | Cotransfection of phosphorothioate CAGA oligonucleotides with PAI-1 reporter vector also blocked Gly-BSA-induced PAI-1 promoter luciferase activity. |
| 3651 | 15198928 | These results indicate that Gly-BSA increases DNA binding activity of Smad3 and that it stimulates PAI-1 transcription through Smad-binding CAGA sequences in the PAI-1 promoter in HMC. |
| 3652 | 15198928 | Thus progression of diabetic nephropathy may be promoted by PAI-1 upregulation mediated by the glycated albumin-induced Smad/DNA interactions. |
| 3653 | 15198928 | Glycated albumin activates PAI-1 transcription through Smad DNA binding sites in mesangial cells. |
| 3654 | 15198928 | Amadori-modified glycated albumin stimulates extracellular matrix and transforming growth factor-beta (TGF-beta) expression in cultured mesangial cells. |
| 3655 | 15198928 | Smad proteins transduce the TGF-beta-mediated signal, and Smad-binding CAGA sequences are present in the plasminogen activator inhibitor-1 (PAI-1) promoter. |
| 3656 | 15198928 | This study examined whether glycated albumin induces PAI-1 transcription in human mesangial cells (HMC) through Smad-binding sites in the PAI-1 promoter. |
| 3657 | 15198928 | At 24 h, Gly-BSA stimulated TGF-beta1 and PAI-1 mRNA expression in HMC to 1.8 and 3.2 times that in the BSA-treated control cells. |
| 3658 | 15198928 | Gly-BSA-treated cells enhanced Smad2 and Smad3 protein levels 2.5 times the control levels in the nuclei. |
| 3659 | 15198928 | Transfection of phosphorothioate CAGA oligonucleotide, a CAGA antisense analog, inhibited Gly-BSA-induced PAI-1 mRNA expression. |
| 3660 | 15198928 | Cotransfection of phosphorothioate CAGA oligonucleotides with PAI-1 reporter vector also blocked Gly-BSA-induced PAI-1 promoter luciferase activity. |
| 3661 | 15198928 | These results indicate that Gly-BSA increases DNA binding activity of Smad3 and that it stimulates PAI-1 transcription through Smad-binding CAGA sequences in the PAI-1 promoter in HMC. |
| 3662 | 15198928 | Thus progression of diabetic nephropathy may be promoted by PAI-1 upregulation mediated by the glycated albumin-induced Smad/DNA interactions. |
| 3663 | 15198928 | Glycated albumin activates PAI-1 transcription through Smad DNA binding sites in mesangial cells. |
| 3664 | 15198928 | Amadori-modified glycated albumin stimulates extracellular matrix and transforming growth factor-beta (TGF-beta) expression in cultured mesangial cells. |
| 3665 | 15198928 | Smad proteins transduce the TGF-beta-mediated signal, and Smad-binding CAGA sequences are present in the plasminogen activator inhibitor-1 (PAI-1) promoter. |
| 3666 | 15198928 | This study examined whether glycated albumin induces PAI-1 transcription in human mesangial cells (HMC) through Smad-binding sites in the PAI-1 promoter. |
| 3667 | 15198928 | At 24 h, Gly-BSA stimulated TGF-beta1 and PAI-1 mRNA expression in HMC to 1.8 and 3.2 times that in the BSA-treated control cells. |
| 3668 | 15198928 | Gly-BSA-treated cells enhanced Smad2 and Smad3 protein levels 2.5 times the control levels in the nuclei. |
| 3669 | 15198928 | Transfection of phosphorothioate CAGA oligonucleotide, a CAGA antisense analog, inhibited Gly-BSA-induced PAI-1 mRNA expression. |
| 3670 | 15198928 | Cotransfection of phosphorothioate CAGA oligonucleotides with PAI-1 reporter vector also blocked Gly-BSA-induced PAI-1 promoter luciferase activity. |
| 3671 | 15198928 | These results indicate that Gly-BSA increases DNA binding activity of Smad3 and that it stimulates PAI-1 transcription through Smad-binding CAGA sequences in the PAI-1 promoter in HMC. |
| 3672 | 15198928 | Thus progression of diabetic nephropathy may be promoted by PAI-1 upregulation mediated by the glycated albumin-induced Smad/DNA interactions. |
| 3673 | 15215651 | Furthermore, the expression of transforming growth factor beta1 mRNA in kidney cortex by RT-PCR analysis was markedly declined. |
| 3674 | 15220206 | Diabetes was also accompanied by aortic accumulation of total collagen, specifically collagens I, III, and IV, as well as increases in the profibrotic cytokines transforming growth factor-beta and connective tissue growth factor and in cellular alpha-smooth muscle actin. |
| 3675 | 15223229 | There was a positive correlation between urinary betaig-h3 and TGF-beta excretion rate and a positive correlation between urinary betaig-h3 and albumin excretion rate (AER). |
| 3676 | 15223984 | Finally, ROS and lipid peroxidation increase the generation of several cytokines (TNF-alpha, TGF-B, Fas ligand) that play sundry roles in the pathogenesis of NASH. |
| 3677 | 15240736 | RAGE expression was detected on CD4(+), CD8(+), and B cells from diabetic mice and transferred to NOD/scid recipients. |
| 3678 | 15240736 | RAGE blockade was associated with increased expression of IL-10 and TGF-beta in the islets from protected mice. |
| 3679 | 15256362 | We examined the induction of steatohepatitis and liver fibrosis in obese and type 2 diabetic db/db mice in a nutritional model of NASH and determined the relationship of the expressions of osteopontin (OPN) and leptin receptors to the pathogenesis of NASH. db/db mice and the corresponding lean and nondiabetic db/m mice were fed a diet deficient in methionine and choline (MCD diet) or control diet for 4 wk. |
| 3680 | 15256362 | Collagen I mRNA expression was increased 10-fold in db/db mice, 4-fold in db/m mice, and was unchanged in ob/ob mice. mRNA expressions of OPN, TNF-alpha, TGF-beta, and short-form leptin receptors (Ob-Ra) were significantly increased in db/db mice compared with db/m or ob/ob mice. |
| 3681 | 15256362 | Cultured hepatocytes expressed only Ob-Ra, and leptin stimulated OPN mRNA and protein expression in these cells. |
| 3682 | 15258755 | All the PDCL showed resistance to Fas-mediated apoptosis but were significantly sensitive to the pro-apoptotic effect of inflammatory cytokines [interleukin (IL)-1beta, tumor necrosis factor (TNF)alpha and interferon gamma]. |
| 3683 | 15258755 | Vascular endothelial growth factor, CCL2, CCL5 and transforming growth factor beta were the factors most frequently released; less frequent was the secretion of CXCL8, CCL22, IL-6 and sporadically CXCL12, IL-10 and hepatocyte growth factor. |
| 3684 | 15258755 | The cytokines IL-1beta and TNFalpha were always undetectable. |
| 3685 | 15270841 | However, DNA vaccination encoding microbial or reporter antigens is known to induce specific long-lasting CD4 Th1 and strong cytolytic CD8 T cell responses. |
| 3686 | 15270841 | Simultaneously, DNA immunization induced GAD-specific CD4 T cells secreting interleukin (IL)-4 (P < 0.05) and transforming growth factor (TGF)-beta (P = 0.03). |
| 3687 | 15270841 | Furthermore, vaccination produced high amounts of Th2 cytokine-related IgG1 (P < 3.10(-3)) and TGF-beta-related IgG2b to GAD (P = 0.015). |
| 3688 | 15270841 | Surprisingly, diabetes onset was correlated positively with Th2-related GAD-specific IgG1 (P < 10(-4)) and TGF-beta-related IgG2b (P < 3.10(-3)). |
| 3689 | 15270841 | However, DNA vaccination encoding microbial or reporter antigens is known to induce specific long-lasting CD4 Th1 and strong cytolytic CD8 T cell responses. |
| 3690 | 15270841 | Simultaneously, DNA immunization induced GAD-specific CD4 T cells secreting interleukin (IL)-4 (P < 0.05) and transforming growth factor (TGF)-beta (P = 0.03). |
| 3691 | 15270841 | Furthermore, vaccination produced high amounts of Th2 cytokine-related IgG1 (P < 3.10(-3)) and TGF-beta-related IgG2b to GAD (P = 0.015). |
| 3692 | 15270841 | Surprisingly, diabetes onset was correlated positively with Th2-related GAD-specific IgG1 (P < 10(-4)) and TGF-beta-related IgG2b (P < 3.10(-3)). |
| 3693 | 15276022 | Salutary effects of attenuation of angiotensin II on coronary perivascular fibrosis associated with insulin resistance and obesity. |
| 3694 | 15276022 | We have previously shown that inhibition of angiotensin-converting enzyme (ACE) prevents coronary perimicrovascular fibrosis in genetically obese mice that develop insulin resistance. |
| 3695 | 15276022 | Genetically obese ob/ob mice were given ACE inhibitor (temocapril) or Ang II type 1 (AT(1)) receptor blocker (olmesartan) from 10 to 20 weeks. |
| 3696 | 15276022 | Cardiac expressions of plasminogen activator inhibitor (PAI)-1, the major physiologic inhibitor of fibrinolysis, and transforming growth factor (TGF)-beta(1), a prototypic profibrotic molecule, were determined and extent of perivascular coronary fibrosis was measured. |
| 3697 | 15276022 | Twenty-week-old obese mice exhibited increased plasma levels of PAI-1 and TGF-beta(1) compared with the values in lean counterpart. |
| 3698 | 15276022 | Markedly increased PAI-1 and TGF-beta were seen immunohistochemically in coronary vascular wall and confirmed by western blotting. |
| 3699 | 15276022 | When obese mice were treated with temocapril or olmesartan from 10 to 20 weeks, both were equally effective and prevented increases in perivascular fibrosis, plasma PAI-1 and TGF-beta(1), left ventricular collagen and mural immunoreactivity for PAI-1, TGF-beta and collagen type 1. |
| 3700 | 15276022 | The c-Jun NH(2)-terminal kinase (JNK) activity was elevated in the left ventricle of obese mice (western) and blocked by temocapril and olmesartan. |
| 3701 | 15276022 | Ang II-mediated upregulation of PAI-1 and TGF-beta(1) with collagen deposition may explain the mechanism of perivascular fibrosis in obese mice. |
| 3702 | 15276022 | ACE inhibition and blockade of AT(1) receptor may prevent coronary perivascular fibrosis and collagen deposition even before development of overt diabetes. |
| 3703 | 15276022 | Salutary effects of attenuation of angiotensin II on coronary perivascular fibrosis associated with insulin resistance and obesity. |
| 3704 | 15276022 | We have previously shown that inhibition of angiotensin-converting enzyme (ACE) prevents coronary perimicrovascular fibrosis in genetically obese mice that develop insulin resistance. |
| 3705 | 15276022 | Genetically obese ob/ob mice were given ACE inhibitor (temocapril) or Ang II type 1 (AT(1)) receptor blocker (olmesartan) from 10 to 20 weeks. |
| 3706 | 15276022 | Cardiac expressions of plasminogen activator inhibitor (PAI)-1, the major physiologic inhibitor of fibrinolysis, and transforming growth factor (TGF)-beta(1), a prototypic profibrotic molecule, were determined and extent of perivascular coronary fibrosis was measured. |
| 3707 | 15276022 | Twenty-week-old obese mice exhibited increased plasma levels of PAI-1 and TGF-beta(1) compared with the values in lean counterpart. |
| 3708 | 15276022 | Markedly increased PAI-1 and TGF-beta were seen immunohistochemically in coronary vascular wall and confirmed by western blotting. |
| 3709 | 15276022 | When obese mice were treated with temocapril or olmesartan from 10 to 20 weeks, both were equally effective and prevented increases in perivascular fibrosis, plasma PAI-1 and TGF-beta(1), left ventricular collagen and mural immunoreactivity for PAI-1, TGF-beta and collagen type 1. |
| 3710 | 15276022 | The c-Jun NH(2)-terminal kinase (JNK) activity was elevated in the left ventricle of obese mice (western) and blocked by temocapril and olmesartan. |
| 3711 | 15276022 | Ang II-mediated upregulation of PAI-1 and TGF-beta(1) with collagen deposition may explain the mechanism of perivascular fibrosis in obese mice. |
| 3712 | 15276022 | ACE inhibition and blockade of AT(1) receptor may prevent coronary perivascular fibrosis and collagen deposition even before development of overt diabetes. |
| 3713 | 15276022 | Salutary effects of attenuation of angiotensin II on coronary perivascular fibrosis associated with insulin resistance and obesity. |
| 3714 | 15276022 | We have previously shown that inhibition of angiotensin-converting enzyme (ACE) prevents coronary perimicrovascular fibrosis in genetically obese mice that develop insulin resistance. |
| 3715 | 15276022 | Genetically obese ob/ob mice were given ACE inhibitor (temocapril) or Ang II type 1 (AT(1)) receptor blocker (olmesartan) from 10 to 20 weeks. |
| 3716 | 15276022 | Cardiac expressions of plasminogen activator inhibitor (PAI)-1, the major physiologic inhibitor of fibrinolysis, and transforming growth factor (TGF)-beta(1), a prototypic profibrotic molecule, were determined and extent of perivascular coronary fibrosis was measured. |
| 3717 | 15276022 | Twenty-week-old obese mice exhibited increased plasma levels of PAI-1 and TGF-beta(1) compared with the values in lean counterpart. |
| 3718 | 15276022 | Markedly increased PAI-1 and TGF-beta were seen immunohistochemically in coronary vascular wall and confirmed by western blotting. |
| 3719 | 15276022 | When obese mice were treated with temocapril or olmesartan from 10 to 20 weeks, both were equally effective and prevented increases in perivascular fibrosis, plasma PAI-1 and TGF-beta(1), left ventricular collagen and mural immunoreactivity for PAI-1, TGF-beta and collagen type 1. |
| 3720 | 15276022 | The c-Jun NH(2)-terminal kinase (JNK) activity was elevated in the left ventricle of obese mice (western) and blocked by temocapril and olmesartan. |
| 3721 | 15276022 | Ang II-mediated upregulation of PAI-1 and TGF-beta(1) with collagen deposition may explain the mechanism of perivascular fibrosis in obese mice. |
| 3722 | 15276022 | ACE inhibition and blockade of AT(1) receptor may prevent coronary perivascular fibrosis and collagen deposition even before development of overt diabetes. |
| 3723 | 15276022 | Salutary effects of attenuation of angiotensin II on coronary perivascular fibrosis associated with insulin resistance and obesity. |
| 3724 | 15276022 | We have previously shown that inhibition of angiotensin-converting enzyme (ACE) prevents coronary perimicrovascular fibrosis in genetically obese mice that develop insulin resistance. |
| 3725 | 15276022 | Genetically obese ob/ob mice were given ACE inhibitor (temocapril) or Ang II type 1 (AT(1)) receptor blocker (olmesartan) from 10 to 20 weeks. |
| 3726 | 15276022 | Cardiac expressions of plasminogen activator inhibitor (PAI)-1, the major physiologic inhibitor of fibrinolysis, and transforming growth factor (TGF)-beta(1), a prototypic profibrotic molecule, were determined and extent of perivascular coronary fibrosis was measured. |
| 3727 | 15276022 | Twenty-week-old obese mice exhibited increased plasma levels of PAI-1 and TGF-beta(1) compared with the values in lean counterpart. |
| 3728 | 15276022 | Markedly increased PAI-1 and TGF-beta were seen immunohistochemically in coronary vascular wall and confirmed by western blotting. |
| 3729 | 15276022 | When obese mice were treated with temocapril or olmesartan from 10 to 20 weeks, both were equally effective and prevented increases in perivascular fibrosis, plasma PAI-1 and TGF-beta(1), left ventricular collagen and mural immunoreactivity for PAI-1, TGF-beta and collagen type 1. |
| 3730 | 15276022 | The c-Jun NH(2)-terminal kinase (JNK) activity was elevated in the left ventricle of obese mice (western) and blocked by temocapril and olmesartan. |
| 3731 | 15276022 | Ang II-mediated upregulation of PAI-1 and TGF-beta(1) with collagen deposition may explain the mechanism of perivascular fibrosis in obese mice. |
| 3732 | 15276022 | ACE inhibition and blockade of AT(1) receptor may prevent coronary perivascular fibrosis and collagen deposition even before development of overt diabetes. |
| 3733 | 15277392 | The hyperglycemia-induced downregulation of the negatively charged basement membrane heparan sulfate proteoglycan perlecan was completely prevented in the PKC-alpha(-/-) mice, compared with controls. |
| 3734 | 15277392 | We then asked whether transforming growth factor-beta1 (TGF-beta1) and/or vascular endothelial growth factor (VEGF) is implicated in the PKC-alpha-mediated changes in the basement membrane. |
| 3735 | 15277392 | The hyperglycemia-induced expression of VEGF165 and its receptor VEGF receptor II (flk-1) was ameliorated in PKC-alpha(-/-) mice, whereas expression of TGF-beta1 was not affected by the lack of PKC-alpha. |
| 3736 | 15277392 | The glucose-induced albuminuria seems to be mediated by PKC-alpha via downregulation of proteoglycans in the basement membrane and regulation of VEGF expression. |
| 3737 | 15277392 | The hyperglycemia-induced downregulation of the negatively charged basement membrane heparan sulfate proteoglycan perlecan was completely prevented in the PKC-alpha(-/-) mice, compared with controls. |
| 3738 | 15277392 | We then asked whether transforming growth factor-beta1 (TGF-beta1) and/or vascular endothelial growth factor (VEGF) is implicated in the PKC-alpha-mediated changes in the basement membrane. |
| 3739 | 15277392 | The hyperglycemia-induced expression of VEGF165 and its receptor VEGF receptor II (flk-1) was ameliorated in PKC-alpha(-/-) mice, whereas expression of TGF-beta1 was not affected by the lack of PKC-alpha. |
| 3740 | 15277392 | The glucose-induced albuminuria seems to be mediated by PKC-alpha via downregulation of proteoglycans in the basement membrane and regulation of VEGF expression. |
| 3741 | 15284298 | These abnormalities were associated with increased expression of collagen type I and type IV and transforming growth factor-beta1 (TGF-beta1), increased alpha-smooth muscle actin immunostaining and macrophage infiltration, and increased serum and renal AGE. |
| 3742 | 15284298 | The two treatments, which attenuated renal AGE accumulation in a disparate manner, were associated with less albuminuria, structural injury, macrophage infiltration, TGF-beta1, and collagen expression. |
| 3743 | 15284298 | These abnormalities were associated with increased expression of collagen type I and type IV and transforming growth factor-beta1 (TGF-beta1), increased alpha-smooth muscle actin immunostaining and macrophage infiltration, and increased serum and renal AGE. |
| 3744 | 15284298 | The two treatments, which attenuated renal AGE accumulation in a disparate manner, were associated with less albuminuria, structural injury, macrophage infiltration, TGF-beta1, and collagen expression. |
| 3745 | 15305298 | Extracellular matrix accumulates in adult tissues in response to hyperglycemia, and transforming growth factor-beta1 (TGF beta1) likely mediates this effect. |
| 3746 | 15326185 | No changes in transforming growth factor beta1 (expression or biological activity) occurred that could account for our observations, whereas incubation of tTg with collagen III indicated that cross-linking could directly increase the rate of collagen fibril/gel formation. |
| 3747 | 15326185 | We conclude that Tg inhibition reduces glucose-induced deposition of ECM proteins independently of changes in ECM and transforming growth factor beta1 synthesis thus opening up its possible application in the treatment other fibrotic and scarring diseases where tTg has been implicated. |
| 3748 | 15326185 | No changes in transforming growth factor beta1 (expression or biological activity) occurred that could account for our observations, whereas incubation of tTg with collagen III indicated that cross-linking could directly increase the rate of collagen fibril/gel formation. |
| 3749 | 15326185 | We conclude that Tg inhibition reduces glucose-induced deposition of ECM proteins independently of changes in ECM and transforming growth factor beta1 synthesis thus opening up its possible application in the treatment other fibrotic and scarring diseases where tTg has been implicated. |
| 3750 | 15337504 | Some of these effects were shown to be mediated by the up-regulation of endothelial transforming growth factor-beta1 (TGFbeta1) secretion and activation. |
| 3751 | 15337504 | By blocking the coupling of CS chains to the core protein with p-nitrophenyl-beta-D-xyloside and by chondroitinase ABC treatment, we demonstrated that the increased accumulation of pericellular CS is accompanied by increased cell attachment to immobilized hyaluronic acid (HA), while the expression of cell surface CD44 remains unaltered. |
| 3752 | 15345671 | Connective tissue growth factor (CTGF) expression is increased in diabetic nephropathy and is a downstream mediator of TGF-beta actions. |
| 3753 | 15345671 | Matrix degradation was inhibited by rhCTGF in a dose-dependent manner, and the decrease in matrix degradation caused by high glucose and by TGF-beta was significantly attenuated by addition of CTGF-neutralizing antibody (by 40.2 and 69.1%, respectively). |
| 3754 | 15345671 | Similar to 25 mM glucose, addition of rhCTGF increased MMP-2, TIMP-1, and TIMP-3 mRNA by 2.5-, 2.1-, and 1.6-fold, respectively (P < 0.05) but had no effect on membrane-type (MT)1-MMP or TIMP-2. |
| 3755 | 15345671 | In vivo studies of glomeruli from diabetic and control rats showed that intensive insulin treatment prevented the increase in expression of CTGF and TIMP-1 and attenuated the decreased matrix degradation seen in diabetes. |
| 3756 | 15345671 | In summary, CTGF inhibits matrix degradation by increasing TIMP-1 expression, and by this action it contributes to the inhibition of matrix breakdown by high glucose, implying that CTGF has a role in the reduced matrix degradation observed in diabetic nephropathy. |
| 3757 | 15345671 | Connective tissue growth factor (CTGF) expression is increased in diabetic nephropathy and is a downstream mediator of TGF-beta actions. |
| 3758 | 15345671 | Matrix degradation was inhibited by rhCTGF in a dose-dependent manner, and the decrease in matrix degradation caused by high glucose and by TGF-beta was significantly attenuated by addition of CTGF-neutralizing antibody (by 40.2 and 69.1%, respectively). |
| 3759 | 15345671 | Similar to 25 mM glucose, addition of rhCTGF increased MMP-2, TIMP-1, and TIMP-3 mRNA by 2.5-, 2.1-, and 1.6-fold, respectively (P < 0.05) but had no effect on membrane-type (MT)1-MMP or TIMP-2. |
| 3760 | 15345671 | In vivo studies of glomeruli from diabetic and control rats showed that intensive insulin treatment prevented the increase in expression of CTGF and TIMP-1 and attenuated the decreased matrix degradation seen in diabetes. |
| 3761 | 15345671 | In summary, CTGF inhibits matrix degradation by increasing TIMP-1 expression, and by this action it contributes to the inhibition of matrix breakdown by high glucose, implying that CTGF has a role in the reduced matrix degradation observed in diabetic nephropathy. |
| 3762 | 15356668 | Plasminogen activator inhibitor-1 (PAI-1) is the most important endogenous inhibitor of tissue plasminogen activator and uro-plasminogen activator, and is a main determinant of fibrinolytic activity. |
| 3763 | 15356668 | Studies in human adipocytes indicate that PAI-1 synthesis is upregulated by insulin, glucocorticoids, angiotensin II, some fatty acids and, most potently, by cytokines such as tumour necrosis factor-alpha and transforming growth factor-beta, whereas catecholamines reduce PAI-1 production. |
| 3764 | 15367428 | Despite their opposite effects on growth, stem cell factor (SCF) and transforming growth factor beta (TGF-B) had synergistic effects with respect to fetal hemoglobin (HbF): average HbF/HbF + adult hemoglobin (HbA) ratio in erythropoietin (EPO) = 1.4 +/- 1.0%; EPO + TGF-B = 10.8 +/- 1.9%; EPO + SCF = 19.1 +/- 6.2%; and EPO + SCF + TGF-B (EST) = 39.3 +/- 6.3%. |
| 3765 | 15367428 | Polymerase chain reaction (PCR) revealed significant increases in gamma-globin transcripts that were balanced by reduced beta-globin transcripts. |
| 3766 | 15373787 | For the studies of transforming growth factor-beta1 (TGF-beta1) local expression and therapeutic effects, full thickness excisional wound model of db/db mice was used, we measured TGF-beta1 cytokine level at 24 h postwounding and examined wounds histologically. |
| 3767 | 15373787 | Five to seven days postapplication of intradermal injection of plasmid TGF-beta1 followed by electroporation, the wound bed showed an increased reepithelialization rate, collagen synthesis, and angiogenesis. |
| 3768 | 15373787 | For the studies of transforming growth factor-beta1 (TGF-beta1) local expression and therapeutic effects, full thickness excisional wound model of db/db mice was used, we measured TGF-beta1 cytokine level at 24 h postwounding and examined wounds histologically. |
| 3769 | 15373787 | Five to seven days postapplication of intradermal injection of plasmid TGF-beta1 followed by electroporation, the wound bed showed an increased reepithelialization rate, collagen synthesis, and angiogenesis. |
| 3770 | 15380036 | Three forms of these regulatory T cells have been described: those that function via the production of the cytokine IL-10 (T regulatory 1 cells), transforming growth factor beta (Th3 cells), and a population of T cells that suppresses proliferation via a cell-contact-dependent mechanism (CD4+CD25+ TR cells). |
| 3771 | 15454392 | Diabetes was associated with an increase in urine albumin excretion (UAE; ND, 0.39 +/- 0.03; D, 5.9 +/- 0.8 mg/day; P < 0.001), decrease in creatinine clearance (CrCl; ND, 0.69 +/- 0.03; D, 0.43 +/- 0.09 mg x min(-1) x 100 g body wt(-1); P < 0.05), increase in the index of glomerulosclerosis [GSI; ND, 0.01 +/- 0.01; D, 0.15 +/- 0.04 arbitrary units (AU); P < 0.01], tubulointerstitial fibrosis (TIFI; ND, 0.04 +/- 0.04; D, 0.68 +/- 0.2 AU; P < 0.01), and transforming growth factor-beta (TGF-beta) protein expression (ND, 0.61 +/- 0.02; D, 1.25 +/- 0.07 AU; P < 0.01). |
| 3772 | 15465639 | Effects of culture with TNF-alpha, TGF-beta and insulin on sulphotransferase (SULT 1A1 and 1A3) activity in human colon and neuronal cell lines. |
| 3773 | 15465639 | The effects of cytokines (TNF-alpha and TGF-beta) and insulin on sulphotransferase (SULT 1A1 and 1A3) activity were studied in a human neuronal cell line (SK-N-SH) and a human gastrointestinal tract cell line (HT-29). |
| 3774 | 15465639 | Cells were cultured with varying concentrations of TNF-alpha, TGF-beta or insulin for 24 h; the SULT 1A1 isoform in the 2 cell lines showed different optimal substrate concentrations. |
| 3775 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 3776 | 15465639 | Effects of culture with TNF-alpha, TGF-beta and insulin on sulphotransferase (SULT 1A1 and 1A3) activity in human colon and neuronal cell lines. |
| 3777 | 15465639 | The effects of cytokines (TNF-alpha and TGF-beta) and insulin on sulphotransferase (SULT 1A1 and 1A3) activity were studied in a human neuronal cell line (SK-N-SH) and a human gastrointestinal tract cell line (HT-29). |
| 3778 | 15465639 | Cells were cultured with varying concentrations of TNF-alpha, TGF-beta or insulin for 24 h; the SULT 1A1 isoform in the 2 cell lines showed different optimal substrate concentrations. |
| 3779 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 3780 | 15465639 | Effects of culture with TNF-alpha, TGF-beta and insulin on sulphotransferase (SULT 1A1 and 1A3) activity in human colon and neuronal cell lines. |
| 3781 | 15465639 | The effects of cytokines (TNF-alpha and TGF-beta) and insulin on sulphotransferase (SULT 1A1 and 1A3) activity were studied in a human neuronal cell line (SK-N-SH) and a human gastrointestinal tract cell line (HT-29). |
| 3782 | 15465639 | Cells were cultured with varying concentrations of TNF-alpha, TGF-beta or insulin for 24 h; the SULT 1A1 isoform in the 2 cell lines showed different optimal substrate concentrations. |
| 3783 | 15465639 | Culture with TNF-alpha increased activity of both SULT 1A1 and 1A3 in the HT-29 cells; TGF-beta also increased activities of both isoforms but to a lesser extent; insulin increased activity of SULT 1A1 only. |
| 3784 | 15466268 | HGF attenuated urine albumin and total protein excretion in diabetic mice. |
| 3785 | 15466268 | Exogenous HGF also mitigated glomerular mesangial expansion, reduced fibronectin and type I collagen deposition, and prevented interstitial myofibroblast activation. |
| 3786 | 15466268 | Moreover, expression of HGF inhibited renal expression of TGF-beta1 and reduced urine level of TGF-beta1 protein. |
| 3787 | 15468055 | Distinct roles of CTLA-4 and TGF-beta in CD4+CD25+ regulatory T cell function. |
| 3788 | 15468055 | Both CTLA-4 and TGF-beta have been implicated in suppression by CD4+CD25+ regulatory T cells (Treg). |
| 3789 | 15468055 | In this study, the relationship between CTLA-4 and TGF-beta in Treg function was examined. |
| 3790 | 15468055 | These CTLA-4-deficient Treg expressed increased levels of the suppressive cytokines IL-10 and TGF-beta, and in vitro suppression mediated by CTLA-4(-/-) Treg was markedly reduced by neutralizing TGF-beta, suggesting that CTLA-4-deficient Treg develop a compensatory suppressive mechanism through CTLA-4-independent production of TGF-beta. |
| 3791 | 15468055 | Distinct roles of CTLA-4 and TGF-beta in CD4+CD25+ regulatory T cell function. |
| 3792 | 15468055 | Both CTLA-4 and TGF-beta have been implicated in suppression by CD4+CD25+ regulatory T cells (Treg). |
| 3793 | 15468055 | In this study, the relationship between CTLA-4 and TGF-beta in Treg function was examined. |
| 3794 | 15468055 | These CTLA-4-deficient Treg expressed increased levels of the suppressive cytokines IL-10 and TGF-beta, and in vitro suppression mediated by CTLA-4(-/-) Treg was markedly reduced by neutralizing TGF-beta, suggesting that CTLA-4-deficient Treg develop a compensatory suppressive mechanism through CTLA-4-independent production of TGF-beta. |
| 3795 | 15468055 | Distinct roles of CTLA-4 and TGF-beta in CD4+CD25+ regulatory T cell function. |
| 3796 | 15468055 | Both CTLA-4 and TGF-beta have been implicated in suppression by CD4+CD25+ regulatory T cells (Treg). |
| 3797 | 15468055 | In this study, the relationship between CTLA-4 and TGF-beta in Treg function was examined. |
| 3798 | 15468055 | These CTLA-4-deficient Treg expressed increased levels of the suppressive cytokines IL-10 and TGF-beta, and in vitro suppression mediated by CTLA-4(-/-) Treg was markedly reduced by neutralizing TGF-beta, suggesting that CTLA-4-deficient Treg develop a compensatory suppressive mechanism through CTLA-4-independent production of TGF-beta. |
| 3799 | 15468055 | Distinct roles of CTLA-4 and TGF-beta in CD4+CD25+ regulatory T cell function. |
| 3800 | 15468055 | Both CTLA-4 and TGF-beta have been implicated in suppression by CD4+CD25+ regulatory T cells (Treg). |
| 3801 | 15468055 | In this study, the relationship between CTLA-4 and TGF-beta in Treg function was examined. |
| 3802 | 15468055 | These CTLA-4-deficient Treg expressed increased levels of the suppressive cytokines IL-10 and TGF-beta, and in vitro suppression mediated by CTLA-4(-/-) Treg was markedly reduced by neutralizing TGF-beta, suggesting that CTLA-4-deficient Treg develop a compensatory suppressive mechanism through CTLA-4-independent production of TGF-beta. |
| 3803 | 15481803 | The latter, in turn, lead to the formation, within the brain, of proinflammatory cytokines including interleukin (IL)-1alpha, IL-1beta, IL-6, tumor necrosis factor alpha (TNF-alpha), and one or more antinflammatory cytokines including tumor growth factor beta (TGF-beta), and IL-10. |
| 3804 | 15481803 | De Simoni et al. were the first to show that the intracerebroventricular (icv) injection of IL-1beta in rats induced a dramatic increase in the concentration of circulating IL-6 that was much greater and more prolonged than that induced by intravenous bolus injection of the same dose of cytokine. |
| 3805 | 15481803 | Although IL-6, TNF-alpha and LPS are passively transferred from brain to blood (as shown by radioiodine-labeled tracer studies) peripheral cytokine responses to central injection differ from responses to IL-1beta. |
| 3806 | 15504962 | Interplay of glucagon-like peptide-1 and transforming growth factor-beta signaling in insulin-positive differentiation of AR42J cells. |
| 3807 | 15504962 | Exogenous activin, possibly working through intracellular smad 2 and/or smad 3, as well as exogenous exendin-4 (a long-acting glucagon-like peptide-1 agonist) have both been shown to induce insulin-positive/endocrine differentiation in AR42J cells. |
| 3808 | 15504962 | In particular, insulin-positive differentiation seems to entail an exendin-4-induced drop in smad 2 and elevation in smad 3 in RNA levels. |
| 3809 | 15504962 | The coapplication of exogenous exendin-4 and, specifically, low-dose exogenous TGF-beta1 led to a dramatic 20-fold increase in insulin mRNA levels, supporting a novel synergistic and codependent relationship between exendin-4 signaling and TGF-beta isoform signaling. |
| 3810 | 15504962 | Interplay of glucagon-like peptide-1 and transforming growth factor-beta signaling in insulin-positive differentiation of AR42J cells. |
| 3811 | 15504962 | Exogenous activin, possibly working through intracellular smad 2 and/or smad 3, as well as exogenous exendin-4 (a long-acting glucagon-like peptide-1 agonist) have both been shown to induce insulin-positive/endocrine differentiation in AR42J cells. |
| 3812 | 15504962 | In particular, insulin-positive differentiation seems to entail an exendin-4-induced drop in smad 2 and elevation in smad 3 in RNA levels. |
| 3813 | 15504962 | The coapplication of exogenous exendin-4 and, specifically, low-dose exogenous TGF-beta1 led to a dramatic 20-fold increase in insulin mRNA levels, supporting a novel synergistic and codependent relationship between exendin-4 signaling and TGF-beta isoform signaling. |
| 3814 | 15504975 | Podocyte-derived vascular endothelial growth factor mediates the stimulation of alpha3(IV) collagen production by transforming growth factor-beta1 in mouse podocytes. |
| 3815 | 15504975 | Exogenous VEGF(164) increased the production of alpha3(IV) collagen, an integral component of the glomerular basement membrane (GBM); this effect was completely prevented by SU5416, a pan-VEGF receptor inhibitor. |
| 3816 | 15504975 | The VEGF inhibitor also partially prevented the stimulation of alpha3(IV) collagen by transforming growth factor (TGF)-beta1, establishing a novel role for endogenous VEGF. |
| 3817 | 15504975 | However, VEGF did not influence the production of another novel chain of collagen IV, alpha5(IV) collagen, and SU5416 failed to reverse the known inhibitory effect of TGF-beta1 on alpha5(IV) collagen production. |
| 3818 | 15504975 | VEGF signaling proceeds via autophosphorylation of VEGFR-1 and activation of the phosphatidylinositol 3-kinase (PI3K) pathway. |
| 3819 | 15504975 | Thus, podocyte-derived VEGF operates in an autocrine loop, likely through VEGFR-1 and PI3K, to stimulate alpha3(IV) collagen production. |
| 3820 | 15504975 | Podocyte-derived vascular endothelial growth factor mediates the stimulation of alpha3(IV) collagen production by transforming growth factor-beta1 in mouse podocytes. |
| 3821 | 15504975 | Exogenous VEGF(164) increased the production of alpha3(IV) collagen, an integral component of the glomerular basement membrane (GBM); this effect was completely prevented by SU5416, a pan-VEGF receptor inhibitor. |
| 3822 | 15504975 | The VEGF inhibitor also partially prevented the stimulation of alpha3(IV) collagen by transforming growth factor (TGF)-beta1, establishing a novel role for endogenous VEGF. |
| 3823 | 15504975 | However, VEGF did not influence the production of another novel chain of collagen IV, alpha5(IV) collagen, and SU5416 failed to reverse the known inhibitory effect of TGF-beta1 on alpha5(IV) collagen production. |
| 3824 | 15504975 | VEGF signaling proceeds via autophosphorylation of VEGFR-1 and activation of the phosphatidylinositol 3-kinase (PI3K) pathway. |
| 3825 | 15504975 | Thus, podocyte-derived VEGF operates in an autocrine loop, likely through VEGFR-1 and PI3K, to stimulate alpha3(IV) collagen production. |
| 3826 | 15504980 | Overexpression of transforming growth factor-beta1, mesangial cell transdifferentiation by expression of alpha-smooth muscle actin, and aberrant deposition of collagen type IV, fibronectin, and laminin were found in classic diabetic glomerulopathy. |
| 3827 | 15509792 | Therefore, to investigate the mechanism of Wt1 R394W-induced renal failure, the expression of genes whose deletion leads to glomerulosclerosis (NPHS1, NPHS2, and CD2AP) was quantitated. |
| 3828 | 15509792 | In mutant kidneys, NPHS1 and NPHS2 were only moderately downregulated (25 to 30%) at birth but not at 2 or 4 months. |
| 3829 | 15509792 | Two other genes implicated in glomerulosclerosis, TGFB1 and IGF1, were upregulated at 2 months and at 2 and 4 months, respectively. |
| 3830 | 15509792 | However, the data do suggest that Wt1 R394W-induced glomerulosclerosis may be independent of downregulation of the genes for NPHS1, NPHS2, CD2AP, and podocalyxin and may involve other genes yet to be implicated in renal failure. |
| 3831 | 15526251 | Renin-angiotensin system blockade prevents the increase in plasma transforming growth factor beta 1, and reduces proteinuria and kidney hypertrophy in the streptozotocin-diabetic rat. |
| 3832 | 15533578 | However, it is not known whether they are also involved in the homeostasis of intracellular fibronectin content via upregulation of protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and transforming growth factor-beta1 (TGF-beta1). |
| 3833 | 15533578 | To determine this, we have studied the effect of multiple amines on fibronectin, TGF-beta1, ERK, and PKC levels in mesangial cells under high glucose conditions. |
| 3834 | 15533578 | Agmatine reduced TGF-beta1 and ERK levels but not PKC at concentrations of 0.1-1 mM. |
| 3835 | 15533578 | However, levels of fibronectin, TGF-beta1, ERK, and PKC were unaffected by either putrescine or spermidine. |
| 3836 | 15533578 | A decrease in fibronectin secretion was accompanied by decreases in TGF-beta1 and ERK. |
| 3837 | 15533578 | However, it is not known whether they are also involved in the homeostasis of intracellular fibronectin content via upregulation of protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and transforming growth factor-beta1 (TGF-beta1). |
| 3838 | 15533578 | To determine this, we have studied the effect of multiple amines on fibronectin, TGF-beta1, ERK, and PKC levels in mesangial cells under high glucose conditions. |
| 3839 | 15533578 | Agmatine reduced TGF-beta1 and ERK levels but not PKC at concentrations of 0.1-1 mM. |
| 3840 | 15533578 | However, levels of fibronectin, TGF-beta1, ERK, and PKC were unaffected by either putrescine or spermidine. |
| 3841 | 15533578 | A decrease in fibronectin secretion was accompanied by decreases in TGF-beta1 and ERK. |
| 3842 | 15533578 | However, it is not known whether they are also involved in the homeostasis of intracellular fibronectin content via upregulation of protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and transforming growth factor-beta1 (TGF-beta1). |
| 3843 | 15533578 | To determine this, we have studied the effect of multiple amines on fibronectin, TGF-beta1, ERK, and PKC levels in mesangial cells under high glucose conditions. |
| 3844 | 15533578 | Agmatine reduced TGF-beta1 and ERK levels but not PKC at concentrations of 0.1-1 mM. |
| 3845 | 15533578 | However, levels of fibronectin, TGF-beta1, ERK, and PKC were unaffected by either putrescine or spermidine. |
| 3846 | 15533578 | A decrease in fibronectin secretion was accompanied by decreases in TGF-beta1 and ERK. |
| 3847 | 15533578 | However, it is not known whether they are also involved in the homeostasis of intracellular fibronectin content via upregulation of protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and transforming growth factor-beta1 (TGF-beta1). |
| 3848 | 15533578 | To determine this, we have studied the effect of multiple amines on fibronectin, TGF-beta1, ERK, and PKC levels in mesangial cells under high glucose conditions. |
| 3849 | 15533578 | Agmatine reduced TGF-beta1 and ERK levels but not PKC at concentrations of 0.1-1 mM. |
| 3850 | 15533578 | However, levels of fibronectin, TGF-beta1, ERK, and PKC were unaffected by either putrescine or spermidine. |
| 3851 | 15533578 | A decrease in fibronectin secretion was accompanied by decreases in TGF-beta1 and ERK. |
| 3852 | 15533578 | However, it is not known whether they are also involved in the homeostasis of intracellular fibronectin content via upregulation of protein kinase C (PKC), extracellular signal-regulated kinase (ERK), and transforming growth factor-beta1 (TGF-beta1). |
| 3853 | 15533578 | To determine this, we have studied the effect of multiple amines on fibronectin, TGF-beta1, ERK, and PKC levels in mesangial cells under high glucose conditions. |
| 3854 | 15533578 | Agmatine reduced TGF-beta1 and ERK levels but not PKC at concentrations of 0.1-1 mM. |
| 3855 | 15533578 | However, levels of fibronectin, TGF-beta1, ERK, and PKC were unaffected by either putrescine or spermidine. |
| 3856 | 15533578 | A decrease in fibronectin secretion was accompanied by decreases in TGF-beta1 and ERK. |
| 3857 | 15536593 | OLETF rats showed glomerular hyperfiltration (an increase in creatinine clearance and a decrease in fractional excretion of Na) and microalbuminuria at the insulin-resistant prediabetic stage, and both were related to expression of transforming growth factor (TGF)-beta(1) and extracellular matrix protein such as fibronectin and collagen (a(1)) IV. |
| 3858 | 15536593 | Cilostazol, a selective type III cyclic nucleotide phosphodiesterase (PDE) inhibitor, normalized glomerular hyperfiltration and microalbuminuria with a parallel decline of TGF-beta(1) and extracellular matrix protein mRNA expression. |
| 3859 | 15544523 | The involvement of growth hormone (GH), insulin-like growth factors (IGFs) and vascular endothelial growth factor (VEGF) in diabetic kidney disease. |
| 3860 | 15544523 | These include metabolic factors beyond blood glucose (e.g. advanced glycation endproducts (AGEs)), haemodynamic factors (e.g. the renin angiotensin system (RAS)), intracellular signaling molecule proteins (e.g. protein kinase C (PKC)) and growth factors/cytokines (e.g. growth hormone (GH), insulin-like growth factors (IGFs), transforming growth factor beta (TGF-beta) and vascular endothelial growth factor (VEGF)). |
| 3861 | 15546028 | Plasma transforming growth factor-beta1 levels in patients with erectile dysfunction. |
| 3862 | 15579446 | Advanced glycation end-products induce connective tissue growth factor-mediated renal fibrosis predominantly through transforming growth factor beta-independent pathway. |
| 3863 | 15579446 | AGE treatment also caused significant increases in renal CTGF and transforming growth factor (TGF)-beta 1 mRNA and protein expression. |
| 3864 | 15579446 | AGE treatment also significantly increased both TGF-beta 1 and CTGF mRNA expression; however, inhibition of TGF-beta 1 mRNA expression by shRNA or neutralization of TGF-beta 1 protein by anti-TGF-beta 1 antibody did not significantly prevent AGE-increased expression of CTGF mRNA and protein. |
| 3865 | 15579446 | These results suggest that AGE-induced CTGF expression, predominantly through a TGF-beta 1-independent pathway, plays a critical role in renal ECM accumulation leading to diabetic nephropathy. |
| 3866 | 15579446 | Advanced glycation end-products induce connective tissue growth factor-mediated renal fibrosis predominantly through transforming growth factor beta-independent pathway. |
| 3867 | 15579446 | AGE treatment also caused significant increases in renal CTGF and transforming growth factor (TGF)-beta 1 mRNA and protein expression. |
| 3868 | 15579446 | AGE treatment also significantly increased both TGF-beta 1 and CTGF mRNA expression; however, inhibition of TGF-beta 1 mRNA expression by shRNA or neutralization of TGF-beta 1 protein by anti-TGF-beta 1 antibody did not significantly prevent AGE-increased expression of CTGF mRNA and protein. |
| 3869 | 15579446 | These results suggest that AGE-induced CTGF expression, predominantly through a TGF-beta 1-independent pathway, plays a critical role in renal ECM accumulation leading to diabetic nephropathy. |
| 3870 | 15579446 | Advanced glycation end-products induce connective tissue growth factor-mediated renal fibrosis predominantly through transforming growth factor beta-independent pathway. |
| 3871 | 15579446 | AGE treatment also caused significant increases in renal CTGF and transforming growth factor (TGF)-beta 1 mRNA and protein expression. |
| 3872 | 15579446 | AGE treatment also significantly increased both TGF-beta 1 and CTGF mRNA expression; however, inhibition of TGF-beta 1 mRNA expression by shRNA or neutralization of TGF-beta 1 protein by anti-TGF-beta 1 antibody did not significantly prevent AGE-increased expression of CTGF mRNA and protein. |
| 3873 | 15579446 | These results suggest that AGE-induced CTGF expression, predominantly through a TGF-beta 1-independent pathway, plays a critical role in renal ECM accumulation leading to diabetic nephropathy. |
| 3874 | 15583025 | Furthermore, the contribution of hemodynamic factors, the renin-angiotensin system, the endothelin system, and the nitric oxide system, as well as the prominent role of the intracellular signaling molecule protein kinase C are discussed. |
| 3875 | 15583025 | Finally, the respective roles of TGF-beta, GH and IGFs, vascular endothelial growth factor, and platelet-derived growth factor are covered. |
| 3876 | 15598843 | Other related changes observed in the PTCs that could be reversed by treatment with either aminoguanidine, pyridoxamine, rotenone, apocynin, or DPI included an increase in transforming growth factor-beta1 secretion and the activation of the NF-kappaB signal transduction pathway. |
| 3877 | 15615821 | It is interesting that direct treatment of RMC with 12(S)-HETE increased TGF-beta mRNA and protein levels, as well as p-Smad2/3, which are TGF-beta-specific target transcription factors. 12(S)-HETE also increased transcription from a minimal TGF-beta promoter. |
| 3878 | 15615821 | Furthermore, TGF-beta expression and p-Smad2/3 levels were lower in MC from 12/15-LO knockout mice relative to control mice. |
| 3879 | 15615821 | Reciprocally, mouse MC stably overexpressing 12/15-LO had greater TGF-beta mRNA and also nuclear p-Smad2/3 relative to mock-transfected cells. 12/15-LO and TGF-beta could functionally signal and increase ECM expression via the p38 mitogen-activated protein kinase signaling pathway. |
| 3880 | 15615821 | It is interesting that direct treatment of RMC with 12(S)-HETE increased TGF-beta mRNA and protein levels, as well as p-Smad2/3, which are TGF-beta-specific target transcription factors. 12(S)-HETE also increased transcription from a minimal TGF-beta promoter. |
| 3881 | 15615821 | Furthermore, TGF-beta expression and p-Smad2/3 levels were lower in MC from 12/15-LO knockout mice relative to control mice. |
| 3882 | 15615821 | Reciprocally, mouse MC stably overexpressing 12/15-LO had greater TGF-beta mRNA and also nuclear p-Smad2/3 relative to mock-transfected cells. 12/15-LO and TGF-beta could functionally signal and increase ECM expression via the p38 mitogen-activated protein kinase signaling pathway. |
| 3883 | 15615821 | It is interesting that direct treatment of RMC with 12(S)-HETE increased TGF-beta mRNA and protein levels, as well as p-Smad2/3, which are TGF-beta-specific target transcription factors. 12(S)-HETE also increased transcription from a minimal TGF-beta promoter. |
| 3884 | 15615821 | Furthermore, TGF-beta expression and p-Smad2/3 levels were lower in MC from 12/15-LO knockout mice relative to control mice. |
| 3885 | 15615821 | Reciprocally, mouse MC stably overexpressing 12/15-LO had greater TGF-beta mRNA and also nuclear p-Smad2/3 relative to mock-transfected cells. 12/15-LO and TGF-beta could functionally signal and increase ECM expression via the p38 mitogen-activated protein kinase signaling pathway. |
| 3886 | 15616013 | Treatment with granulocyte colony-stimulating factor prevents diabetes in NOD mice by recruiting plasmacytoid dendritic cells and functional CD4(+)CD25(+) regulatory T-cells. |
| 3887 | 15616013 | Accumulating evidence that granulocyte colony-stimulating factor (G-CSF), the key hematopoietic growth factor of the myeloid lineage, not only represents a major component of the endogenous response to infections, but also affects adaptive immune responses, prompted us to investigate the therapeutic potential of G-CSF in autoimmune type 1 diabetes. |
| 3888 | 15616013 | G-CSF recipients further displayed accumulation of functional CD4(+)CD25(+) regulatory T-cells that produce transforming growth factor-beta1 (TGF-beta1) and actively suppressed diabetes transfer by diabetogenic effector cells in secondary NOD-SCID recipients. |
| 3889 | 15616013 | G-CSF's ability to promote key tolerogenic interactions between DCs and regulatory T-cells was demonstrated by enhanced recruitment of TGF-beta1-expressing CD4(+)CD25(+) cells after adoptive transfer of DCs isolated from G-CSF- relative to vehicle-treated mice into naive NOD recipients. |
| 3890 | 15616035 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor. |
| 3891 | 15616035 | In the present study, we demonstrated for the first time that the expression of PEDF was decreased at both the mRNA and protein levels in the kidney of diabetic rats, whereas transforming growth factor-beta (TGF-beta) and fibronectin levels were increased in the same diabetic kidneys. |
| 3892 | 15616035 | Toward the function of PEDF, we showed that PEDF blocked the high-glucose-induced overexpression of TGF-beta, a major pathogenic factor in diabetic nephropathy, and fibronectin in primary HMCs, suggesting that PEDF may function as an endogenous inhibitor of TGF-beta expression and fibronectin production in glomeruli. |
| 3893 | 15616035 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor. |
| 3894 | 15616035 | In the present study, we demonstrated for the first time that the expression of PEDF was decreased at both the mRNA and protein levels in the kidney of diabetic rats, whereas transforming growth factor-beta (TGF-beta) and fibronectin levels were increased in the same diabetic kidneys. |
| 3895 | 15616035 | Toward the function of PEDF, we showed that PEDF blocked the high-glucose-induced overexpression of TGF-beta, a major pathogenic factor in diabetic nephropathy, and fibronectin in primary HMCs, suggesting that PEDF may function as an endogenous inhibitor of TGF-beta expression and fibronectin production in glomeruli. |
| 3896 | 15622443 | TNF-alpha, TGF-beta1, IL-10, IL-6, gene polymorphisms in latent autoimmune diabetes of adults (LADA) and type 2 diabetes mellitus. |
| 3897 | 15622443 | In this study, healthy individuals LADA and type 2 diabetic patients were genotyped for IL-6-174G/C, TNF-alpha-308A/G, TGF-beta1-codon10T/C, TGF-beta1-codon25G/C, IL-10-1082A/G, IL-10-819T/C, IL-10-592A/C gene polymorphisms, by sequence-specific-primer polymerase chain reaction methodology. |
| 3898 | 15637419 | Concentration of transforming growth factor beta2 in aqueous humor. |
| 3899 | 15637419 | It was found that the total TGF-beta(2) concentration (1) decreases with age, (2) shows slight changes with axial length, (3) has slight changes with difference of localization of opacification, (4) is significantly high in patients with concurrent open-angle glaucoma (p < 0.05), (5) is high in patients with complicating diabetes who have undergone panretinal photocoagulation for diabetic retinopathy (p < 0.05) and (6) is low in patients with atopic cataracts. |
| 3900 | 15637419 | These findings provide useful information on the intraocular activity of TGF-beta(2). |
| 3901 | 15637419 | Concentration of transforming growth factor beta2 in aqueous humor. |
| 3902 | 15637419 | It was found that the total TGF-beta(2) concentration (1) decreases with age, (2) shows slight changes with axial length, (3) has slight changes with difference of localization of opacification, (4) is significantly high in patients with concurrent open-angle glaucoma (p < 0.05), (5) is high in patients with complicating diabetes who have undergone panretinal photocoagulation for diabetic retinopathy (p < 0.05) and (6) is low in patients with atopic cataracts. |
| 3903 | 15637419 | These findings provide useful information on the intraocular activity of TGF-beta(2). |
| 3904 | 15677501 | Bone marrow (BM) was cultured in granulocyte macrophage colony-stimulating factor (GM-CSF) and transforming growth factor-beta1, a cytokine combination that expands myeloid cells but inhibits terminal DC differentiation, to yield Gr-1(+)/CD11b(+)/CD11c(-) myeloid progenitor cells and a minor population of CD11c(+)/CD11b(+)/CD86(lo) immature DCs. |
| 3905 | 15677501 | After transfer, Gr-1(+) myeloid cells acquired the characteristics of resting DCs (CD11c(+)/MHC classII(int)/CD86(lo)/CD40(lo)). |
| 3906 | 15677501 | Gr-1(+) myeloid cells generated from transgenic NOD mice that expressed proinsulin controlled by a major histocompatibility complex (MHC) class II promoter, but not from wild-type NOD mice, transferred into 4-week-old female NOD mice significantly suppressed diabetes development. |
| 3907 | 15689403 | Exposure of CF to pioglitazone caused an antiproliferative (P < 0.0001) and hypertrophic (P < 0.0001) effect; reduced type IV collagen secretion (P < 0.01), fibronectin secretion (P < 0.0001), and proline incorporation (P < 0.0001); decreased MMP-9 activity (P < 0.05); and reduced tissue inhibitor of metalloproteinase-1 (TIMP-1) and TIMP-2 secretion (P < 0.001 and P < 0.0001, respectively). |
| 3908 | 15689403 | Exposure of CF to high glucose conditions induced an increase in the expression of collagen IV (P < 0.05), which was reversed both in the presence of pioglitazone (1 and 3 muM) and by L-805645. |
| 3909 | 15689403 | In summary, exposure of human CF to pioglitazone causes an antiproliferative effect and reduces ECM production through mechanisms that include reducing TIMP activity, independent of TGF-beta1. |
| 3910 | 15692059 | The present study examined the influence of streptozotocin-induced diabetes on the renal expression of bradykinin (BK) B2 receptors (B2KR), connective tissue growth factor (CTGF), transforming growth factor-beta (TGF-beta), and TGF-beta type II receptor (TGF-betaRII) and assessed the signaling mechanisms through which B2KR activation may promote glomerular injury. |
| 3911 | 15692059 | Eight weeks after the induction of diabetes, renal mRNA levels of B2KR, CTGF, and TGF-beta as well as protein levels of CTGF and TGF-betaRII were measured in control (C), diabetic (D), and insulin-treated diabetic (D+I) rats. |
| 3912 | 15692059 | Renal B2KR and TGF-beta mRNA levels expressed relative to beta-actin mRNA levels and CTGF and TGF-betaRII protein levels were significantly increased in D and D+I rats compared with C rats (P < 0.03, n = 5). |
| 3913 | 15692059 | To assess the contribution of B2KR activation on modulating the expression of CTGF, TGF-betaRII, and collagen I, mesangial cells (MC) were treated with BK (10(-8) M) for 24 h and CTGF and TGF-betaRII protein levels were measured by Western blots and collagen I mRNA levels were measured by RT-PCR. |
| 3914 | 15692059 | In addition, a marked increase in collagen I mRNA levels was observed in response to BK stimulation. |
| 3915 | 15692059 | Treatment of MC with BK (10(-8) M) for 5 min significantly increased the tyrosine phosphorylation of p60src kinase and of p42/p44 MAPK (P < 0.05, n = 4). |
| 3916 | 15692059 | Inhibition of src kinase by PP1 (10 microM) inhibited the increase in p42/p44 MAPK activation in response to BK. |
| 3917 | 15692059 | Finally, to determine whether BK stimulates CTGF, TGF-betaRII, and collagen I expression via activation of MAPK pathways, MC were pretreated with an inhibitor of p42/p44 MAPK (PD-98059) for 45 min, followed by BK (10(-8) M) stimulation for 24 h. |
| 3918 | 15692059 | Selective inhibition of p42/p44 MAPK significantly inhibited the BK-induced increase in CTGF, TGF-betaRII, and collagen I levels. |
| 3919 | 15692059 | These findings are the first to demonstrate that BK regulates the expression of CTGF, TGF-betaRII, and collagen I in MC and provide a mechanistic pathway through which B2KR activation may contribute to the development of diabetic nephropathy. |
| 3920 | 15692059 | The present study examined the influence of streptozotocin-induced diabetes on the renal expression of bradykinin (BK) B2 receptors (B2KR), connective tissue growth factor (CTGF), transforming growth factor-beta (TGF-beta), and TGF-beta type II receptor (TGF-betaRII) and assessed the signaling mechanisms through which B2KR activation may promote glomerular injury. |
| 3921 | 15692059 | Eight weeks after the induction of diabetes, renal mRNA levels of B2KR, CTGF, and TGF-beta as well as protein levels of CTGF and TGF-betaRII were measured in control (C), diabetic (D), and insulin-treated diabetic (D+I) rats. |
| 3922 | 15692059 | Renal B2KR and TGF-beta mRNA levels expressed relative to beta-actin mRNA levels and CTGF and TGF-betaRII protein levels were significantly increased in D and D+I rats compared with C rats (P < 0.03, n = 5). |
| 3923 | 15692059 | To assess the contribution of B2KR activation on modulating the expression of CTGF, TGF-betaRII, and collagen I, mesangial cells (MC) were treated with BK (10(-8) M) for 24 h and CTGF and TGF-betaRII protein levels were measured by Western blots and collagen I mRNA levels were measured by RT-PCR. |
| 3924 | 15692059 | In addition, a marked increase in collagen I mRNA levels was observed in response to BK stimulation. |
| 3925 | 15692059 | Treatment of MC with BK (10(-8) M) for 5 min significantly increased the tyrosine phosphorylation of p60src kinase and of p42/p44 MAPK (P < 0.05, n = 4). |
| 3926 | 15692059 | Inhibition of src kinase by PP1 (10 microM) inhibited the increase in p42/p44 MAPK activation in response to BK. |
| 3927 | 15692059 | Finally, to determine whether BK stimulates CTGF, TGF-betaRII, and collagen I expression via activation of MAPK pathways, MC were pretreated with an inhibitor of p42/p44 MAPK (PD-98059) for 45 min, followed by BK (10(-8) M) stimulation for 24 h. |
| 3928 | 15692059 | Selective inhibition of p42/p44 MAPK significantly inhibited the BK-induced increase in CTGF, TGF-betaRII, and collagen I levels. |
| 3929 | 15692059 | These findings are the first to demonstrate that BK regulates the expression of CTGF, TGF-betaRII, and collagen I in MC and provide a mechanistic pathway through which B2KR activation may contribute to the development of diabetic nephropathy. |
| 3930 | 15692059 | The present study examined the influence of streptozotocin-induced diabetes on the renal expression of bradykinin (BK) B2 receptors (B2KR), connective tissue growth factor (CTGF), transforming growth factor-beta (TGF-beta), and TGF-beta type II receptor (TGF-betaRII) and assessed the signaling mechanisms through which B2KR activation may promote glomerular injury. |
| 3931 | 15692059 | Eight weeks after the induction of diabetes, renal mRNA levels of B2KR, CTGF, and TGF-beta as well as protein levels of CTGF and TGF-betaRII were measured in control (C), diabetic (D), and insulin-treated diabetic (D+I) rats. |
| 3932 | 15692059 | Renal B2KR and TGF-beta mRNA levels expressed relative to beta-actin mRNA levels and CTGF and TGF-betaRII protein levels were significantly increased in D and D+I rats compared with C rats (P < 0.03, n = 5). |
| 3933 | 15692059 | To assess the contribution of B2KR activation on modulating the expression of CTGF, TGF-betaRII, and collagen I, mesangial cells (MC) were treated with BK (10(-8) M) for 24 h and CTGF and TGF-betaRII protein levels were measured by Western blots and collagen I mRNA levels were measured by RT-PCR. |
| 3934 | 15692059 | In addition, a marked increase in collagen I mRNA levels was observed in response to BK stimulation. |
| 3935 | 15692059 | Treatment of MC with BK (10(-8) M) for 5 min significantly increased the tyrosine phosphorylation of p60src kinase and of p42/p44 MAPK (P < 0.05, n = 4). |
| 3936 | 15692059 | Inhibition of src kinase by PP1 (10 microM) inhibited the increase in p42/p44 MAPK activation in response to BK. |
| 3937 | 15692059 | Finally, to determine whether BK stimulates CTGF, TGF-betaRII, and collagen I expression via activation of MAPK pathways, MC were pretreated with an inhibitor of p42/p44 MAPK (PD-98059) for 45 min, followed by BK (10(-8) M) stimulation for 24 h. |
| 3938 | 15692059 | Selective inhibition of p42/p44 MAPK significantly inhibited the BK-induced increase in CTGF, TGF-betaRII, and collagen I levels. |
| 3939 | 15692059 | These findings are the first to demonstrate that BK regulates the expression of CTGF, TGF-betaRII, and collagen I in MC and provide a mechanistic pathway through which B2KR activation may contribute to the development of diabetic nephropathy. |
| 3940 | 15699123 | These experiments reveal that cytokines such as IL-4, IL-10, IL-13, and TGF-beta, that have been involved in other functions of NKT cells, play only a minor role if any in the blockade of T cell differentiation by NKT cells. |
| 3941 | 15699123 | Diabetes is still prevented by NKT cells in the absence of functional IL-4, IL-10, IL-13, and TGF-beta. |
| 3942 | 15699123 | These experiments reveal that cytokines such as IL-4, IL-10, IL-13, and TGF-beta, that have been involved in other functions of NKT cells, play only a minor role if any in the blockade of T cell differentiation by NKT cells. |
| 3943 | 15699123 | Diabetes is still prevented by NKT cells in the absence of functional IL-4, IL-10, IL-13, and TGF-beta. |
| 3944 | 15703175 | Na+/Ca2+ exchanger activity modulates connective tissue growth factor mRNA expression in transforming growth factor beta1- and Des-Arg10-kallidin-stimulated myofibroblasts. |
| 3945 | 15703175 | Transforming growth factor (TGF)-beta and des-Arg(10)-kallidin stimulate the expression of connective tissue growth factor (CTGF), a matrix signaling molecule that is frequently overexpressed in fibrotic disorders. |
| 3946 | 15703175 | Because the early signal transduction events regulating CTGF expression are unclear, we investigated the role of Ca(2+) homeostasis in CTGF mRNA expression in TGF-beta1- and des-Arg(10)-kallidin-stimulated human lung myofibroblasts. |
| 3947 | 15703175 | We also found that KB-R7943 or 2',4'-dichlorobenzamil, an amiloride analog that inhibits the Na(+)/Ca(2+) exchanger activity, blocked the TGF-beta1- and des-Arg(10)-kallidin-stimulated increases of CTGF mRNA. |
| 3948 | 15703175 | Pretreatment with KB-R7943 also reduced the basal and TGF-beta1-stimulated levels of alpha1(I) collagen and alpha smooth muscle actin mRNAs. |
| 3949 | 15703175 | These data suggest that, in addition to regulating ion homeostasis, Na(+)/Ca(2+) exchanger acts as a signal transducer regulating CTGF, alpha1(I) collagen, and alpha smooth muscle actin expression. |
| 3950 | 15703175 | Na+/Ca2+ exchanger activity modulates connective tissue growth factor mRNA expression in transforming growth factor beta1- and Des-Arg10-kallidin-stimulated myofibroblasts. |
| 3951 | 15703175 | Transforming growth factor (TGF)-beta and des-Arg(10)-kallidin stimulate the expression of connective tissue growth factor (CTGF), a matrix signaling molecule that is frequently overexpressed in fibrotic disorders. |
| 3952 | 15703175 | Because the early signal transduction events regulating CTGF expression are unclear, we investigated the role of Ca(2+) homeostasis in CTGF mRNA expression in TGF-beta1- and des-Arg(10)-kallidin-stimulated human lung myofibroblasts. |
| 3953 | 15703175 | We also found that KB-R7943 or 2',4'-dichlorobenzamil, an amiloride analog that inhibits the Na(+)/Ca(2+) exchanger activity, blocked the TGF-beta1- and des-Arg(10)-kallidin-stimulated increases of CTGF mRNA. |
| 3954 | 15703175 | Pretreatment with KB-R7943 also reduced the basal and TGF-beta1-stimulated levels of alpha1(I) collagen and alpha smooth muscle actin mRNAs. |
| 3955 | 15703175 | These data suggest that, in addition to regulating ion homeostasis, Na(+)/Ca(2+) exchanger acts as a signal transducer regulating CTGF, alpha1(I) collagen, and alpha smooth muscle actin expression. |
| 3956 | 15703175 | Na+/Ca2+ exchanger activity modulates connective tissue growth factor mRNA expression in transforming growth factor beta1- and Des-Arg10-kallidin-stimulated myofibroblasts. |
| 3957 | 15703175 | Transforming growth factor (TGF)-beta and des-Arg(10)-kallidin stimulate the expression of connective tissue growth factor (CTGF), a matrix signaling molecule that is frequently overexpressed in fibrotic disorders. |
| 3958 | 15703175 | Because the early signal transduction events regulating CTGF expression are unclear, we investigated the role of Ca(2+) homeostasis in CTGF mRNA expression in TGF-beta1- and des-Arg(10)-kallidin-stimulated human lung myofibroblasts. |
| 3959 | 15703175 | We also found that KB-R7943 or 2',4'-dichlorobenzamil, an amiloride analog that inhibits the Na(+)/Ca(2+) exchanger activity, blocked the TGF-beta1- and des-Arg(10)-kallidin-stimulated increases of CTGF mRNA. |
| 3960 | 15703175 | Pretreatment with KB-R7943 also reduced the basal and TGF-beta1-stimulated levels of alpha1(I) collagen and alpha smooth muscle actin mRNAs. |
| 3961 | 15703175 | These data suggest that, in addition to regulating ion homeostasis, Na(+)/Ca(2+) exchanger acts as a signal transducer regulating CTGF, alpha1(I) collagen, and alpha smooth muscle actin expression. |
| 3962 | 15712349 | In an effort to identify genetic polymorphisms in potential candidate genes for type 2 diabetes mellitus (T2DM), we have sequenced the transforming growth factor beta-induced gene (TGFBI), and examined the association with T2DM and diabetic phenotypes in a Korean T2DM study (775 T2DM patients and 316 normal controls). |
| 3963 | 15712349 | The present study provides, for the first time, information about genetic polymorphisms in TGFBI and positive associations of those polymorphisms with levels of insulin and BMI in the Korean population. |
| 3964 | 15721303 | High levels of glucose also increase EDB(+) FN expression in endothelial cells (ECs) via transforming growth factor-beta1 (TGF-beta1) and endothelin-1 (ET-1). |
| 3965 | 15721303 | Using human macro- and microvascular ECs, we show that high levels of glucose, TGF-beta1, and ET-1 increase the EDB(+) FN expression via SGK-1 alteration at the mRNA, protein, and activity levels. |
| 3966 | 15721303 | Inhibition of TGF-beta1 and ET-1 prevented glucose-induced SGK-1 activation and the EDB(+) FN expression. |
| 3967 | 15721303 | High levels of glucose also increase EDB(+) FN expression in endothelial cells (ECs) via transforming growth factor-beta1 (TGF-beta1) and endothelin-1 (ET-1). |
| 3968 | 15721303 | Using human macro- and microvascular ECs, we show that high levels of glucose, TGF-beta1, and ET-1 increase the EDB(+) FN expression via SGK-1 alteration at the mRNA, protein, and activity levels. |
| 3969 | 15721303 | Inhibition of TGF-beta1 and ET-1 prevented glucose-induced SGK-1 activation and the EDB(+) FN expression. |
| 3970 | 15721303 | High levels of glucose also increase EDB(+) FN expression in endothelial cells (ECs) via transforming growth factor-beta1 (TGF-beta1) and endothelin-1 (ET-1). |
| 3971 | 15721303 | Using human macro- and microvascular ECs, we show that high levels of glucose, TGF-beta1, and ET-1 increase the EDB(+) FN expression via SGK-1 alteration at the mRNA, protein, and activity levels. |
| 3972 | 15721303 | Inhibition of TGF-beta1 and ET-1 prevented glucose-induced SGK-1 activation and the EDB(+) FN expression. |
| 3973 | 15734860 | Pioglitazone induces vascular smooth muscle cell apoptosis through a peroxisome proliferator-activated receptor-gamma, transforming growth factor-beta1, and a Smad2-dependent mechanism. |
| 3974 | 15734860 | Extracellular TGF-beta1 levels were rapidly increased after treatment with pioglitazone in a peroxisome proliferator-activated receptor (PPAR)-gamma-dependent mechanism because this secretion was blocked by the PPAR-gamma inhibitor GW9662. |
| 3975 | 15734860 | According to our results, we propose that the apoptotic effect of pioglitazone on VSMC depends on the following sequence: PPAR-gamma activation, TGF-beta1 release, and selective phospho-Smad2 nuclear recruitment. |
| 3976 | 15734860 | Pioglitazone induces vascular smooth muscle cell apoptosis through a peroxisome proliferator-activated receptor-gamma, transforming growth factor-beta1, and a Smad2-dependent mechanism. |
| 3977 | 15734860 | Extracellular TGF-beta1 levels were rapidly increased after treatment with pioglitazone in a peroxisome proliferator-activated receptor (PPAR)-gamma-dependent mechanism because this secretion was blocked by the PPAR-gamma inhibitor GW9662. |
| 3978 | 15734860 | According to our results, we propose that the apoptotic effect of pioglitazone on VSMC depends on the following sequence: PPAR-gamma activation, TGF-beta1 release, and selective phospho-Smad2 nuclear recruitment. |
| 3979 | 15734860 | Pioglitazone induces vascular smooth muscle cell apoptosis through a peroxisome proliferator-activated receptor-gamma, transforming growth factor-beta1, and a Smad2-dependent mechanism. |
| 3980 | 15734860 | Extracellular TGF-beta1 levels were rapidly increased after treatment with pioglitazone in a peroxisome proliferator-activated receptor (PPAR)-gamma-dependent mechanism because this secretion was blocked by the PPAR-gamma inhibitor GW9662. |
| 3981 | 15734860 | According to our results, we propose that the apoptotic effect of pioglitazone on VSMC depends on the following sequence: PPAR-gamma activation, TGF-beta1 release, and selective phospho-Smad2 nuclear recruitment. |
| 3982 | 15734863 | We have previously reported that N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP), which is a tetrapeptide hydrolyzed by ACE, inhibits the transforming growth factor-beta (TGF-beta)-induced expression of extracellular matrix proteins via inhibition of the Smad signaling in human mesangial cells. |
| 3983 | 15755259 | There were also pro-inflammatory and profibrotic responses, including increased IL-1beta (interleukin-1beta) expression in intact epidermis, TNF-alpha (tumour necrosis factor-alpha) in regions of angiogenesis, CTGF (connective tissue growth factor) in medial layers of arteries, and TGF-beta (transforming growth factor-beta) in glomerular tufts, tubular epithelial cells and interstitial endothelial cells. |
| 3984 | 15823702 | Oxidative stress and inflammatory cytokines such as monocyte chemoattractant protein 1 (MCP-1), TGF-beta, and IL-2 are supposed to play crucial roles in the pathogenesis of insulin resistance (IR). |
| 3985 | 15823702 | Tranilast is an anti-allergic drug which exerts anti-inflammatory and anti-angiogenesis effects through inhibition of expression of MCP-1, TGF-beta, and antigen-induced IL-2 lymphocyte responsiveness. |
| 3986 | 15823702 | Oxidative stress and inflammatory cytokines such as monocyte chemoattractant protein 1 (MCP-1), TGF-beta, and IL-2 are supposed to play crucial roles in the pathogenesis of insulin resistance (IR). |
| 3987 | 15823702 | Tranilast is an anti-allergic drug which exerts anti-inflammatory and anti-angiogenesis effects through inhibition of expression of MCP-1, TGF-beta, and antigen-induced IL-2 lymphocyte responsiveness. |
| 3988 | 15826820 | Using quantitative real-time PCR we could show that basal TGF-beta mRNA expression is about 2-fold decreased in end-stage renal failure patients, while expression of TNF-alpha becomes 2-fold increased, further doubling during hemodialysis. |
| 3989 | 15827346 | Compared with normal mice, diabetic Gpx1+/+ and -/- mice had a two- to threefold increase in urine albumin excretion at 2 and 4 mo of diabetes. |
| 3990 | 15827346 | At 4 mo, diabetic Gpx1+/+ and -/- mice had equivalent levels of oxidative renal injury (increased kidney reactive oxygen species, kidney lipid peroxidation, urine isoprostanes, kidney deposition of advanced glycoxidation, and nitrosylation end products) and a similar degree of glomerular damage (hypertrophy, hypercellularity, sclerosis), tubular injury (apoptosis and vimentin expression), and renal fibrosis (myofibroblasts, collagen, TGF-beta excretion). |
| 3991 | 15827346 | A lack of Gpx1 was not compensated for by increased levels of catalase or other Gpx isoforms in diabetic kidneys. |
| 3992 | 15838489 | Overexpression of transforming growth factor-beta1 correlates with increased synthesis of nitric oxide synthase in varicose veins. |
| 3993 | 15840049 | Circulating vitamin E, transforming growth factor beta1, and the association with renal disease susceptibility in two racial groups with type 2 diabetes. |
| 3994 | 15840669 | Angiotensin II stimulates alpha3(IV) collagen production in mouse podocytes via TGF-beta and VEGF signalling: implications for diabetic glomerulopathy. |
| 3995 | 15843473 | Although cell culture studies indicate that protein kinase C (PKC) mediates the expression of osteopontin, its role in the in vivo setting is unknown. |
| 3996 | 15843473 | After 12 wk, diabetic rats showed increases in osteopontin expression in tubular epithelial cells of the cortex in association with macrophage infiltration, interstitial fibrosis, and activity of TGF-beta as indicated by the expression of its receptor activated protein phospho-Smad2 (P < 0.05 for all parameters). |
| 3997 | 15850715 | GLUT-4 (glucose transporter) receptor, tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), daf-genes and PPARs (peroxisomal proliferation activator receptors) play a role in the development of insulin resistance syndrome and associated conditions. |
| 3998 | 15850715 | Long chain polyunsaturated fatty acids (LCPUFAs) increase cell membrane fluidity and enhance the number of insulin receptors and the affinity of insulin to its receptors; suppress TNF-alpha, IL-6, macrophage migration inhibitory factor (MIF) and leptin synthesis; increase the number of GLUT-4 receptors, serve as endogenous ligands of PPARs, modify lipolysis, and regulate the balance between pro- and anti-oxidants, and thus, play a critical role in the pathogenesis of insulin resistance. |
| 3999 | 15850715 | In the nematode, Caenorhabditis elegans, the protein encoded by daf-2 is 35% identical to the human insulin receptor; daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 enhances superoxide dismutase (SOD) expression. |
| 4000 | 15850715 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 4001 | 15850715 | These evidences suggest that the activities of Delta6 and Delta5 enzymes play a critical role in the expression and regulation of GLUT-4, TNF-alpha, IL-6, MIF, daf-genes, melatonin, and leptin by modulating the synthesis and tissue concentrations of LCPUFAs. |
| 4002 | 15850715 | Both insulin and insulin-like growth factor-1 (IGF-1) attenuated this response. |
| 4003 | 15850715 | SIRT1 sequesters the proapoptotic factor Bax, prevents stress-induced apoptosis of cells, and thus, prolongs survival. |
| 4004 | 15850715 | In addition, SIRT1 repressed PPAR-gamma, and overexpression of SIRT1 attenuated adipogenesis, and upregulation of SIRT in differentiated fat cells triggered lipolysis and loss of fat, events that are known to attenuate insulin resistance and prolong life span. |
| 4005 | 15850715 | GLUT-4 (glucose transporter) receptor, tumor necrosis factor-alpha (TNF-alpha), interleukins-6 (IL-6), daf-genes and PPARs (peroxisomal proliferation activator receptors) play a role in the development of insulin resistance syndrome and associated conditions. |
| 4006 | 15850715 | Long chain polyunsaturated fatty acids (LCPUFAs) increase cell membrane fluidity and enhance the number of insulin receptors and the affinity of insulin to its receptors; suppress TNF-alpha, IL-6, macrophage migration inhibitory factor (MIF) and leptin synthesis; increase the number of GLUT-4 receptors, serve as endogenous ligands of PPARs, modify lipolysis, and regulate the balance between pro- and anti-oxidants, and thus, play a critical role in the pathogenesis of insulin resistance. |
| 4007 | 15850715 | In the nematode, Caenorhabditis elegans, the protein encoded by daf-2 is 35% identical to the human insulin receptor; daf-7 codes a transforming growth factor-beta (TGF-beta) type signal and daf-16 enhances superoxide dismutase (SOD) expression. |
| 4008 | 15850715 | Melatonin has anti-oxidant actions similar to daf-16, TGF-beta and SOD. |
| 4009 | 15850715 | These evidences suggest that the activities of Delta6 and Delta5 enzymes play a critical role in the expression and regulation of GLUT-4, TNF-alpha, IL-6, MIF, daf-genes, melatonin, and leptin by modulating the synthesis and tissue concentrations of LCPUFAs. |
| 4010 | 15850715 | Both insulin and insulin-like growth factor-1 (IGF-1) attenuated this response. |
| 4011 | 15850715 | SIRT1 sequesters the proapoptotic factor Bax, prevents stress-induced apoptosis of cells, and thus, prolongs survival. |
| 4012 | 15850715 | In addition, SIRT1 repressed PPAR-gamma, and overexpression of SIRT1 attenuated adipogenesis, and upregulation of SIRT in differentiated fat cells triggered lipolysis and loss of fat, events that are known to attenuate insulin resistance and prolong life span. |
| 4013 | 15855327 | Functional defects and the influence of age on the frequency of CD4+ CD25+ T-cells in type 1 diabetes. |
| 4014 | 15855327 | CD4+ CD25+ T-cells appear to play a crucial role in regulating the immune response. |
| 4015 | 15855327 | Therefore, we evaluated the peripheral blood frequency and function of CD4+ CD25+ T-cells in 70 type 1 diabetic patients and 37 healthy individuals. |
| 4016 | 15855327 | Interestingly, a positive correlation was observed between increasing age and CD4+ CD25+ T-cell frequency in both subject groups. |
| 4017 | 15855327 | In contrast to previous studies of nonobese diabetic mice and type 1 diabetic patients, similar frequencies of CD4+ CD25+ and CD4+ CD25(+Bright) T-cells were observed in healthy control subjects and type 1 diabetic patients of similar age. |
| 4018 | 15855327 | There was no difference between type 1 diabetic subjects of recent-onset versus those with established disease in terms of their CD4+ CD25+ or CD4+ CD25(+Bright) T-cell frequency. |
| 4019 | 15855327 | This type 1 diabetes-associated defect in suppression was associated with reduced production of interleukin (IL)-2, gamma-interferon, and transforming growth factor-beta, whereas other cytokines including those of adaptive and innate immunity (IL-10, IL-1beta, IL-6, IL-8, IL-12p70, and tumor necrosis factor-alpha) were similar in control subjects and type 1 diabetic patients. |
| 4020 | 15855327 | These data suggest that age strongly influences the frequency of CD4+ CD25+ T-cells and that function, rather than frequency, may represent the means by which these cells associate with type 1 diabetes in humans. |
| 4021 | 15857924 | The development of renal fibrosis (expression of TGF-beta1, collagen IV, and interstitial alpha-smooth muscle actin) was also strikingly attenuated in the ICAM-1-deficient db/db mice. |
| 4022 | 15857946 | The effects of tranilast on urinary albumin excretion, mesangial expansion, expression of transforming growth factor-beta (TGF-beta) and type I collagen mRNAs, number of anionic sites on the glomerular basement membrane (GBM), and urinary TGF-beta and 8-hydroxy-2'-deoxyguanosine (8-OHdG) excretion were assessed. |
| 4023 | 15857946 | The levels of TGF-beta and type I collagen mRNA expression were increased in the renal cortex in untreated diabetic SHR at 24 weeks, as determined by real-time quantitative polymerase chain reaction. |
| 4024 | 15857946 | Tranilast treatment inhibited the up-regulation of TGF-beta and type I collagen mRNA expression by 65 and 36%, respectively, in diabetic SHR. |
| 4025 | 15857946 | The effects of tranilast on urinary albumin excretion, mesangial expansion, expression of transforming growth factor-beta (TGF-beta) and type I collagen mRNAs, number of anionic sites on the glomerular basement membrane (GBM), and urinary TGF-beta and 8-hydroxy-2'-deoxyguanosine (8-OHdG) excretion were assessed. |
| 4026 | 15857946 | The levels of TGF-beta and type I collagen mRNA expression were increased in the renal cortex in untreated diabetic SHR at 24 weeks, as determined by real-time quantitative polymerase chain reaction. |
| 4027 | 15857946 | Tranilast treatment inhibited the up-regulation of TGF-beta and type I collagen mRNA expression by 65 and 36%, respectively, in diabetic SHR. |
| 4028 | 15857946 | The effects of tranilast on urinary albumin excretion, mesangial expansion, expression of transforming growth factor-beta (TGF-beta) and type I collagen mRNAs, number of anionic sites on the glomerular basement membrane (GBM), and urinary TGF-beta and 8-hydroxy-2'-deoxyguanosine (8-OHdG) excretion were assessed. |
| 4029 | 15857946 | The levels of TGF-beta and type I collagen mRNA expression were increased in the renal cortex in untreated diabetic SHR at 24 weeks, as determined by real-time quantitative polymerase chain reaction. |
| 4030 | 15857946 | Tranilast treatment inhibited the up-regulation of TGF-beta and type I collagen mRNA expression by 65 and 36%, respectively, in diabetic SHR. |
| 4031 | 15876977 | CSF-TNF-alpha, VEGF, and TGF-beta were increased in both AD and VaD. |
| 4032 | 15880049 | Systemic transforming growth factor-beta1 gene therapy induces Foxp3+ regulatory cells, restores self-tolerance, and facilitates regeneration of beta cell function in overtly diabetic nonobese diabetic mice. |
| 4033 | 15918106 | Among several growth factors, transforming growth factor beta1 (TGF-beta1) plays a major role. |
| 4034 | 15919782 | A key mediator of nephrin suppression is angiotensin II (ANG II), which can activate other cytokine pathways such as transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF) systems. |
| 4035 | 15920148 | An in vitro experiment further demonstrated that raloxifene inhibited transforming growth factor beta-1-induced fibronectin transcription and AP-1 activity. |
| 4036 | 15934303 | The serum creatinine (Scr), protein kinase C (PKC), creatinine clearance (Ccr), transforming growth factor-beta, (TGF-beta1), type IV collagen were compared among the groups after 24 weeks. |
| 4037 | 15934303 | The results showed that after 24 weeks, Scr, PKC, TGF-beta1 in group D were significantly lower than in group C, meanwhile, renal pathologic changes in group D were improved. |
| 4038 | 15934303 | The serum creatinine (Scr), protein kinase C (PKC), creatinine clearance (Ccr), transforming growth factor-beta, (TGF-beta1), type IV collagen were compared among the groups after 24 weeks. |
| 4039 | 15934303 | The results showed that after 24 weeks, Scr, PKC, TGF-beta1 in group D were significantly lower than in group C, meanwhile, renal pathologic changes in group D were improved. |
| 4040 | 15938030 | TGF-beta1 causes augmented extracellular matrix protein deposition (collagen types I, IV, V, and VI; fibronectin, and laminin) at the glomerular level, thus inducing mesangial expansion and glomerular basement membrane thickening. |
| 4041 | 15959620 | The diagnosis of PDD/CED in this family was confirmed at the molecular level by detection of a C-to-T transition at position 466, leading to an arginine-to-cysteine amino acid change (position 156) in exon 2 of the transforming growth factor-beta1 (TGFB1) gene. |
| 4042 | 15959781 | Lamina propria (LP) mononuclear cells from helminth-colonized mice make less interleukin (IL)-12 p40 and IFN-gamma, but more IL-4, IL-13, IL-10, TGF-beta, and PGE(2) compared to LP mononuclear cells from naive mice. |
| 4043 | 15980944 | Connective tissue growth factor mediates the profibrotic effects of transforming growth factor-beta produced by tubular epithelial cells in response to high glucose. |
| 4044 | 15983197 | Role of upstream stimulatory factors in regulation of renal transforming growth factor-beta1. |
| 4045 | 15983197 | We previously identified an E-box to be implicated in high-glucose-induced transforming growth factor-beta1 (TGF-beta1) gene stimulation in murine mesangial cells. |
| 4046 | 15983197 | Mesangial cells cultured in glucose concentrations exceeding 2.7 mmol/l D-glucose exhibited increased levels of USF1 and USF2 protein by Western analysis and electrophoretic mobility shift assay (EMSA). |
| 4047 | 15983197 | An E-box element from the murine TGF-beta1 promoter revealed USF1 and USF2 binding by EMSA. |
| 4048 | 15983197 | Chromatin immunoprecipitation assay revealed in vivo binding of USF1 to a glucose-responsive region of the TGF-beta1 promoter. |
| 4049 | 15983197 | Transient cotransfection studies of 293 cells with USF1 led to a twofold increase in TGF-beta1 promoter activity and a 46% increase in secreted TGF-beta1 protein levels. |
| 4050 | 15983197 | Wild-type and USF2 knockout mice exhibited a 2.5-fold stimulation of renal TGF-beta1 expression upon fasting and refeeding with a carbohydrate-rich diet, whereas USF1 knockout mice exhibited only a minimal increase of renal TGF-beta1 upon refeeding. |
| 4051 | 15983197 | We conclude that USF1 is stimulated by modest increases in glucose concentration in murine mesangial cells, bind to the murine TGF-beta1 promoter, contribute to carbohydrate-induced renal TGF-beta1 expression, and may play a role in diabetes-related gene regulation in the kidney. |
| 4052 | 15983197 | Role of upstream stimulatory factors in regulation of renal transforming growth factor-beta1. |
| 4053 | 15983197 | We previously identified an E-box to be implicated in high-glucose-induced transforming growth factor-beta1 (TGF-beta1) gene stimulation in murine mesangial cells. |
| 4054 | 15983197 | Mesangial cells cultured in glucose concentrations exceeding 2.7 mmol/l D-glucose exhibited increased levels of USF1 and USF2 protein by Western analysis and electrophoretic mobility shift assay (EMSA). |
| 4055 | 15983197 | An E-box element from the murine TGF-beta1 promoter revealed USF1 and USF2 binding by EMSA. |
| 4056 | 15983197 | Chromatin immunoprecipitation assay revealed in vivo binding of USF1 to a glucose-responsive region of the TGF-beta1 promoter. |
| 4057 | 15983197 | Transient cotransfection studies of 293 cells with USF1 led to a twofold increase in TGF-beta1 promoter activity and a 46% increase in secreted TGF-beta1 protein levels. |
| 4058 | 15983197 | Wild-type and USF2 knockout mice exhibited a 2.5-fold stimulation of renal TGF-beta1 expression upon fasting and refeeding with a carbohydrate-rich diet, whereas USF1 knockout mice exhibited only a minimal increase of renal TGF-beta1 upon refeeding. |
| 4059 | 15983197 | We conclude that USF1 is stimulated by modest increases in glucose concentration in murine mesangial cells, bind to the murine TGF-beta1 promoter, contribute to carbohydrate-induced renal TGF-beta1 expression, and may play a role in diabetes-related gene regulation in the kidney. |
| 4060 | 15983197 | Role of upstream stimulatory factors in regulation of renal transforming growth factor-beta1. |
| 4061 | 15983197 | We previously identified an E-box to be implicated in high-glucose-induced transforming growth factor-beta1 (TGF-beta1) gene stimulation in murine mesangial cells. |
| 4062 | 15983197 | Mesangial cells cultured in glucose concentrations exceeding 2.7 mmol/l D-glucose exhibited increased levels of USF1 and USF2 protein by Western analysis and electrophoretic mobility shift assay (EMSA). |
| 4063 | 15983197 | An E-box element from the murine TGF-beta1 promoter revealed USF1 and USF2 binding by EMSA. |
| 4064 | 15983197 | Chromatin immunoprecipitation assay revealed in vivo binding of USF1 to a glucose-responsive region of the TGF-beta1 promoter. |
| 4065 | 15983197 | Transient cotransfection studies of 293 cells with USF1 led to a twofold increase in TGF-beta1 promoter activity and a 46% increase in secreted TGF-beta1 protein levels. |
| 4066 | 15983197 | Wild-type and USF2 knockout mice exhibited a 2.5-fold stimulation of renal TGF-beta1 expression upon fasting and refeeding with a carbohydrate-rich diet, whereas USF1 knockout mice exhibited only a minimal increase of renal TGF-beta1 upon refeeding. |
| 4067 | 15983197 | We conclude that USF1 is stimulated by modest increases in glucose concentration in murine mesangial cells, bind to the murine TGF-beta1 promoter, contribute to carbohydrate-induced renal TGF-beta1 expression, and may play a role in diabetes-related gene regulation in the kidney. |
| 4068 | 15983197 | Role of upstream stimulatory factors in regulation of renal transforming growth factor-beta1. |
| 4069 | 15983197 | We previously identified an E-box to be implicated in high-glucose-induced transforming growth factor-beta1 (TGF-beta1) gene stimulation in murine mesangial cells. |
| 4070 | 15983197 | Mesangial cells cultured in glucose concentrations exceeding 2.7 mmol/l D-glucose exhibited increased levels of USF1 and USF2 protein by Western analysis and electrophoretic mobility shift assay (EMSA). |
| 4071 | 15983197 | An E-box element from the murine TGF-beta1 promoter revealed USF1 and USF2 binding by EMSA. |
| 4072 | 15983197 | Chromatin immunoprecipitation assay revealed in vivo binding of USF1 to a glucose-responsive region of the TGF-beta1 promoter. |
| 4073 | 15983197 | Transient cotransfection studies of 293 cells with USF1 led to a twofold increase in TGF-beta1 promoter activity and a 46% increase in secreted TGF-beta1 protein levels. |
| 4074 | 15983197 | Wild-type and USF2 knockout mice exhibited a 2.5-fold stimulation of renal TGF-beta1 expression upon fasting and refeeding with a carbohydrate-rich diet, whereas USF1 knockout mice exhibited only a minimal increase of renal TGF-beta1 upon refeeding. |
| 4075 | 15983197 | We conclude that USF1 is stimulated by modest increases in glucose concentration in murine mesangial cells, bind to the murine TGF-beta1 promoter, contribute to carbohydrate-induced renal TGF-beta1 expression, and may play a role in diabetes-related gene regulation in the kidney. |
| 4076 | 15983197 | Role of upstream stimulatory factors in regulation of renal transforming growth factor-beta1. |
| 4077 | 15983197 | We previously identified an E-box to be implicated in high-glucose-induced transforming growth factor-beta1 (TGF-beta1) gene stimulation in murine mesangial cells. |
| 4078 | 15983197 | Mesangial cells cultured in glucose concentrations exceeding 2.7 mmol/l D-glucose exhibited increased levels of USF1 and USF2 protein by Western analysis and electrophoretic mobility shift assay (EMSA). |
| 4079 | 15983197 | An E-box element from the murine TGF-beta1 promoter revealed USF1 and USF2 binding by EMSA. |
| 4080 | 15983197 | Chromatin immunoprecipitation assay revealed in vivo binding of USF1 to a glucose-responsive region of the TGF-beta1 promoter. |
| 4081 | 15983197 | Transient cotransfection studies of 293 cells with USF1 led to a twofold increase in TGF-beta1 promoter activity and a 46% increase in secreted TGF-beta1 protein levels. |
| 4082 | 15983197 | Wild-type and USF2 knockout mice exhibited a 2.5-fold stimulation of renal TGF-beta1 expression upon fasting and refeeding with a carbohydrate-rich diet, whereas USF1 knockout mice exhibited only a minimal increase of renal TGF-beta1 upon refeeding. |
| 4083 | 15983197 | We conclude that USF1 is stimulated by modest increases in glucose concentration in murine mesangial cells, bind to the murine TGF-beta1 promoter, contribute to carbohydrate-induced renal TGF-beta1 expression, and may play a role in diabetes-related gene regulation in the kidney. |
| 4084 | 15983197 | Role of upstream stimulatory factors in regulation of renal transforming growth factor-beta1. |
| 4085 | 15983197 | We previously identified an E-box to be implicated in high-glucose-induced transforming growth factor-beta1 (TGF-beta1) gene stimulation in murine mesangial cells. |
| 4086 | 15983197 | Mesangial cells cultured in glucose concentrations exceeding 2.7 mmol/l D-glucose exhibited increased levels of USF1 and USF2 protein by Western analysis and electrophoretic mobility shift assay (EMSA). |
| 4087 | 15983197 | An E-box element from the murine TGF-beta1 promoter revealed USF1 and USF2 binding by EMSA. |
| 4088 | 15983197 | Chromatin immunoprecipitation assay revealed in vivo binding of USF1 to a glucose-responsive region of the TGF-beta1 promoter. |
| 4089 | 15983197 | Transient cotransfection studies of 293 cells with USF1 led to a twofold increase in TGF-beta1 promoter activity and a 46% increase in secreted TGF-beta1 protein levels. |
| 4090 | 15983197 | Wild-type and USF2 knockout mice exhibited a 2.5-fold stimulation of renal TGF-beta1 expression upon fasting and refeeding with a carbohydrate-rich diet, whereas USF1 knockout mice exhibited only a minimal increase of renal TGF-beta1 upon refeeding. |
| 4091 | 15983197 | We conclude that USF1 is stimulated by modest increases in glucose concentration in murine mesangial cells, bind to the murine TGF-beta1 promoter, contribute to carbohydrate-induced renal TGF-beta1 expression, and may play a role in diabetes-related gene regulation in the kidney. |
| 4092 | 15983197 | Role of upstream stimulatory factors in regulation of renal transforming growth factor-beta1. |
| 4093 | 15983197 | We previously identified an E-box to be implicated in high-glucose-induced transforming growth factor-beta1 (TGF-beta1) gene stimulation in murine mesangial cells. |
| 4094 | 15983197 | Mesangial cells cultured in glucose concentrations exceeding 2.7 mmol/l D-glucose exhibited increased levels of USF1 and USF2 protein by Western analysis and electrophoretic mobility shift assay (EMSA). |
| 4095 | 15983197 | An E-box element from the murine TGF-beta1 promoter revealed USF1 and USF2 binding by EMSA. |
| 4096 | 15983197 | Chromatin immunoprecipitation assay revealed in vivo binding of USF1 to a glucose-responsive region of the TGF-beta1 promoter. |
| 4097 | 15983197 | Transient cotransfection studies of 293 cells with USF1 led to a twofold increase in TGF-beta1 promoter activity and a 46% increase in secreted TGF-beta1 protein levels. |
| 4098 | 15983197 | Wild-type and USF2 knockout mice exhibited a 2.5-fold stimulation of renal TGF-beta1 expression upon fasting and refeeding with a carbohydrate-rich diet, whereas USF1 knockout mice exhibited only a minimal increase of renal TGF-beta1 upon refeeding. |
| 4099 | 15983197 | We conclude that USF1 is stimulated by modest increases in glucose concentration in murine mesangial cells, bind to the murine TGF-beta1 promoter, contribute to carbohydrate-induced renal TGF-beta1 expression, and may play a role in diabetes-related gene regulation in the kidney. |
| 4100 | 15996232 | The effect of RGTZ on CsA-induced renal injury was evaluated by assessing renal function and pathology; mediators of inflammation and fibrosis such as angiotensin II (AngII), osteopontin (OPN) and transforming growth factor-beta1 (TGF-beta1) and apoptotic cell death. |
| 4101 | 15996232 | Pro-inflammatory and pro-fibrotic molecules such as AngII, OPN and TGF-beta1, and apoptotic cell death also decreased with RGTZ treatment. |
| 4102 | 15996232 | The effect of RGTZ on CsA-induced renal injury was evaluated by assessing renal function and pathology; mediators of inflammation and fibrosis such as angiotensin II (AngII), osteopontin (OPN) and transforming growth factor-beta1 (TGF-beta1) and apoptotic cell death. |
| 4103 | 15996232 | Pro-inflammatory and pro-fibrotic molecules such as AngII, OPN and TGF-beta1, and apoptotic cell death also decreased with RGTZ treatment. |
| 4104 | 16020542 | Cross-talk between bone morphogenetic protein and transforming growth factor-beta signaling is essential for exendin-4-induced insulin-positive differentiation of AR42J cells. |
| 4105 | 16020542 | We found that the canonical intracellular mediators of BMP signaling, Smad-1 and Smad-8, were significantly elevated in AR42J cells undergoing insulin-positive differentiation in response to exendin-4 treatment, suggesting a role for BMP signaling in beta-cell formation. |
| 4106 | 16020542 | Similarly, endogenous BMP-2 ligand and ALK-1 receptor (activin receptor-like kinase-1; known to activate Smads 1 and 8) mRNAs were specifically up-regulated in exendin-4-treated AR42J cells. |
| 4107 | 16020542 | Surprisingly, Smad-1 and Smad-8 levels were suppressed by the addition of BMP-soluble receptor inhibition of BMP ligand binding to its receptor. |
| 4108 | 16020542 | BMP-2 ligand antisense also strongly inhibited Smad-1 and Smad-8 expression, again with the abolition of insulin-positive differentiation. |
| 4109 | 16020542 | In short, BMP signaling may represent a novel downstream target of exendin-4 (glucagon-like peptide 1) signaling and potentially serve as an upstream regulator of transforming growth factor-beta isoform signaling to differentiate the acinar-like AR42J cells into insulin-secreting cells. |
| 4110 | 16020542 | Cross-talk between bone morphogenetic protein and transforming growth factor-beta signaling is essential for exendin-4-induced insulin-positive differentiation of AR42J cells. |
| 4111 | 16020542 | We found that the canonical intracellular mediators of BMP signaling, Smad-1 and Smad-8, were significantly elevated in AR42J cells undergoing insulin-positive differentiation in response to exendin-4 treatment, suggesting a role for BMP signaling in beta-cell formation. |
| 4112 | 16020542 | Similarly, endogenous BMP-2 ligand and ALK-1 receptor (activin receptor-like kinase-1; known to activate Smads 1 and 8) mRNAs were specifically up-regulated in exendin-4-treated AR42J cells. |
| 4113 | 16020542 | Surprisingly, Smad-1 and Smad-8 levels were suppressed by the addition of BMP-soluble receptor inhibition of BMP ligand binding to its receptor. |
| 4114 | 16020542 | BMP-2 ligand antisense also strongly inhibited Smad-1 and Smad-8 expression, again with the abolition of insulin-positive differentiation. |
| 4115 | 16020542 | In short, BMP signaling may represent a novel downstream target of exendin-4 (glucagon-like peptide 1) signaling and potentially serve as an upstream regulator of transforming growth factor-beta isoform signaling to differentiate the acinar-like AR42J cells into insulin-secreting cells. |
| 4116 | 16041601 | No correlation between the p38 MAPK pathway and the contractile dysfunction in diabetic cardiomyocytes: hyperglycaemia-induced signalling and contractile function. |
| 4117 | 16041601 | TGFbeta expression and p38 MAP-kinase (MAPK) activation were measured by Western blotting. |
| 4118 | 16041601 | Glucose (30 mM) caused an increase in formation of radicals, phosphorylation of p38 MAPK, and TGFbeta expression. |
| 4119 | 16041601 | Neither inhibition of p38 MAPK with SB 202190 (1 microM) nor inhibition of reactive oxygen species with vitamin C did alter these measured functional parameters. |
| 4120 | 16041601 | No correlation between the p38 MAPK pathway and the contractile dysfunction in diabetic cardiomyocytes: hyperglycaemia-induced signalling and contractile function. |
| 4121 | 16041601 | TGFbeta expression and p38 MAP-kinase (MAPK) activation were measured by Western blotting. |
| 4122 | 16041601 | Glucose (30 mM) caused an increase in formation of radicals, phosphorylation of p38 MAPK, and TGFbeta expression. |
| 4123 | 16041601 | Neither inhibition of p38 MAPK with SB 202190 (1 microM) nor inhibition of reactive oxygen species with vitamin C did alter these measured functional parameters. |
| 4124 | 16046298 | In the present study, we found that db/db mice on the FVB genetic background with loss-of-function mutation of the leptin receptor (FVB-Lepr(db) mice or FVBdb/db) develop severe diabetic nephropathy, including glomerulosclerosis, tubulointerstitial fibrosis, increased expression of type IV collagen and fibronectin, and proteinuria, which is associated with increased renal mRNA abundance of transforming growth factor-beta, plasminogen activator inhibitor-1, and vascular endothelial growth factor. |
| 4125 | 16046298 | We also detected a significant increase in the renal expression of adipocyte differentiation-related protein (adipophilin), a marker of cytoplasmic lipid droplets. |
| 4126 | 16046298 | We found significant increases in SREBP-1 and -2 protein levels in nuclear extracts from the kidneys of FVBdb/db mice, with increases in the mRNA abundance of acetyl-CoA carboxylase, fatty acid synthase, and 3-hydroxy-3-methylglutaryl-CoA reductase, which mediates the increase in renal triglyceride and cholesterol content. |
| 4127 | 16046298 | Our results indicate that in FVBdb/db mice, renal triglyceride and cholesterol accumulation is mediated by increased activity of SREBP-1 and -2. |
| 4128 | 16046297 | Carnosine inhibited the increased production of fibronectin and collagen type VI in podocytes and the increased production of TGF-beta in mesangial cells induced by 25 mmol/l glucose. |
| 4129 | 16048553 | Oral antigen induces T-helper 2 [interleukin (IL)-4/IL-10] and Th3 [transforming growth factor (TGF)-beta] T cells plus CD4+CD25+ regulatory cells and latency-associated peptide+ T cells. |
| 4130 | 16048553 | Induction of oral tolerance is enhanced by IL-4, IL-10, anti-IL-12, TGF-beta, cholera toxin B subunit, Flt-3 ligand, and anti-CD40 ligand. |
| 4131 | 16105242 | Hachimi-jio-gan also reduced fibronectin and transforming growth factor beta1 (TGF-beta1) protein expression in the renal cortex. |
| 4132 | 16174288 | High glucose (HG) induces cellular ROS through protein kinase C (PKC)-dependent activation of NADPH oxidase and through mitochondrial metabolism. |
| 4133 | 16174288 | ROS thus generated activate signal transduction cascade (PKC, mitogen-activated protein kinases, and janus kinase/signal transducers and activators of transcription) and transcription factors (nuclear factor-kappaB, activated protein-1, and specificity protein-1), up-regulate transforming growth factor-beta1 (TGF-beta1), angiotensin II (Ang II), monocyte chemoattractant protein-1 (MCP-1), and plasminogen activator inhibitor-1 (PAI-1) gene and protein expression, and promote formation of advanced glycation end-products (AGE). |
| 4134 | 16174288 | PKC, TGF-beta1, Ang II, and AGE also induce cellular ROS and signal through ROS leading to enhanced ECM synthesis. |
| 4135 | 16174288 | High glucose (HG) induces cellular ROS through protein kinase C (PKC)-dependent activation of NADPH oxidase and through mitochondrial metabolism. |
| 4136 | 16174288 | ROS thus generated activate signal transduction cascade (PKC, mitogen-activated protein kinases, and janus kinase/signal transducers and activators of transcription) and transcription factors (nuclear factor-kappaB, activated protein-1, and specificity protein-1), up-regulate transforming growth factor-beta1 (TGF-beta1), angiotensin II (Ang II), monocyte chemoattractant protein-1 (MCP-1), and plasminogen activator inhibitor-1 (PAI-1) gene and protein expression, and promote formation of advanced glycation end-products (AGE). |
| 4137 | 16174288 | PKC, TGF-beta1, Ang II, and AGE also induce cellular ROS and signal through ROS leading to enhanced ECM synthesis. |
| 4138 | 16177004 | Galectin-9 (Gal-9) was identified previously and demonstrated to have apoptotic potential to thymocytes in mice and activated CD8(+) T cells in nephrotoxic serum nephritis model. |
| 4139 | 16177004 | Gal-9 reduced glomerular expression of TGF-beta1 and the number of p27(Kip1)- and p21(Cip1)-positive cells in glomeruli. |
| 4140 | 16177004 | Double staining with nephrin and type IV collagen revealed that podocytes were mainly positive for p27(Kip1). |
| 4141 | 16177004 | Gal-9 reversed the high-glucose-mediated upregulation of p27(Kip1) and p21(Cip1) and inhibited cell-cycle-dependent hypertrophy, i.e., reduced [(3)H]proline incorporation. |
| 4142 | 16186390 | Here, we examine the effect of endostatin peptide, a potent inhibitor of angiogenesis derived from type XVIII collagen, in preventing progression in the type 1 diabetic nephropathy mouse model. |
| 4143 | 16186390 | Glomerular mesangial matrix expansion, the increase of glomerular type IV collagen, endothelial area (CD31(+)), and F4/80(+) monocyte/macrophage accumulation were significantly inhibited by endostatin peptide. |
| 4144 | 16186390 | Increase in the renal expression of VEGF-A, flk-1, Ang-2, an antagonist of angiopoietin-1, transforming growth factor-beta1, interleukin-6, and monocyte chemoattractant protein-1 was inhibited by endostatin peptide in diabetic mice. |
| 4145 | 16186390 | Decrease of nephrin mRNA and protein in diabetic mice was suppressed by treatment with endostatin peptide. |
| 4146 | 16186390 | Endogenous renal levels of endostatin were decreased in endostatin peptide-treated groups in parallel with VEGF-A. |
| 4147 | 16194052 | To clarify the mechanism involved in anti-proliferative activity of these medicines, this study examined the effects of Cnidii rhizoma and Tabanus on high glucose-stimulated extracellular matrix (ECM) protein accumulation and transforming growth factor-beta1 (TGF-beta1) production. |
| 4148 | 16194052 | Exposure of GMCs to high glucose significantly stimulated the ECM protein, collagen and fibronectin, accumulation and TGF-beta1 secretion, and these changes were dramatically diminished by treatment of GMCs with extracts of Cnidii rhizoma or Tabanus (10 microg/ml). |
| 4149 | 16194052 | To clarify the mechanism involved in anti-proliferative activity of these medicines, this study examined the effects of Cnidii rhizoma and Tabanus on high glucose-stimulated extracellular matrix (ECM) protein accumulation and transforming growth factor-beta1 (TGF-beta1) production. |
| 4150 | 16194052 | Exposure of GMCs to high glucose significantly stimulated the ECM protein, collagen and fibronectin, accumulation and TGF-beta1 secretion, and these changes were dramatically diminished by treatment of GMCs with extracts of Cnidii rhizoma or Tabanus (10 microg/ml). |
| 4151 | 16198623 | Xenobiotics-induced liver fibrosis was extremely diminished in ob/ob mice and Zucker (fa/fa) rats, an inborn leptin- and leptin receptor (Ob-R)-deficient animal, respectively. |
| 4152 | 16198623 | Further, leptin increased transforming growth factor (TGF)-beta mRNA in isolated sinusoidal endothelial cells and Kupffer cells, suggesting that leptin promotes hepatic fibrogenesis through up-regulation of TGF-beta in the liver. |
| 4153 | 16198623 | Moreover, leptin augmented PDGF-dependent proliferation of HSCs by enhancing downstream intracellular signaling pathways via mitogen-activated protein kinase (MAPK) and phosphatidylinositol 3 kinase (PI3K)/Akt. |
| 4154 | 16220017 | Modulation of the transforming growth factor beta1 by vitamin E in early nephropathy. |
| 4155 | 16222610 | Amadori-glycated albumin induces the activation of glomerular mesangial and endothelial cells to a phenotype that may be linked to the pathogenesis of diabetic microangiopathy, that is, by the stimulation of protein kinase C, activation of transforming growth factor beta, and the expression of extracellular matrix proteins. |
| 4156 | 16225463 | White adipose tissue is secreting several hormones, particularly leptin and adiponectin, and a variety of other protein signals: the adipocytokines. |
| 4157 | 16225463 | A growing list of adipocytokines involved in inflammation (IL-1beta, IL-6, IL-8, IL-10, TNF-alpha, TGF-beta,) and the acute-phase response (serum amyloid A, PAI-1) have been found to be increased in the metabolic syndrome. |
| 4158 | 16247347 | PPAR-gamma ligands, including thiazolidinediones, have recently become clinically available for treating insulin-resistant diabetes mellitus. |
| 4159 | 16247347 | Moreover, troglitazone reduced expression of ECM proteins and transforming growth factor-beta in glomeruli from streptozotocin-induced diabetic rats. |
| 4160 | 16247347 | Many other properties including antiproteinuric, hemodynamic, and antihypertensive effects in insulin-dependent diabetes mellitus suggest that PPAR-gamma ligands might have a direct, beneficial renal effect, independent of their capacity to improve glucose tolerance. |
| 4161 | 16270194 | Glomerular expression of thrombospondin-1, transforming growth factor beta and connective tissue growth factor at different stages of diabetic nephropathy and their interdependent roles in mesangial response to diabetic stimuli. |
| 4162 | 16272194 | To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). |
| 4163 | 16272194 | Treatment of HAECs with LDL (50 microg/ml) for 24 h produced a significant increase in the mRNA and the protein levels of CTGF and collagen IV compared with unstimulated controls. |
| 4164 | 16272194 | To explore the mechanisms by which LDL regulates CTGF and collagen IV expression in HAECs, we determined first if CTGF and collagen IV are downstream targets for regulation by transforming growth factor-beta (TGF-beta). |
| 4165 | 16272194 | The results demonstrated that TGF-beta produced a concentration-dependent increase in the protein levels of CTGF. |
| 4166 | 16272194 | To assess whether the induction of CTGF in response to LDL is mediated via autocrine activation of TGF-beta, HAECs were treated with LDL for 24 h in the presence and absence of anti-TGF-beta neutralizing antibodies (anti-TGF-beta NA). |
| 4167 | 16272194 | To investigate the upstream mediators of TGF-beta on activity of CTGF in response to LDL, HAECs were treated with LDL for 24 h in the presence and absence of cell-permeable MAPK inhibitors. |
| 4168 | 16272194 | Inhibition of p38(mapk) activities did not affect LDL-induced TGF-beta1, CTGF, and collagen IV expression. |
| 4169 | 16272194 | On the other hand, SP-600125, a specific inhibitor of c-Jun NH(2)-terminal kinase, suppressed LDL-induced TGF-beta, CTGF, and collagen IV expression, and PD-98059, a selective inhibitor of p44/42(mapk), suppressed LDL-induced TGF-beta and CTGF expression. |
| 4170 | 16272194 | These findings are the first to implicate the MAPK pathway and TGF-beta as key players in LDL signaling, leading to CTGF and collagen IV expression in HAECs. |
| 4171 | 16272194 | To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). |
| 4172 | 16272194 | Treatment of HAECs with LDL (50 microg/ml) for 24 h produced a significant increase in the mRNA and the protein levels of CTGF and collagen IV compared with unstimulated controls. |
| 4173 | 16272194 | To explore the mechanisms by which LDL regulates CTGF and collagen IV expression in HAECs, we determined first if CTGF and collagen IV are downstream targets for regulation by transforming growth factor-beta (TGF-beta). |
| 4174 | 16272194 | The results demonstrated that TGF-beta produced a concentration-dependent increase in the protein levels of CTGF. |
| 4175 | 16272194 | To assess whether the induction of CTGF in response to LDL is mediated via autocrine activation of TGF-beta, HAECs were treated with LDL for 24 h in the presence and absence of anti-TGF-beta neutralizing antibodies (anti-TGF-beta NA). |
| 4176 | 16272194 | To investigate the upstream mediators of TGF-beta on activity of CTGF in response to LDL, HAECs were treated with LDL for 24 h in the presence and absence of cell-permeable MAPK inhibitors. |
| 4177 | 16272194 | Inhibition of p38(mapk) activities did not affect LDL-induced TGF-beta1, CTGF, and collagen IV expression. |
| 4178 | 16272194 | On the other hand, SP-600125, a specific inhibitor of c-Jun NH(2)-terminal kinase, suppressed LDL-induced TGF-beta, CTGF, and collagen IV expression, and PD-98059, a selective inhibitor of p44/42(mapk), suppressed LDL-induced TGF-beta and CTGF expression. |
| 4179 | 16272194 | These findings are the first to implicate the MAPK pathway and TGF-beta as key players in LDL signaling, leading to CTGF and collagen IV expression in HAECs. |
| 4180 | 16272194 | To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). |
| 4181 | 16272194 | Treatment of HAECs with LDL (50 microg/ml) for 24 h produced a significant increase in the mRNA and the protein levels of CTGF and collagen IV compared with unstimulated controls. |
| 4182 | 16272194 | To explore the mechanisms by which LDL regulates CTGF and collagen IV expression in HAECs, we determined first if CTGF and collagen IV are downstream targets for regulation by transforming growth factor-beta (TGF-beta). |
| 4183 | 16272194 | The results demonstrated that TGF-beta produced a concentration-dependent increase in the protein levels of CTGF. |
| 4184 | 16272194 | To assess whether the induction of CTGF in response to LDL is mediated via autocrine activation of TGF-beta, HAECs were treated with LDL for 24 h in the presence and absence of anti-TGF-beta neutralizing antibodies (anti-TGF-beta NA). |
| 4185 | 16272194 | To investigate the upstream mediators of TGF-beta on activity of CTGF in response to LDL, HAECs were treated with LDL for 24 h in the presence and absence of cell-permeable MAPK inhibitors. |
| 4186 | 16272194 | Inhibition of p38(mapk) activities did not affect LDL-induced TGF-beta1, CTGF, and collagen IV expression. |
| 4187 | 16272194 | On the other hand, SP-600125, a specific inhibitor of c-Jun NH(2)-terminal kinase, suppressed LDL-induced TGF-beta, CTGF, and collagen IV expression, and PD-98059, a selective inhibitor of p44/42(mapk), suppressed LDL-induced TGF-beta and CTGF expression. |
| 4188 | 16272194 | These findings are the first to implicate the MAPK pathway and TGF-beta as key players in LDL signaling, leading to CTGF and collagen IV expression in HAECs. |
| 4189 | 16272194 | To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). |
| 4190 | 16272194 | Treatment of HAECs with LDL (50 microg/ml) for 24 h produced a significant increase in the mRNA and the protein levels of CTGF and collagen IV compared with unstimulated controls. |
| 4191 | 16272194 | To explore the mechanisms by which LDL regulates CTGF and collagen IV expression in HAECs, we determined first if CTGF and collagen IV are downstream targets for regulation by transforming growth factor-beta (TGF-beta). |
| 4192 | 16272194 | The results demonstrated that TGF-beta produced a concentration-dependent increase in the protein levels of CTGF. |
| 4193 | 16272194 | To assess whether the induction of CTGF in response to LDL is mediated via autocrine activation of TGF-beta, HAECs were treated with LDL for 24 h in the presence and absence of anti-TGF-beta neutralizing antibodies (anti-TGF-beta NA). |
| 4194 | 16272194 | To investigate the upstream mediators of TGF-beta on activity of CTGF in response to LDL, HAECs were treated with LDL for 24 h in the presence and absence of cell-permeable MAPK inhibitors. |
| 4195 | 16272194 | Inhibition of p38(mapk) activities did not affect LDL-induced TGF-beta1, CTGF, and collagen IV expression. |
| 4196 | 16272194 | On the other hand, SP-600125, a specific inhibitor of c-Jun NH(2)-terminal kinase, suppressed LDL-induced TGF-beta, CTGF, and collagen IV expression, and PD-98059, a selective inhibitor of p44/42(mapk), suppressed LDL-induced TGF-beta and CTGF expression. |
| 4197 | 16272194 | These findings are the first to implicate the MAPK pathway and TGF-beta as key players in LDL signaling, leading to CTGF and collagen IV expression in HAECs. |
| 4198 | 16272194 | To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). |
| 4199 | 16272194 | Treatment of HAECs with LDL (50 microg/ml) for 24 h produced a significant increase in the mRNA and the protein levels of CTGF and collagen IV compared with unstimulated controls. |
| 4200 | 16272194 | To explore the mechanisms by which LDL regulates CTGF and collagen IV expression in HAECs, we determined first if CTGF and collagen IV are downstream targets for regulation by transforming growth factor-beta (TGF-beta). |
| 4201 | 16272194 | The results demonstrated that TGF-beta produced a concentration-dependent increase in the protein levels of CTGF. |
| 4202 | 16272194 | To assess whether the induction of CTGF in response to LDL is mediated via autocrine activation of TGF-beta, HAECs were treated with LDL for 24 h in the presence and absence of anti-TGF-beta neutralizing antibodies (anti-TGF-beta NA). |
| 4203 | 16272194 | To investigate the upstream mediators of TGF-beta on activity of CTGF in response to LDL, HAECs were treated with LDL for 24 h in the presence and absence of cell-permeable MAPK inhibitors. |
| 4204 | 16272194 | Inhibition of p38(mapk) activities did not affect LDL-induced TGF-beta1, CTGF, and collagen IV expression. |
| 4205 | 16272194 | On the other hand, SP-600125, a specific inhibitor of c-Jun NH(2)-terminal kinase, suppressed LDL-induced TGF-beta, CTGF, and collagen IV expression, and PD-98059, a selective inhibitor of p44/42(mapk), suppressed LDL-induced TGF-beta and CTGF expression. |
| 4206 | 16272194 | These findings are the first to implicate the MAPK pathway and TGF-beta as key players in LDL signaling, leading to CTGF and collagen IV expression in HAECs. |
| 4207 | 16272194 | To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). |
| 4208 | 16272194 | Treatment of HAECs with LDL (50 microg/ml) for 24 h produced a significant increase in the mRNA and the protein levels of CTGF and collagen IV compared with unstimulated controls. |
| 4209 | 16272194 | To explore the mechanisms by which LDL regulates CTGF and collagen IV expression in HAECs, we determined first if CTGF and collagen IV are downstream targets for regulation by transforming growth factor-beta (TGF-beta). |
| 4210 | 16272194 | The results demonstrated that TGF-beta produced a concentration-dependent increase in the protein levels of CTGF. |
| 4211 | 16272194 | To assess whether the induction of CTGF in response to LDL is mediated via autocrine activation of TGF-beta, HAECs were treated with LDL for 24 h in the presence and absence of anti-TGF-beta neutralizing antibodies (anti-TGF-beta NA). |
| 4212 | 16272194 | To investigate the upstream mediators of TGF-beta on activity of CTGF in response to LDL, HAECs were treated with LDL for 24 h in the presence and absence of cell-permeable MAPK inhibitors. |
| 4213 | 16272194 | Inhibition of p38(mapk) activities did not affect LDL-induced TGF-beta1, CTGF, and collagen IV expression. |
| 4214 | 16272194 | On the other hand, SP-600125, a specific inhibitor of c-Jun NH(2)-terminal kinase, suppressed LDL-induced TGF-beta, CTGF, and collagen IV expression, and PD-98059, a selective inhibitor of p44/42(mapk), suppressed LDL-induced TGF-beta and CTGF expression. |
| 4215 | 16272194 | These findings are the first to implicate the MAPK pathway and TGF-beta as key players in LDL signaling, leading to CTGF and collagen IV expression in HAECs. |
| 4216 | 16272194 | To define the mechanisms through which low-density lipoproteins (LDL) promote vascular injury, we evaluated whether LDL can modulate the expression of CTGF and collagen IV in human aortic endothelial cells (HAECs). |
| 4217 | 16272194 | Treatment of HAECs with LDL (50 microg/ml) for 24 h produced a significant increase in the mRNA and the protein levels of CTGF and collagen IV compared with unstimulated controls. |
| 4218 | 16272194 | To explore the mechanisms by which LDL regulates CTGF and collagen IV expression in HAECs, we determined first if CTGF and collagen IV are downstream targets for regulation by transforming growth factor-beta (TGF-beta). |
| 4219 | 16272194 | The results demonstrated that TGF-beta produced a concentration-dependent increase in the protein levels of CTGF. |
| 4220 | 16272194 | To assess whether the induction of CTGF in response to LDL is mediated via autocrine activation of TGF-beta, HAECs were treated with LDL for 24 h in the presence and absence of anti-TGF-beta neutralizing antibodies (anti-TGF-beta NA). |
| 4221 | 16272194 | To investigate the upstream mediators of TGF-beta on activity of CTGF in response to LDL, HAECs were treated with LDL for 24 h in the presence and absence of cell-permeable MAPK inhibitors. |
| 4222 | 16272194 | Inhibition of p38(mapk) activities did not affect LDL-induced TGF-beta1, CTGF, and collagen IV expression. |
| 4223 | 16272194 | On the other hand, SP-600125, a specific inhibitor of c-Jun NH(2)-terminal kinase, suppressed LDL-induced TGF-beta, CTGF, and collagen IV expression, and PD-98059, a selective inhibitor of p44/42(mapk), suppressed LDL-induced TGF-beta and CTGF expression. |
| 4224 | 16272194 | These findings are the first to implicate the MAPK pathway and TGF-beta as key players in LDL signaling, leading to CTGF and collagen IV expression in HAECs. |
| 4225 | 16278277 | Previously, we demonstrated that 5-chloro-2-{(1E)-3-[2-(4-methoxybenzoyl)-4-methyl-1H-pyrrol-1-yl]prop-1-en-1-yl}-N-(methylsulfonyl)benzamide (SMP-534) reduces extracellular matrix (ECM) production induced by transforming growth factor-beta (TGF-beta) in vitro and prevents the accumulation of ECM in glomeruli in rat Thy-1 nephritis models. |
| 4226 | 16278277 | Treatment with SMP-534 dose dependently suppressed the increase of urinary albumin and type IV collagen excretion in db/db mice. |
| 4227 | 16290123 | We investigated the relationship between the efficacy of renin angiotensin system (RAS) inhibitors and angiotensin-converting enzyme (ACE) genotypes. |
| 4228 | 16290123 | Patients with type 2 diabetes without proteinuria, were treated with RAS inhibitors, the first being an ACE inhibitor (ACEI) and the second, an angiotensin II (ATII) receptor blocker (ARB) for 8 weeks each. |
| 4229 | 16290123 | However, by analysis segregated with ACE gene polymorphism, ARB significantly decreased transforming growth factor-beta1 (TGF-beta) compared to ACEI in patients with the I/I genotype but not in patients with the D/I+D/D genotype. |
| 4230 | 16290123 | We suggest that in I/I patients, TGF-beta was reduced by ARB via effects on (ATII) type 2 receptors (AT2). |
| 4231 | 16290123 | In our experiments, the effect of ARB on TGF-beta reduction was only detected by segregation of ACE genotypes. |
| 4232 | 16290123 | We investigated the relationship between the efficacy of renin angiotensin system (RAS) inhibitors and angiotensin-converting enzyme (ACE) genotypes. |
| 4233 | 16290123 | Patients with type 2 diabetes without proteinuria, were treated with RAS inhibitors, the first being an ACE inhibitor (ACEI) and the second, an angiotensin II (ATII) receptor blocker (ARB) for 8 weeks each. |
| 4234 | 16290123 | However, by analysis segregated with ACE gene polymorphism, ARB significantly decreased transforming growth factor-beta1 (TGF-beta) compared to ACEI in patients with the I/I genotype but not in patients with the D/I+D/D genotype. |
| 4235 | 16290123 | We suggest that in I/I patients, TGF-beta was reduced by ARB via effects on (ATII) type 2 receptors (AT2). |
| 4236 | 16290123 | In our experiments, the effect of ARB on TGF-beta reduction was only detected by segregation of ACE genotypes. |
| 4237 | 16290123 | We investigated the relationship between the efficacy of renin angiotensin system (RAS) inhibitors and angiotensin-converting enzyme (ACE) genotypes. |
| 4238 | 16290123 | Patients with type 2 diabetes without proteinuria, were treated with RAS inhibitors, the first being an ACE inhibitor (ACEI) and the second, an angiotensin II (ATII) receptor blocker (ARB) for 8 weeks each. |
| 4239 | 16290123 | However, by analysis segregated with ACE gene polymorphism, ARB significantly decreased transforming growth factor-beta1 (TGF-beta) compared to ACEI in patients with the I/I genotype but not in patients with the D/I+D/D genotype. |
| 4240 | 16290123 | We suggest that in I/I patients, TGF-beta was reduced by ARB via effects on (ATII) type 2 receptors (AT2). |
| 4241 | 16290123 | In our experiments, the effect of ARB on TGF-beta reduction was only detected by segregation of ACE genotypes. |
| 4242 | 16303001 | However, transcription of genes previously linked to AR including CD8 (65.9 +/- 18.8) and related molecules IFN-gamma(55.1 +/- 17.0), CXCR3 (49.9 +/- 12.8) and perforin (153.8 +/- 50.4) were significantly higher in PVN compared to AR (30.9 +/- 2.0, 14.0 +/- 7.3, 12.1 +/- 7.3 and 15.6 +/- 3.8-fold, respectively; p < 0.01). |
| 4243 | 16303001 | Importantly, transcription of molecules associated with graft fibrosis including matrix collagens, TGFbeta, MMP2 and 9, as well as markers of epithelial-mesenchymal transformation (EMT) were significantly higher in PVN than AR. |
| 4244 | 16306354 | Moreover, HA-specific CD4+ T-cells from anti-DEC-HA-treated INS-HA/TCR-HA mice exhibited increased expression of Foxp3, cytotoxic T-lymphocyte-associated antigen-4, and the immunosuppressive cytokines interleukin-10 and transforming growth factor-beta. |
| 4245 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4246 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4247 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4248 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4249 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4250 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4251 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4252 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4253 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4254 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4255 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4256 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4257 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4258 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4259 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4260 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4261 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4262 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4263 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4264 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4265 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4266 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4267 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4268 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4269 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4270 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4271 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4272 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4273 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4274 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4275 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4276 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4277 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4278 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4279 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4280 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4281 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4282 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4283 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4284 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4285 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4286 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4287 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4288 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4289 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4290 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4291 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4292 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4293 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4294 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4295 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4296 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4297 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4298 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4299 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4300 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4301 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4302 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4303 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4304 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4305 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4306 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4307 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4308 | 16310163 | Thrombospondin 1 mediates angiotensin II induction of TGF-beta activation by cardiac and renal cells under both high and low glucose conditions. |
| 4309 | 16310163 | Both glucose and angiotensin II (Ang II) upregulate thrombospondin-1 (TSP1), a major activator of latent TGF-beta, and stimulate increased TGF-beta activity. |
| 4310 | 16310163 | We previously showed that high glucose stimulated TSP1-dependent TGF-beta activation in rat mesangial cells (RMCs). |
| 4311 | 16310163 | In this paper, we examined whether Ang II similarly upregulates TSP1 production and TSP1-dependent TGF-beta activation alone or in combination with high glucose concentrations. |
| 4312 | 16310163 | Ang II and high glucose stimulated increases in TSP1 protein levels in the conditioned media of both rat cardiac fibroblasts (RCFs) and rat mesangial cells (RMCs). |
| 4313 | 16310163 | Meanwhile, Ang II stimulated increases in both TGF-beta activity and protein by RMCs, whereas, RCFs responded to both Ang II and high glucose with increased TGF-beta activity in the absence of altered TGF-beta protein levels. |
| 4314 | 16310163 | A combination of Ang II and high glucose induced synergistic TGF-beta activation by RCFs. |
| 4315 | 16310163 | Moreover, Ang II induction of TSP1 and increased TGF-beta activity were blocked by losartan, an antagonist of the Ang II type 1 (AT1) receptor. |
| 4316 | 16310163 | The increase in TSP1 expression leads to increased TGF-beta activity upon Ang II and/or glucose treatment, since peptide antagonists of TSP1-mediated TGF-beta activation blocked Ang II and glucose-induced TGF-beta activation. |
| 4317 | 16330325 | Transcript levels of genes involved in intestinal iron absorption, including Dcytb, DMT1, and ferroportin, are significantly elevated in the absence of hepcidin. |
| 4318 | 16330325 | Moreover, transcriptional activation of hepcidin is abrogated in SMAD4-deficient hepatocytes in response to iron overload, TGF-beta, BMP, or IL-6. |
| 4319 | 16330325 | Our study uncovers a novel role of TGF-beta/SMAD4 in regulating hepcidin expression and thus intestinal iron transport and iron homeostasis. |
| 4320 | 16371802 | In addition, there appears to be a complex relationship between TNFalpha and tumor growth factor beta (TGF-beta), a cytokine which promotes collagen synthesis and deposition. |
| 4321 | 16380465 | Increased renal fibronectin, fibronectin ED-A, and collagen IValpha1 expression, as well as elevated plasma creatinine levels, were observed after 9 wk. |
| 4322 | 16380465 | In contrast, transforming growth factor-beta1 mRNA content was significantly increased only in the kidney by 9 wk. |
| 4323 | 16392625 | In conclusion, aminoguanidine improves wound healing, restores growth factor TGF-beta1 expression, and preserves collagen ultra structure, whereas it has no prominent effect on NO levels within wound tissue in diabetic rats. |
| 4324 | 16394111 | Moreover, angiostatin treatment downregulated the expression of vascular endothelial growth factor and TGF-beta1, two major pathogenic factors of DN, in diabetic kidneys. |
| 4325 | 16394111 | In cultured human mesangial cells, angiostatin blocked the overexpression of vascular endothelial growth factor and TGF-beta1 that were induced by high glucose while increasing the levels of pigment epithelium-derived factor, an endogenous inhibitor of DN. |
| 4326 | 16394111 | Moreover, angiostatin treatment downregulated the expression of vascular endothelial growth factor and TGF-beta1, two major pathogenic factors of DN, in diabetic kidneys. |
| 4327 | 16394111 | In cultured human mesangial cells, angiostatin blocked the overexpression of vascular endothelial growth factor and TGF-beta1 that were induced by high glucose while increasing the levels of pigment epithelium-derived factor, an endogenous inhibitor of DN. |
| 4328 | 16400005 | Mdk-/- mesangial cells exhibited reduced phosphorylation of protein kinase C and extracellular signal-regulated kinase as well as reduced production of transforming growth factor-beta(1) on high glucose loading. |
| 4329 | 16400005 | Addition of exogenous midkine restored extracellular signal-regulated kinase phosphorylation in Mdk-/- cells under high glucose conditions, whereas a midkine antisense oligodeoxynucleotide suppressed midkine in Mdk+/+ cells. |
| 4330 | 16412937 | Immunohistologic study of interleukin-1, transforming growth factor-beta, and alpha-smooth muscle actin in lens epithelial cells in diabetic eyes. |
| 4331 | 16428080 | Immunohistochemistry for ED-1 macrophages marker, intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein-1 (MCP-1) was performed. |
| 4332 | 16428080 | Activity of AOE such as glutathione peroxidase (GSH-PX) was markedly elevated while superoxide dismutase (SOD) and catalase (CAT) were not changed by MMF treatment. |
| 4333 | 16428080 | In diabetic animals receiving no treatment, there were increases in ED-1-positive cells, ICAM-1 expression and MCP-1 expression in glomeruli and tubulointerstitium, which were effectively suppressed by MMF treatment. |
| 4334 | 16428080 | Our data suggest that MMF treatment ameliorates early renal injury via the inhibition of oxidative stress and overexpression of ICAM-1, MCP-1 and TGF-beta1 in renal tissue in diabetic rats. |
| 4335 | 16433046 | Changes in maternal plasma levels of VEGF, bFGF, TGF-beta1, ET-1 and sKL during uncomplicated pregnancy, hypertensive pregnancy and gestational diabetes. |
| 4336 | 16435884 | Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus. |
| 4337 | 16435884 | Here we describe a conditional system for expressing Smad7, a potent inhibitor of TGF-beta signaling, to identify distinct roles for this pathway in adult and embryonic beta cells. |
| 4338 | 16435884 | Smad7 expression in Pdx1+ embryonic pancreas cells resulted in striking embryonic beta cell hypoplasia and neonatal lethality. |
| 4339 | 16435884 | Conditional expression of Smad7 in adult Pdx1+ cells reduced detectable beta cell expression of MafA, menin, and other factors that regulate beta cell function. |
| 4340 | 16435884 | Reduced pancreatic insulin content and hypoinsulinemia produced overt diabetes that was fully reversed upon resumption of islet TGF-beta signaling. |
| 4341 | 16435884 | Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus. |
| 4342 | 16435884 | Here we describe a conditional system for expressing Smad7, a potent inhibitor of TGF-beta signaling, to identify distinct roles for this pathway in adult and embryonic beta cells. |
| 4343 | 16435884 | Smad7 expression in Pdx1+ embryonic pancreas cells resulted in striking embryonic beta cell hypoplasia and neonatal lethality. |
| 4344 | 16435884 | Conditional expression of Smad7 in adult Pdx1+ cells reduced detectable beta cell expression of MafA, menin, and other factors that regulate beta cell function. |
| 4345 | 16435884 | Reduced pancreatic insulin content and hypoinsulinemia produced overt diabetes that was fully reversed upon resumption of islet TGF-beta signaling. |
| 4346 | 16435884 | Conditional expression of Smad7 in pancreatic beta cells disrupts TGF-beta signaling and induces reversible diabetes mellitus. |
| 4347 | 16435884 | Here we describe a conditional system for expressing Smad7, a potent inhibitor of TGF-beta signaling, to identify distinct roles for this pathway in adult and embryonic beta cells. |
| 4348 | 16435884 | Smad7 expression in Pdx1+ embryonic pancreas cells resulted in striking embryonic beta cell hypoplasia and neonatal lethality. |
| 4349 | 16435884 | Conditional expression of Smad7 in adult Pdx1+ cells reduced detectable beta cell expression of MafA, menin, and other factors that regulate beta cell function. |
| 4350 | 16435884 | Reduced pancreatic insulin content and hypoinsulinemia produced overt diabetes that was fully reversed upon resumption of islet TGF-beta signaling. |
| 4351 | 16436663 | Reverse transcription-polymerase chain reaction analysis showed that relative gene expression levels of matrix metalloproteinases (MMP-2 and MMP-9) and transforming growth factor-beta1 were increased in parallel with calcification. |
| 4352 | 16436663 | Gene expression of core binding factor alpha-1, an osteoblast-specific transcription factor, increased in parallel with elastin calcification and attained approximately 9.5-fold higher expression at 21 days compared to 3 days after implantation. |
| 4353 | 16436663 | Similarly, mRNA levels of the bone markers osteopontin and alkaline phosphatase also increased progressively, but osteocalcin levels remained unchanged. |
| 4354 | 16449286 | Role of TGF-beta/GLUT1 axis in susceptibility vs resistance to diabetic glomerulopathy in the Milan rat model. |
| 4355 | 16476010 | Elimination of CD4+ CD25+ regulatory T cells breaks down reovirus type 2-triggered and CpG ODN-induced prolonged mild autoimmune insulitis in DBA/1 mice. |
| 4356 | 16476010 | Compared with the control mice, newborn mice treated with monoclonal antibody (MoAb) against mouse CD25(+) CD4(+) T cells together with Reo-2 and CpG ODN greatly reduced the absolute number of splenic CD25(+) T cells and resulted in the development of severe insulitis, leading to an overt early diabetes. |
| 4357 | 16476010 | Moreover, the treatment of the MoAb increased production of interferon-gamma (IFN-gamma) and decreased that of interleukin-4 (IL-4) and transforming growth factor-beta1 (TGF-beta1) and developed high titre of autoantibodies against pancreatic islet cells. |
| 4358 | 16476010 | These evidences suggest that CD4(+) CD25(+) T cell may, at least in part, maintain tolerance to Reo-2-triggered and CpG ODN-induced prolonged mild Th1-dependent autoimmune insulitis, leading to the overt disease. |
| 4359 | 16523407 | Suppression of transforming growth factor-beta1 gene expression by Danggui buxue tang, a traditional Chinese herbal preparation, in retarding the progress of renal damage in streptozotocin-induced diabetic rats. |
| 4360 | 16523407 | Streptozotocin-dependent alterations in renal weight/body weight ratio, urinary albumin and beta (2)-microglobulin concentrations, urinary albumin excretion rate, and creatinine clearance were ameliorated after eight weeks of treatment with either DBT or the angiotensin-converting enzyme inhibitor, benazepril. |
| 4361 | 16523407 | However, eight weeks of treatment with DBT failed to modify the concentration of angiotensin II in plasma or kidney, indicating that the ability of the preparation to retard the progression of kidney disease was not attributable to inhibition of the renin-angiotensin system. |
| 4362 | 16528250 | High glucose, angiotensin II, phorbol 12-myristate 13-acetate and transforming growth factor-beta 1 (TGF-beta1) stimulated OPN mRNA expression in IRPTCs in a dose- and time-dependent manner. |
| 4363 | 16528250 | IRPTCs overexpressing dominant-negative protein kinase C-beta 1 (PKC-beta1) cDNA or antisense TGF-beta1 cDNA prevented the high glucose effect on OPN mRNA expression. |
| 4364 | 16528250 | We concluded that high glucose-mediated increases in OPN gene expression in diabetic rat RPTs and IRPTCs are mediated, at least in part, via reactive oxygen species generation, intrarenal rennin-angiotensin system activation, TGF-beta1 expression, and PKC-beta1 signaling. |
| 4365 | 16528250 | High glucose, angiotensin II, phorbol 12-myristate 13-acetate and transforming growth factor-beta 1 (TGF-beta1) stimulated OPN mRNA expression in IRPTCs in a dose- and time-dependent manner. |
| 4366 | 16528250 | IRPTCs overexpressing dominant-negative protein kinase C-beta 1 (PKC-beta1) cDNA or antisense TGF-beta1 cDNA prevented the high glucose effect on OPN mRNA expression. |
| 4367 | 16528250 | We concluded that high glucose-mediated increases in OPN gene expression in diabetic rat RPTs and IRPTCs are mediated, at least in part, via reactive oxygen species generation, intrarenal rennin-angiotensin system activation, TGF-beta1 expression, and PKC-beta1 signaling. |
| 4368 | 16528250 | High glucose, angiotensin II, phorbol 12-myristate 13-acetate and transforming growth factor-beta 1 (TGF-beta1) stimulated OPN mRNA expression in IRPTCs in a dose- and time-dependent manner. |
| 4369 | 16528250 | IRPTCs overexpressing dominant-negative protein kinase C-beta 1 (PKC-beta1) cDNA or antisense TGF-beta1 cDNA prevented the high glucose effect on OPN mRNA expression. |
| 4370 | 16528250 | We concluded that high glucose-mediated increases in OPN gene expression in diabetic rat RPTs and IRPTCs are mediated, at least in part, via reactive oxygen species generation, intrarenal rennin-angiotensin system activation, TGF-beta1 expression, and PKC-beta1 signaling. |
| 4371 | 16543493 | Association of transforming growth factor-beta1 gene polymorphisms with myocardial infarction in patients with angiographically proven coronary heart disease. |
| 4372 | 16556868 | Essential role of Smad3 in angiotensin II-induced vascular fibrosis. |
| 4373 | 16556868 | This was extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) dependent but transforming growth factor-beta (TGF-beta) independent because Ang II-induced Smad signaling was blocked by addition of ERK1/2 inhibitor and by dominant-negative (DN) ERK1/2 but not by DN-TGF-beta receptor II (TbetaRII) or conditional deletion of TbetaRII. |
| 4374 | 16556868 | Second, Ang II was also able to activate the late Smad2/3 signaling pathway at 24 hours, which was TGF-beta dependent because it was blocked by the anti-TGF-beta antibody and DN-TbetaRII. |
| 4375 | 16556868 | Finally, activation of Smad3 but not Smad2 was a key and necessary mechanism of Ang II-induced vascular fibrosis because Ang II induced Smad3/4 promoter activities and collagen matrix expression was abolished in VSMCs null for Smad3 but not Smad2. |
| 4376 | 16556868 | Thus, we concluded that Ang II induces vascular fibrosis via both TGF-beta-dependent and ERK1/2 MAPK-dependent Smad signaling pathways. |
| 4377 | 16556868 | Activation of Smad3 but not Smad2 is a key mechanism by which Ang II mediates arteriosclerosis. |
| 4378 | 16556868 | Essential role of Smad3 in angiotensin II-induced vascular fibrosis. |
| 4379 | 16556868 | This was extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) dependent but transforming growth factor-beta (TGF-beta) independent because Ang II-induced Smad signaling was blocked by addition of ERK1/2 inhibitor and by dominant-negative (DN) ERK1/2 but not by DN-TGF-beta receptor II (TbetaRII) or conditional deletion of TbetaRII. |
| 4380 | 16556868 | Second, Ang II was also able to activate the late Smad2/3 signaling pathway at 24 hours, which was TGF-beta dependent because it was blocked by the anti-TGF-beta antibody and DN-TbetaRII. |
| 4381 | 16556868 | Finally, activation of Smad3 but not Smad2 was a key and necessary mechanism of Ang II-induced vascular fibrosis because Ang II induced Smad3/4 promoter activities and collagen matrix expression was abolished in VSMCs null for Smad3 but not Smad2. |
| 4382 | 16556868 | Thus, we concluded that Ang II induces vascular fibrosis via both TGF-beta-dependent and ERK1/2 MAPK-dependent Smad signaling pathways. |
| 4383 | 16556868 | Activation of Smad3 but not Smad2 is a key mechanism by which Ang II mediates arteriosclerosis. |
| 4384 | 16556868 | Essential role of Smad3 in angiotensin II-induced vascular fibrosis. |
| 4385 | 16556868 | This was extracellular signal-regulated kinase 1/2 (ERK1/2) mitogen-activated protein kinase (MAPK) dependent but transforming growth factor-beta (TGF-beta) independent because Ang II-induced Smad signaling was blocked by addition of ERK1/2 inhibitor and by dominant-negative (DN) ERK1/2 but not by DN-TGF-beta receptor II (TbetaRII) or conditional deletion of TbetaRII. |
| 4386 | 16556868 | Second, Ang II was also able to activate the late Smad2/3 signaling pathway at 24 hours, which was TGF-beta dependent because it was blocked by the anti-TGF-beta antibody and DN-TbetaRII. |
| 4387 | 16556868 | Finally, activation of Smad3 but not Smad2 was a key and necessary mechanism of Ang II-induced vascular fibrosis because Ang II induced Smad3/4 promoter activities and collagen matrix expression was abolished in VSMCs null for Smad3 but not Smad2. |
| 4388 | 16556868 | Thus, we concluded that Ang II induces vascular fibrosis via both TGF-beta-dependent and ERK1/2 MAPK-dependent Smad signaling pathways. |
| 4389 | 16556868 | Activation of Smad3 but not Smad2 is a key mechanism by which Ang II mediates arteriosclerosis. |
| 4390 | 16567507 | Furthermore, they exhibited increased renal immunostaining for type IV collagen and osteopontin, which was associated with increased macrophage infiltration and glomerular apoptosis. |
| 4391 | 16567507 | In vitro studies demonstrated that high glucose levels markedly increased the expression of type IV collagen, transforming growth factor-beta1, and the number of leukocytes adherent to cultured mesangial cells. |
| 4392 | 16572112 | Transforming growth factor (TGF)-beta1, fibronectin expression, Ras, ERK, p38, and c-Jun activation of glomerular mesangial cells or urinary albumin secretion were assessed. |
| 4393 | 16572112 | High glucose and AGEs rapidly enhanced Ras activation and progressively increased cytosolic ERK and nuclear c-Jun activation. |
| 4394 | 16572112 | SOD or PD98059 pretreatment reduced high-glucose and AGE promotion of ERK and c-Jun activation. |
| 4395 | 16572112 | Exogenous SOD treatment in diabetic rats significantly attenuated diabetes induction of superoxide, urinary albumin excretion, 8-hydroxy-2'-deoxyguanosine, TGF-beta1, and fibronectin immunoreactivities in renal glomerular mesangial cells. |
| 4396 | 16575121 | Of these, the cytokine transforming growth factor (TGF-beta) has emerged as having a key role in the development of renal hypertrophy and accumulation of extracellular matrix in diabetes. |
| 4397 | 16585566 | We show that effectors generated from murine islet-specific CD4 cells by TCR stimulation with IL-2 and TGF-beta1 have potent suppressive activity. |
| 4398 | 16585566 | However, the adaptive population does acquire the X-linked forkhead/winged helix transcription factor, FoxP3, which is associated with regulatory T cell function and maintains expression in vivo. |
| 4399 | 16585566 | In vivo, they eliminate Th1 cells in lymphoid tissues, where Fas/FasL interactions potentially play a role because Th1 cells persist when this pathway is blocked. |
| 4400 | 16597372 | Furthermore, long-term administration of Hachimi-jio-gan reduced renal cortical expression of proteins, such as transforming growth factor-beta1 (TGF-beta1), fibronectin, inducible nitric oxide synthase and cyclooxygenase-2. |
| 4401 | 16597691 | Recent data suggest that the phosphatidylinositol 3-kinase (PI3-K)/Akt/mammalian target of rapamycin (mTOR) pathway is important in diabetic nephropathy. |
| 4402 | 16597691 | It is interesting that D+SRL was associated with a significant reduction of renal TGF-beta1 and glomerular connective tissue growth factor. |
| 4403 | 16600163 | We propose that an auto-maintaining mechanism of hemodynamic perturbations and increased tissue angiotensin II may be involved in the initiation and maintenance of a loop in which transforming growth factor beta1 and Glut-1 upregulation play important roles in the pathophysiology of diabetic-induced kidney lesions. |
| 4404 | 16604193 | Renal expression of several genes that encode proteins associated with senescence and/or apoptosis (TGF-beta1, connective tissue growth factor, p53, alpha-synuclein, and forkhead box O1) increases in the same progression. |
| 4405 | 16624630 | These nephropathies were associated with the upregulations of plasminogen activator inhibitor 1 (PAI-1) mRNA expression and its protein activity in the renal cortex, and a significant increase in transforming growth factor beta1 (TGF-beta1) expression. |
| 4406 | 16624630 | These renoprotective effects are likely to be achieved through suppression of PAI-1 and TGF-beta1 in the renal cortex, and consequently less extracellular matrix deposition. |
| 4407 | 16624630 | These nephropathies were associated with the upregulations of plasminogen activator inhibitor 1 (PAI-1) mRNA expression and its protein activity in the renal cortex, and a significant increase in transforming growth factor beta1 (TGF-beta1) expression. |
| 4408 | 16624630 | These renoprotective effects are likely to be achieved through suppression of PAI-1 and TGF-beta1 in the renal cortex, and consequently less extracellular matrix deposition. |
| 4409 | 16628253 | In vivo, expansion of CD25(+)Foxp3(+) and insulin-specific Tregs producing IL-10, TGF-beta, and IL-4 was strongly enhanced. |
| 4410 | 16644677 | One of the mechanisms involved in the progression of diabetic nephropathy, the most common cause of end-stage renal failure, is angiogenic phenomenon associated with the increase of angiogenic factors such as vascular endothelial growth factor (VEGF)-A and angiopoietin (Ang)-2, an antagonist of Ang-1. |
| 4411 | 16644677 | Increases in kidney weight, glomerular volume, creatinine clearance, urinary albumin excretion, total mesangial fraction, glomerular type IV collagen, glomerular endothelial area (CD31(+)), and monocyte/macrophage accumulation (F4/80(+)) observed in control db/db mice were significantly suppressed by daily intraperitoneal injection of NM-3 (100 mg/kg, for 8 weeks). |
| 4412 | 16644677 | Increases in renal expression of VEGF-A, Ang-2, fibrogenic factor transforming growth factor (TGF)-beta1, and chemokine monocyte chemoattractant protein-1 but not tumor necrosis factor-alpha were also inhibited by NM-3 in db/db mice. |
| 4413 | 16644677 | NM-3 significantly suppressed the increase of VEGF induced by high glucose in cultured podocytes and also suppressed the increase of VEGF and TGF-beta induced by high glucose in cultured mesangial cells. |
| 4414 | 16673206 | In this study, we examined TGF-beta 1, TGF-beta type I receptor (TbetaRI) and TGF-beta type II receptor (TbetaRII) expression in SW-13 adrenocortical carcinoma cells by Northern and Western blot analysis. |
| 4415 | 16696316 | The expression of transforming growth factor beta1 (TGF-beta1) and fibronectin (FN) was immunohistochemically examined. |
| 4416 | 16696316 | The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. |
| 4417 | 16696316 | The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-beta1 and FN were down-regulated by fluvastatin. |
| 4418 | 16696316 | The mRNA of SGK1 was positively correlated with the CTGF, TGF-beta1 and FN. |
| 4419 | 16696316 | The expression of transforming growth factor beta1 (TGF-beta1) and fibronectin (FN) was immunohistochemically examined. |
| 4420 | 16696316 | The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. |
| 4421 | 16696316 | The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-beta1 and FN were down-regulated by fluvastatin. |
| 4422 | 16696316 | The mRNA of SGK1 was positively correlated with the CTGF, TGF-beta1 and FN. |
| 4423 | 16696316 | The expression of transforming growth factor beta1 (TGF-beta1) and fibronectin (FN) was immunohistochemically examined. |
| 4424 | 16696316 | The expression of SGK1 was detected by RT-PCR and Western blot, and CTGF mRNA was assessed by RT-PCR. |
| 4425 | 16696316 | The levels of cortex SGK1 mRNA and protein were up-regulated, and both TGF-beta1 and FN were down-regulated by fluvastatin. |
| 4426 | 16696316 | The mRNA of SGK1 was positively correlated with the CTGF, TGF-beta1 and FN. |
| 4427 | 16700888 | CD4+CD25+ regulatory T cells in health and disease. |
| 4428 | 16700888 | Various populations of Treg cells have been described, including thymically derived CD4(+)CD25(+) Treg cells. |
| 4429 | 16700888 | In addition, a second subset of Treg cells, type 1 T regulatoary (Tr1) and Th3 cells, exert their suppressive capacity via cytokines such as interleukin-10 and transforming growth factor-beta and are contact independent. 4. |
| 4430 | 16700888 | The present review summarizes the characteristics and molecular basis of CD4(+)CD25(+) Treg cells, as well as their therapeutic potential in modulating inflammatory diseases, such as inflammatory bowel disease and rheumatoid arthritis. |
| 4431 | 16705146 | Here, we characterized renal changes in the pdx1(PB)-HNF6 transgenic mouse that exhibits beta-cell dysfunction and nonobese hypoinsulinemic diabetes. |
| 4432 | 16705146 | The HNF6 males exhibited albuminuria as early as 10 wk of age, and the urinary albumin excretion increased with age, exceeding 150 microg/24 h at 11 mo of age. |
| 4433 | 16705146 | Immunohistochemistry showed accumulation of type IV collagen and TGF-beta1 in the mesangial area. |
| 4434 | 16715619 | Genetics, oxidative stress: superoxide anion (O2*-) and hydrogen peroxide (H2O2), endothelial nitric oxide (eNO), lipid peroxides, anti-oxidants, endothelin, angiotensin converting enzyme (ACE) activity, angiotensinII, transforming growth factor-beta (TGF-beta), insulin, homocysteine, asymmetrical dimethyl arginine, proinflammatory cytokines: interleukin-6 (IL-6), tumor necrosis factor-a (TNF-alpha), C-reactive protein (hs-CRP), and long-chain polyunsaturated fatty acids (LCPUFAs), and activity of NAD(P)H oxidase have a role in human essential hypertension. |
| 4435 | 16718633 | Counteracting pro- and anti-inflammatory responses of serum cytokines have been reported, but the relevance of TNF-alpha, TGF-beta and IL-6 gene expression in peripheral blood leukocytes and their contribution to systemic inflammation in atherosclerosis, especially after acute myocardial infarction (AMI), has not been investigated yet. |
| 4436 | 16718633 | Gene expression alterations indicate a sophisticated regulation of counteracting TNF-alpha and TGF-beta cytokine expression in peripheral blood leukocytes after AMI with bias towards a pro-inflammatory situation. |
| 4437 | 16718633 | Counteracting pro- and anti-inflammatory responses of serum cytokines have been reported, but the relevance of TNF-alpha, TGF-beta and IL-6 gene expression in peripheral blood leukocytes and their contribution to systemic inflammation in atherosclerosis, especially after acute myocardial infarction (AMI), has not been investigated yet. |
| 4438 | 16718633 | Gene expression alterations indicate a sophisticated regulation of counteracting TNF-alpha and TGF-beta cytokine expression in peripheral blood leukocytes after AMI with bias towards a pro-inflammatory situation. |
| 4439 | 16723984 | In addition, we evaluated the effect of aldosterone and spironolactone on CTGF and collagen production in cultured cells. |
| 4440 | 16723984 | In addition, renal CTGF, collagen synthesis demonstrated marked decreases in the spironolactone treatment group. |
| 4441 | 16723984 | In cultured MC and PTC, aldosterone induced significant increases in CTGF gene expression and protein synthesis associated with increased collagen synthesis, which was abolished by prior treatment with spironolactone. |
| 4442 | 16723984 | However, aldosterone treatment did not induce transforming growth factor (TGF)-beta1 overproduction, and inhibition of TGF-beta1 by neutralization of TGF-beta1 protein did not significantly prevent aldosterone-induced CTGF production. |
| 4443 | 16731830 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor that has been extensively studied in diabetic retinopathy. |
| 4444 | 16731830 | Administration of Ad-PEDF was found to prevent the overexpression of two major fibrogenic factors, transforming growth factor-beta (TGF-beta)1 and connective tissue growth factor (CTGF), and to significantly reduce the production of an extracellular matrix (ECM) protein in the diabetic kidney. |
| 4445 | 16731830 | In cultured human mesangial cells, PEDF significantly inhibited the overexpression of TGF-beta1 and fibronectin induced by angiotensin II. |
| 4446 | 16731830 | PEDF also blocked the fibronectin production induced by TGF-beta1 through inhibition of Smad3 activation. |
| 4447 | 16731830 | A therapeutic potential of PEDF in diabetic nephropathy is supported by its downregulation in diabetes; its prevention of the overexpression of TGF-beta, CTGF, and ECM proteins in diabetic kidney; and its amelioration of proteinuria in diabetic rats following Ad-PEDF injection. |
| 4448 | 16731830 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor that has been extensively studied in diabetic retinopathy. |
| 4449 | 16731830 | Administration of Ad-PEDF was found to prevent the overexpression of two major fibrogenic factors, transforming growth factor-beta (TGF-beta)1 and connective tissue growth factor (CTGF), and to significantly reduce the production of an extracellular matrix (ECM) protein in the diabetic kidney. |
| 4450 | 16731830 | In cultured human mesangial cells, PEDF significantly inhibited the overexpression of TGF-beta1 and fibronectin induced by angiotensin II. |
| 4451 | 16731830 | PEDF also blocked the fibronectin production induced by TGF-beta1 through inhibition of Smad3 activation. |
| 4452 | 16731830 | A therapeutic potential of PEDF in diabetic nephropathy is supported by its downregulation in diabetes; its prevention of the overexpression of TGF-beta, CTGF, and ECM proteins in diabetic kidney; and its amelioration of proteinuria in diabetic rats following Ad-PEDF injection. |
| 4453 | 16731830 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor that has been extensively studied in diabetic retinopathy. |
| 4454 | 16731830 | Administration of Ad-PEDF was found to prevent the overexpression of two major fibrogenic factors, transforming growth factor-beta (TGF-beta)1 and connective tissue growth factor (CTGF), and to significantly reduce the production of an extracellular matrix (ECM) protein in the diabetic kidney. |
| 4455 | 16731830 | In cultured human mesangial cells, PEDF significantly inhibited the overexpression of TGF-beta1 and fibronectin induced by angiotensin II. |
| 4456 | 16731830 | PEDF also blocked the fibronectin production induced by TGF-beta1 through inhibition of Smad3 activation. |
| 4457 | 16731830 | A therapeutic potential of PEDF in diabetic nephropathy is supported by its downregulation in diabetes; its prevention of the overexpression of TGF-beta, CTGF, and ECM proteins in diabetic kidney; and its amelioration of proteinuria in diabetic rats following Ad-PEDF injection. |
| 4458 | 16731830 | Pigment epithelium-derived factor (PEDF) is a potent angiogenic inhibitor that has been extensively studied in diabetic retinopathy. |
| 4459 | 16731830 | Administration of Ad-PEDF was found to prevent the overexpression of two major fibrogenic factors, transforming growth factor-beta (TGF-beta)1 and connective tissue growth factor (CTGF), and to significantly reduce the production of an extracellular matrix (ECM) protein in the diabetic kidney. |
| 4460 | 16731830 | In cultured human mesangial cells, PEDF significantly inhibited the overexpression of TGF-beta1 and fibronectin induced by angiotensin II. |
| 4461 | 16731830 | PEDF also blocked the fibronectin production induced by TGF-beta1 through inhibition of Smad3 activation. |
| 4462 | 16731830 | A therapeutic potential of PEDF in diabetic nephropathy is supported by its downregulation in diabetes; its prevention of the overexpression of TGF-beta, CTGF, and ECM proteins in diabetic kidney; and its amelioration of proteinuria in diabetic rats following Ad-PEDF injection. |
| 4463 | 16733348 | Insulin per se promotes the proliferation of renal cells and stimulates the production of other important growth factors such as insulin-like growth factor-1 and transforming growth factor beta. |
| 4464 | 16733348 | Insulin also upregulates the expression of angiotensin II type 1 receptor in mesangial cells, thus enhancing the deleterious effects of angiotensin II in the kidney, and stimulates production and renal action of endothelin-1. |
| 4465 | 16733556 | The involvement of transforming growth factor beta1 and its activation by thrombospondin-1. |
| 4466 | 16733556 | The cause of the increased high-molecular-weight HA synthesis consisted in the up-regulation of hyaluronan synthase (HAS) 2 mRNA without alterations of the expression of HAS3, which generates HA of lower molecular weight. |
| 4467 | 16733556 | D-Glucose at 30 mM also stimulated the production of transforming growth factor beta1 (TGFbeta1), the excessive activation of which was determined by the up-regulation of thrombospondin-1 (TSP-1). |
| 4468 | 16733556 | The blockage of TGFbeta1 action either by neutralizing anti-TGFbeta1 antibodies or by quenching the TGFbeta1 activation (with TSP-1-derived synthetic GGWSHW peptide) abolished the effect of high glucose on HAS2 mRNA expression and normalized the synthesis of HA. |
| 4469 | 16733556 | The involvement of transforming growth factor beta1 and its activation by thrombospondin-1. |
| 4470 | 16733556 | The cause of the increased high-molecular-weight HA synthesis consisted in the up-regulation of hyaluronan synthase (HAS) 2 mRNA without alterations of the expression of HAS3, which generates HA of lower molecular weight. |
| 4471 | 16733556 | D-Glucose at 30 mM also stimulated the production of transforming growth factor beta1 (TGFbeta1), the excessive activation of which was determined by the up-regulation of thrombospondin-1 (TSP-1). |
| 4472 | 16733556 | The blockage of TGFbeta1 action either by neutralizing anti-TGFbeta1 antibodies or by quenching the TGFbeta1 activation (with TSP-1-derived synthetic GGWSHW peptide) abolished the effect of high glucose on HAS2 mRNA expression and normalized the synthesis of HA. |
| 4473 | 16734145 | Serum TGF-beta1 was significantly positively correlated with albumin excretion rate, fasting and postprandial blood glucose levels, serum cholesterol and HbA1c, these correlations were only found in diabetic patients with nephropathy but not in those without nephropathy or the control group. |
| 4474 | 16741022 | We examined cardiac expression of transforming growth factor-beta(1) (TGFbeta(1)) and endothelin-1 (ET-1) in male OLETF rats. |
| 4475 | 16741022 | Our results suggest that CCBs are effective in normalizing upregulated cardiac TGFbeta1 and ET-1 levels at the insulin-resistant stage in OLETF rats, which may improve cardiac morphology and function in this rat model without altering blood pressure and plasma glucose levels. |
| 4476 | 16766854 | In the presence of high glucose and H2O2, the total antioxidative capability, catalase, reduced glutathione, and superoxide dismutase level of rat mesangial cells were significantly decreased, and transforming growth factor beta1 (TGF-beta1) mRNA level, collagen IV, and laminin level were significantly increased. |
| 4477 | 16766854 | When compared with those in the high glucose group, these 4 indexes of cells incubated in 2.0 and/or 20 micromol/L of AS I were significantly enhanced, and levels of TGF-beta1 mRNA, collagen IV and laminin were statistically decreased. |
| 4478 | 16766854 | In the presence of high glucose and H2O2, the total antioxidative capability, catalase, reduced glutathione, and superoxide dismutase level of rat mesangial cells were significantly decreased, and transforming growth factor beta1 (TGF-beta1) mRNA level, collagen IV, and laminin level were significantly increased. |
| 4479 | 16766854 | When compared with those in the high glucose group, these 4 indexes of cells incubated in 2.0 and/or 20 micromol/L of AS I were significantly enhanced, and levels of TGF-beta1 mRNA, collagen IV and laminin were statistically decreased. |
| 4480 | 16778384 | We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. |
| 4481 | 16778384 | The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. |
| 4482 | 16778384 | TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. |
| 4483 | 16778384 | We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. |
| 4484 | 16778384 | The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. |
| 4485 | 16778384 | TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. |
| 4486 | 16778384 | We also examined the inhibitory effect of TGF-beta1 siRNAs on the expression of plasminogen activator inhibitor (PAI)-1 and Collagen Type I which are down-regulators of TGF-beta1. |
| 4487 | 16778384 | The expression of TGF-beta1, PAI-1 and Collagen Type I was increased in RMCs that were stimulated by 30 mM glucose. |
| 4488 | 16778384 | TGF-beta1 siRNAs reduces high glucose-induced TGF-beta1, PAI-1, and Collagen Type I mRNA and protein expression in a dose-dependent manner. |
| 4489 | 16790365 | However, in this study, we demonstrate protection against disease by covaccination with a mutant B7-1 molecule (B7-1wa) that binds the negative T cell regulator CTLA-4 (CD152), but not CD28. |
| 4490 | 16790365 | In vitro, the T cells of covaccinated mice had negative responses to both insulin and GAD65, and this was restored by adding blocking antibodies to transforming growth factor beta1 (TGF-beta1), suggesting a role for this cytokine. |
| 4491 | 16790365 | Furthermore, vaccinated mice had increased numbers of T cells with Tr-associated markers, such as CTLA-4, Foxp3, and membrane-bound TGF-beta1. |
| 4492 | 16790365 | However, in this study, we demonstrate protection against disease by covaccination with a mutant B7-1 molecule (B7-1wa) that binds the negative T cell regulator CTLA-4 (CD152), but not CD28. |
| 4493 | 16790365 | In vitro, the T cells of covaccinated mice had negative responses to both insulin and GAD65, and this was restored by adding blocking antibodies to transforming growth factor beta1 (TGF-beta1), suggesting a role for this cytokine. |
| 4494 | 16790365 | Furthermore, vaccinated mice had increased numbers of T cells with Tr-associated markers, such as CTLA-4, Foxp3, and membrane-bound TGF-beta1. |
| 4495 | 16803995 | Results regarding genes involved in inflammation (IL-1 cluster, IL-6, IL-10, TNF-alpha, TGF-beta, TLR-4, PPARgamma), insulin/IGF-1 signaling pathway and lipid metabolism (apolipoproteins, CETP, PON1), and oxidative stress (p53, p66(shc)) will be described. |
| 4496 | 16804083 | Gene disruption of the tumor suppressor PTEN, a negative regulator of the phosphatidylinositol 3-kinase/Akt pathway, in fruit flies and mice demonstrated its role in size control in a cell-specific manner. |
| 4497 | 16804083 | We link early renal hypertrophy with significant reduction in PTEN expression in the streptozotocin-induced diabetic kidney cortex and glomeruli, concomitant with activation of Akt. |
| 4498 | 16804083 | Similarly, exposure of mesangial cells to high concentrations of glucose also decreased PTEN expression and its phosphatase activity, resulting in increased Akt activity. |
| 4499 | 16804083 | TGF-beta significantly reduced PTEN expression in mesangial cells, with a reduction in its phosphatase activity and an increase in Akt activation. |
| 4500 | 16804083 | PTEN and dominant-negative Akt attenuated TGF-beta-induced hypertrophy of mesangial cells. |
| 4501 | 16804083 | Finally, we show that inhibition of TGF-beta signal transduction blocks the effect of high glucose on PTEN downregulation. |
| 4502 | 16804083 | These data identify a novel mechanism placing PTEN as a key regulator of diabetic mesangial hypertrophy involving TGF-beta signaling. |
| 4503 | 16804083 | Gene disruption of the tumor suppressor PTEN, a negative regulator of the phosphatidylinositol 3-kinase/Akt pathway, in fruit flies and mice demonstrated its role in size control in a cell-specific manner. |
| 4504 | 16804083 | We link early renal hypertrophy with significant reduction in PTEN expression in the streptozotocin-induced diabetic kidney cortex and glomeruli, concomitant with activation of Akt. |
| 4505 | 16804083 | Similarly, exposure of mesangial cells to high concentrations of glucose also decreased PTEN expression and its phosphatase activity, resulting in increased Akt activity. |
| 4506 | 16804083 | TGF-beta significantly reduced PTEN expression in mesangial cells, with a reduction in its phosphatase activity and an increase in Akt activation. |
| 4507 | 16804083 | PTEN and dominant-negative Akt attenuated TGF-beta-induced hypertrophy of mesangial cells. |
| 4508 | 16804083 | Finally, we show that inhibition of TGF-beta signal transduction blocks the effect of high glucose on PTEN downregulation. |
| 4509 | 16804083 | These data identify a novel mechanism placing PTEN as a key regulator of diabetic mesangial hypertrophy involving TGF-beta signaling. |
| 4510 | 16804083 | Gene disruption of the tumor suppressor PTEN, a negative regulator of the phosphatidylinositol 3-kinase/Akt pathway, in fruit flies and mice demonstrated its role in size control in a cell-specific manner. |
| 4511 | 16804083 | We link early renal hypertrophy with significant reduction in PTEN expression in the streptozotocin-induced diabetic kidney cortex and glomeruli, concomitant with activation of Akt. |
| 4512 | 16804083 | Similarly, exposure of mesangial cells to high concentrations of glucose also decreased PTEN expression and its phosphatase activity, resulting in increased Akt activity. |
| 4513 | 16804083 | TGF-beta significantly reduced PTEN expression in mesangial cells, with a reduction in its phosphatase activity and an increase in Akt activation. |
| 4514 | 16804083 | PTEN and dominant-negative Akt attenuated TGF-beta-induced hypertrophy of mesangial cells. |
| 4515 | 16804083 | Finally, we show that inhibition of TGF-beta signal transduction blocks the effect of high glucose on PTEN downregulation. |
| 4516 | 16804083 | These data identify a novel mechanism placing PTEN as a key regulator of diabetic mesangial hypertrophy involving TGF-beta signaling. |
| 4517 | 16804083 | Gene disruption of the tumor suppressor PTEN, a negative regulator of the phosphatidylinositol 3-kinase/Akt pathway, in fruit flies and mice demonstrated its role in size control in a cell-specific manner. |
| 4518 | 16804083 | We link early renal hypertrophy with significant reduction in PTEN expression in the streptozotocin-induced diabetic kidney cortex and glomeruli, concomitant with activation of Akt. |
| 4519 | 16804083 | Similarly, exposure of mesangial cells to high concentrations of glucose also decreased PTEN expression and its phosphatase activity, resulting in increased Akt activity. |
| 4520 | 16804083 | TGF-beta significantly reduced PTEN expression in mesangial cells, with a reduction in its phosphatase activity and an increase in Akt activation. |
| 4521 | 16804083 | PTEN and dominant-negative Akt attenuated TGF-beta-induced hypertrophy of mesangial cells. |
| 4522 | 16804083 | Finally, we show that inhibition of TGF-beta signal transduction blocks the effect of high glucose on PTEN downregulation. |
| 4523 | 16804083 | These data identify a novel mechanism placing PTEN as a key regulator of diabetic mesangial hypertrophy involving TGF-beta signaling. |
| 4524 | 16825023 | In addition, several active proteins generated in the central adipose tissue, such as leptin, proinflammatory cytokines, plasminogen activator inhibitor-1, angiotensinogen, and growth factors (transforming growth factor-beta1), as well as low levels of the protective adiponectin, may contribute to renal injury. |
| 4525 | 16825023 | In the presence of glomerulopathy and/or hypertension, angiotensin converting enzyme inhibitors or angiotensin II type I receptor blockers are the drugs of choice to improve glomerular hyperfiltration. |
| 4526 | 16828231 | These include vitamin E, which blunts the rise in mesangial diacylglycerol levels induced by hyperglycemia; statins and (possibly) policosanol, which down-regulate NADPH oxidase activity by diminishing isoprenylation of Rac1; lipoic acid, whose potent antioxidant activity antagonizes the impact of oxidant stress on TGF-beta expression; pyridoxamine, which inhibits production of advanced glycation endproducts; arginine, high-dose folate, vitamin C, and salt restriction, which may support glomerular production of nitric oxide; and estrogen and soy isoflavones, which may induce nitric oxide synthase in glomerular capillaries while also interfering with TGF-beta signaling. |
| 4527 | 16835316 | Attractin, a dipeptidyl peptidase IV/CD26-like enzyme, is expressed on human peripheral blood monocytes and potentially influences monocyte function. |
| 4528 | 16835316 | Moreover, this inhibitor significantly modulates the production of interleukin-1 (IL-1) receptor antagonist, IL-6, and transforming growth factor-beta1 in lipopolysaccharide-stimulated monocyte cultures. |
| 4529 | 16838180 | During the past 10 years, CD4(+)CD25(+)Foxp3(+) regulatory T cells (Treg) have been extensively studied for their function in autoimmune disease. |
| 4530 | 16838180 | However, downmodulation of dendritic cell function and secretion of inhibitory cytokines such as IL-10 and TGF-beta might underlie Treg function in vivo. |
| 4531 | 16859672 | The malonaldehyde and transforming growth factor beta-1 (TGF-beta1) concentrations as well as the protein kinase C (PKC) activities in the diabetic kidney were significantly higher than those of the control, which were decreased by treatment with N-hexacosanol. |
| 4532 | 16879245 | The expression of interferon (IFN)-gamma, interleukin (IL)-4, IL-10 and transforming growth factor (TGF)-beta in PBMC was studied with real-time polymerase chain reaction (PCR) in a subgroup of 38 children. |
| 4533 | 16879245 | Rotavirus-stimulated lymphocytes from autoantibody-positive children produced more IL-4 and phytohaemagglutinin (PHA)-stimulated lymphocytes more IL-4 and IFN-gamma than lymphocytes from control children. |
| 4534 | 16879245 | PHA-stimulated lymphocytes from children with diabetes also produced more IL-4 and purified protein derivative (PPD)-stimulated lymphocytes less TGF-beta than lymphocytes from autoantibody-negative control children. |
| 4535 | 16888219 | In the pancreas of VIP-treated animals, regulatory T cell markers predominate, as indicated by the upregulation of FoxP3 and transforming growth factor-beta (TGF-beta), and the downregulation of the transcription factor, T-bet. |
| 4536 | 16889607 | CTGF was highly expressed in tubuloepithelial cells of allografts, along with alpha-smooth muscle actin, a marker of myofibroblasts, and transcriptionally associated with other markers of fibrosis. |
| 4537 | 16889607 | In vitro studies of tubular epithelium indicate that CTGF is capable of inducing EMT, independent of TGF-beta. |
| 4538 | 16901490 | Pioglitazone inhibits connective tissue growth factor expression in advanced atherosclerotic plaques in low-density lipoprotein receptor-deficient mice. |
| 4539 | 16901490 | Recent studies indicate that CTGF may also contribute to plaque destabilization as it induces apoptosis and stimulates MMP-2 expression in VSMCs. |
| 4540 | 16901490 | Quantitative real-time PCR and Western blot showed that pioglitazone inhibited TGF-beta-stimulated CTGF expression. |
| 4541 | 16901964 | Diabetic rats and mice developed albuminuria and histopathological evidence of renal injury, including glomerular hypertrophy, mesangial expansion, and tubulointerstitial injury as well as increased renal cortical levels of MR protein, MR mRNA, TGFbeta mRNA, and osteopontin mRNA. |
| 4542 | 16914537 | EMT was assessed by the expression of alpha-smooth muscle actin, vimentin, E-cadherin, and matrix proteins and the induction of a myofibroblastic phenotype. |
| 4543 | 16914537 | Transfection with siRNA to CTGF was able to attenuate EMT-associated phenotypic changes after treatment with AGE or TGF-beta1. |
| 4544 | 16914537 | These findings suggest that CTGF represents an important independent mediator of tubular EMT, downstream of the actions of AGE or TGF-beta1. |
| 4545 | 16914537 | EMT was assessed by the expression of alpha-smooth muscle actin, vimentin, E-cadherin, and matrix proteins and the induction of a myofibroblastic phenotype. |
| 4546 | 16914537 | Transfection with siRNA to CTGF was able to attenuate EMT-associated phenotypic changes after treatment with AGE or TGF-beta1. |
| 4547 | 16914537 | These findings suggest that CTGF represents an important independent mediator of tubular EMT, downstream of the actions of AGE or TGF-beta1. |
| 4548 | 16933058 | Serum transforming growth factor-beta1 levels and pancreatic cancer risk: a nested case-control study (Japan). |
| 4549 | 16954341 | Betaglycan potentiates TGF-beta; however, soluble betaglycan, which is produced by the shedding of the membrane-bound receptor, is a potent antagonist of TGF-beta. |
| 4550 | 16954341 | These effects were associated with lower kidney levels of mRNAs encoding TGF-beta1, TGF-beta2, TGF-beta3, collagen IV, collagen I, fibronectin, and serum glucocorticoid kinase as well as a reduction in the immunostaining of collagen IV and fibronectin. |
| 4551 | 16954341 | Because SBG has a high affinity for all TGF-beta isoforms, in particular TGF-beta2, it is found naturally in serum and tissues and its shedding may be regulated. |
| 4552 | 16954341 | Betaglycan potentiates TGF-beta; however, soluble betaglycan, which is produced by the shedding of the membrane-bound receptor, is a potent antagonist of TGF-beta. |
| 4553 | 16954341 | These effects were associated with lower kidney levels of mRNAs encoding TGF-beta1, TGF-beta2, TGF-beta3, collagen IV, collagen I, fibronectin, and serum glucocorticoid kinase as well as a reduction in the immunostaining of collagen IV and fibronectin. |
| 4554 | 16954341 | Because SBG has a high affinity for all TGF-beta isoforms, in particular TGF-beta2, it is found naturally in serum and tissues and its shedding may be regulated. |
| 4555 | 16954341 | Betaglycan potentiates TGF-beta; however, soluble betaglycan, which is produced by the shedding of the membrane-bound receptor, is a potent antagonist of TGF-beta. |
| 4556 | 16954341 | These effects were associated with lower kidney levels of mRNAs encoding TGF-beta1, TGF-beta2, TGF-beta3, collagen IV, collagen I, fibronectin, and serum glucocorticoid kinase as well as a reduction in the immunostaining of collagen IV and fibronectin. |
| 4557 | 16954341 | Because SBG has a high affinity for all TGF-beta isoforms, in particular TGF-beta2, it is found naturally in serum and tissues and its shedding may be regulated. |
| 4558 | 16964407 | Transforming growth factor beta (TGFbeta) both inhibits proliferation of macrovascular endothelial cells and promotes their transdifferentiation to alpha-smooth-muscle-actin (alphaSMA)-expressing mesenchymal cells in vitro. |
| 4559 | 16964407 | Depending on the type of culture medium, 5-40% of these cells strongly expressed alphaSMA after approximately 6 days whereas expression of the endothelial cell-specific marker proteins von Willebrand factor and VE Cadherin (CD144) declined. |
| 4560 | 16964407 | TGFbeta2-induced phenotypic alterations were specific, as they were not caused by treatment of iBREC with VEGF, IGF-1 or bFGF. |
| 4561 | 16964407 | Induction of alphaSMA expression but not effects on morphology was strongly inhibited by bFGF, whereas IGF-1 enhanced TGFbeta2-induced alphaSMA expression. |
| 4562 | 16964424 | In addition, the expression of many genes associated with oxidative stress, collagen synthesis, and transforming growth factor-beta signaling was enhanced in the diabetic mice, and this enhancement was slightly inhibited in the astaxanthin-treated mice. |
| 4563 | 16980181 | The role of Smad3-dependent TGF-beta signal in vascular response to injury. |
| 4564 | 16980181 | We recently discovered that mice lacking Smad3, a major downstream mediator of TGF-beta, show enhanced neointimal hyperplasia with decreased matrix deposition in response to vascular injury. |
| 4565 | 16980181 | This review summarizes the current view on involvement of TGF-beta in atherosclerotic vascular disease and discusses the role of Smad3-dependent TGF-beta signal in vascular response to injury. |
| 4566 | 16980181 | The role of Smad3-dependent TGF-beta signal in vascular response to injury. |
| 4567 | 16980181 | We recently discovered that mice lacking Smad3, a major downstream mediator of TGF-beta, show enhanced neointimal hyperplasia with decreased matrix deposition in response to vascular injury. |
| 4568 | 16980181 | This review summarizes the current view on involvement of TGF-beta in atherosclerotic vascular disease and discusses the role of Smad3-dependent TGF-beta signal in vascular response to injury. |
| 4569 | 16980181 | The role of Smad3-dependent TGF-beta signal in vascular response to injury. |
| 4570 | 16980181 | We recently discovered that mice lacking Smad3, a major downstream mediator of TGF-beta, show enhanced neointimal hyperplasia with decreased matrix deposition in response to vascular injury. |
| 4571 | 16980181 | This review summarizes the current view on involvement of TGF-beta in atherosclerotic vascular disease and discusses the role of Smad3-dependent TGF-beta signal in vascular response to injury. |
| 4572 | 16980342 | Expression of atrial natriuretic peptide and transforming growth factor-beta1 was significantly increased in the WT-D group. |
| 4573 | 16984461 | Reversal of the wound healing deficit in diabetic rats by combined basic fibroblast growth factor and transforming growth factor-beta1 therapy. |
| 4574 | 16984461 | In this study, the implantation of a combination of basic fibroblast growth factor and transforming growth factor-beta in rats induced fivefold to sevenfold increases in granulation tissue formation in comparison with implantation of each growth factor alone. |
| 4575 | 16984461 | Incisional wounds and sponge granulation tissue were produced in separate groups and then treated with an injection of 2 microg transforming growth factor-beta1 combined with 10 microg basic fibroblast growth factor on day 3. |
| 4576 | 16984461 | The combination of transforming growth factor-beta1 and basic fibroblast growth factor had marked, positive effects on biochemical parameters of wound healing and reversed the tensile strength deficit of diabetic wounds. |
| 4577 | 16984461 | Nonradioactive in situ hybridization showed increased expression of messenger RNA for type I and III procollagen and transforming growth factor-beta1 in normal and diabetic wounds, whereas ultrastructural examination showed a marked reorganization of collagen fibrils. |
| 4578 | 16984461 | Reversal of the wound healing deficit in diabetic rats by combined basic fibroblast growth factor and transforming growth factor-beta1 therapy. |
| 4579 | 16984461 | In this study, the implantation of a combination of basic fibroblast growth factor and transforming growth factor-beta in rats induced fivefold to sevenfold increases in granulation tissue formation in comparison with implantation of each growth factor alone. |
| 4580 | 16984461 | Incisional wounds and sponge granulation tissue were produced in separate groups and then treated with an injection of 2 microg transforming growth factor-beta1 combined with 10 microg basic fibroblast growth factor on day 3. |
| 4581 | 16984461 | The combination of transforming growth factor-beta1 and basic fibroblast growth factor had marked, positive effects on biochemical parameters of wound healing and reversed the tensile strength deficit of diabetic wounds. |
| 4582 | 16984461 | Nonradioactive in situ hybridization showed increased expression of messenger RNA for type I and III procollagen and transforming growth factor-beta1 in normal and diabetic wounds, whereas ultrastructural examination showed a marked reorganization of collagen fibrils. |
| 4583 | 16984461 | Reversal of the wound healing deficit in diabetic rats by combined basic fibroblast growth factor and transforming growth factor-beta1 therapy. |
| 4584 | 16984461 | In this study, the implantation of a combination of basic fibroblast growth factor and transforming growth factor-beta in rats induced fivefold to sevenfold increases in granulation tissue formation in comparison with implantation of each growth factor alone. |
| 4585 | 16984461 | Incisional wounds and sponge granulation tissue were produced in separate groups and then treated with an injection of 2 microg transforming growth factor-beta1 combined with 10 microg basic fibroblast growth factor on day 3. |
| 4586 | 16984461 | The combination of transforming growth factor-beta1 and basic fibroblast growth factor had marked, positive effects on biochemical parameters of wound healing and reversed the tensile strength deficit of diabetic wounds. |
| 4587 | 16984461 | Nonradioactive in situ hybridization showed increased expression of messenger RNA for type I and III procollagen and transforming growth factor-beta1 in normal and diabetic wounds, whereas ultrastructural examination showed a marked reorganization of collagen fibrils. |
| 4588 | 16984461 | Reversal of the wound healing deficit in diabetic rats by combined basic fibroblast growth factor and transforming growth factor-beta1 therapy. |
| 4589 | 16984461 | In this study, the implantation of a combination of basic fibroblast growth factor and transforming growth factor-beta in rats induced fivefold to sevenfold increases in granulation tissue formation in comparison with implantation of each growth factor alone. |
| 4590 | 16984461 | Incisional wounds and sponge granulation tissue were produced in separate groups and then treated with an injection of 2 microg transforming growth factor-beta1 combined with 10 microg basic fibroblast growth factor on day 3. |
| 4591 | 16984461 | The combination of transforming growth factor-beta1 and basic fibroblast growth factor had marked, positive effects on biochemical parameters of wound healing and reversed the tensile strength deficit of diabetic wounds. |
| 4592 | 16984461 | Nonradioactive in situ hybridization showed increased expression of messenger RNA for type I and III procollagen and transforming growth factor-beta1 in normal and diabetic wounds, whereas ultrastructural examination showed a marked reorganization of collagen fibrils. |
| 4593 | 16984461 | Reversal of the wound healing deficit in diabetic rats by combined basic fibroblast growth factor and transforming growth factor-beta1 therapy. |
| 4594 | 16984461 | In this study, the implantation of a combination of basic fibroblast growth factor and transforming growth factor-beta in rats induced fivefold to sevenfold increases in granulation tissue formation in comparison with implantation of each growth factor alone. |
| 4595 | 16984461 | Incisional wounds and sponge granulation tissue were produced in separate groups and then treated with an injection of 2 microg transforming growth factor-beta1 combined with 10 microg basic fibroblast growth factor on day 3. |
| 4596 | 16984461 | The combination of transforming growth factor-beta1 and basic fibroblast growth factor had marked, positive effects on biochemical parameters of wound healing and reversed the tensile strength deficit of diabetic wounds. |
| 4597 | 16984461 | Nonradioactive in situ hybridization showed increased expression of messenger RNA for type I and III procollagen and transforming growth factor-beta1 in normal and diabetic wounds, whereas ultrastructural examination showed a marked reorganization of collagen fibrils. |
| 4598 | 17014667 | Our study found significantly elevated expression of transforming growth factor-beta1 (TGF-beta1) and type I TGF-beta receptors (TGFbetaR1), granulocyte macrophage colony-stimulating factor (GM-CSF), and epidermal growth factor (EGF) in keratinocytes in the ulcer margin (p < 0.05). |
| 4599 | 17014667 | Significantly increased expression of monocyte chemotactic protein-1, GM-CSF, CXCR1, and TGFbetaRI and decreased expression of interleukin (IL)-10, IL-15, and TGF-beta1 were observed in ulcer dermal endothelial cells (p < 0.05). |
| 4600 | 17014667 | There was a lack of up-regulation of IL-8, CCR2A, IL-10 receptor, GM-CSF receptor, platelet-derived growth factors and their receptors, vascular endothelial growth factor and its type II receptor, EGF receptor, insulin-like growth factor-1, and nitric oxide synthase-2 in both KCs and endothelial cells in the ulcer. |
| 4601 | 17014667 | Finally, there was a lack of up-regulation of IL-10 and IL-15 in keratinocytes and of EGF, basic fibroblast growth factor, and nitric oxide synthase-3 in endothelial cells in the ulcer margins. |
| 4602 | 17014667 | Our study found significantly elevated expression of transforming growth factor-beta1 (TGF-beta1) and type I TGF-beta receptors (TGFbetaR1), granulocyte macrophage colony-stimulating factor (GM-CSF), and epidermal growth factor (EGF) in keratinocytes in the ulcer margin (p < 0.05). |
| 4603 | 17014667 | Significantly increased expression of monocyte chemotactic protein-1, GM-CSF, CXCR1, and TGFbetaRI and decreased expression of interleukin (IL)-10, IL-15, and TGF-beta1 were observed in ulcer dermal endothelial cells (p < 0.05). |
| 4604 | 17014667 | There was a lack of up-regulation of IL-8, CCR2A, IL-10 receptor, GM-CSF receptor, platelet-derived growth factors and their receptors, vascular endothelial growth factor and its type II receptor, EGF receptor, insulin-like growth factor-1, and nitric oxide synthase-2 in both KCs and endothelial cells in the ulcer. |
| 4605 | 17014667 | Finally, there was a lack of up-regulation of IL-10 and IL-15 in keratinocytes and of EGF, basic fibroblast growth factor, and nitric oxide synthase-3 in endothelial cells in the ulcer margins. |
| 4606 | 17014924 | Transforming growth factor-beta 1 (TGF-beta1) is a key cytokine in obesity and insulin resistance and also play important roles in the development of atherosclerosis. |
| 4607 | 17014924 | The inflammatory response to hyperglycemia and insulin resistance could be the major factors for the increased expression of TGF-beta1. |
| 4608 | 17014924 | Transforming growth factor-beta 1 (TGF-beta1) is a key cytokine in obesity and insulin resistance and also play important roles in the development of atherosclerosis. |
| 4609 | 17014924 | The inflammatory response to hyperglycemia and insulin resistance could be the major factors for the increased expression of TGF-beta1. |
| 4610 | 17018841 | These high-glucose-induced changes in protein synthesis were phosphatidylinositol 3-kinase, Akt, and mammalian target of rapamycin (mTOR) dependent and transforming growth factor-beta independent. |
| 4611 | 17018841 | High glucose reduced AMPK alpha-subunit theronine (Thr) 172 phosphorylation, which required Akt activation. |
| 4612 | 17018841 | Metformin and 5-aminoimidazole-4-carboxamide-1beta-riboside (AICAR) increased AMPK phosphorylation, inhibited high-glucose stimulation of protein synthesis, and prevented high-glucose-induced changes in phosphorylation of 4E binding protein 1 and eukaryotic elongation factor 2. |
| 4613 | 17018841 | In diabetic rats, metformin and AICAR increased renal AMPK phosphorylation, reversed mTOR activation, and inhibited renal hypertrophy, without affecting hyperglycemia. |
| 4614 | 17018845 | Inhibiting albumin glycation attenuates dysregulation of VEGFR-1 and collagen IV subchain production and the development of renal insufficiency. |
| 4615 | 17018845 | Glomerular cells in culture respond to albumin containing Amadori glucose adducts (the principal serum glycated protein), with activation of protein kinase C-beta(1), increased expression of transforming growth factor (TGF)-beta1, the TGF-beta type II signaling receptor, and the extracellular matrix proteins alpha(1)(IV) collagen and fibronectin and with decreased production of the podocyte protein nephrin. |
| 4616 | 17018845 | Decreasing the burden of glycated albumin in diabetic db/db mice significantly reduces glomerular overexpression of TGF-beta1 mRNA, restores glomerular nephrin immunofluorescence, and lessens proteinuria, mesangial expansion, renal extracellular matrix protein production, and increased glomerular vascular endothelial growth factor (VEGF) immunostaining. |
| 4617 | 17018845 | In the present study, db/db mice were treated with a small molecule, designated 23CPPA, that inhibits the nonenzymatic condensation of glucose with the albumin protein to evaluate whether increased glycated albumin influences the production of VEGF receptors (VEGFRs) and type IV collagen subchains and ameliorates the development of renal insufficiency. |
| 4618 | 17018845 | Renal levels of VEGF and VEGFR-1 proteins and serum creatinine concentrations were significantly higher and renal levels of alpha(3)(IV) collagen and nephrin proteins and endogenous creatinine clearance values were significantly lower in control diabetic than in age-matched nondiabetic (db/m) mice. |
| 4619 | 17018845 | Inhibiting albumin glycation attenuates dysregulation of VEGFR-1 and collagen IV subchain production and the development of renal insufficiency. |
| 4620 | 17018845 | Glomerular cells in culture respond to albumin containing Amadori glucose adducts (the principal serum glycated protein), with activation of protein kinase C-beta(1), increased expression of transforming growth factor (TGF)-beta1, the TGF-beta type II signaling receptor, and the extracellular matrix proteins alpha(1)(IV) collagen and fibronectin and with decreased production of the podocyte protein nephrin. |
| 4621 | 17018845 | Decreasing the burden of glycated albumin in diabetic db/db mice significantly reduces glomerular overexpression of TGF-beta1 mRNA, restores glomerular nephrin immunofluorescence, and lessens proteinuria, mesangial expansion, renal extracellular matrix protein production, and increased glomerular vascular endothelial growth factor (VEGF) immunostaining. |
| 4622 | 17018845 | In the present study, db/db mice were treated with a small molecule, designated 23CPPA, that inhibits the nonenzymatic condensation of glucose with the albumin protein to evaluate whether increased glycated albumin influences the production of VEGF receptors (VEGFRs) and type IV collagen subchains and ameliorates the development of renal insufficiency. |
| 4623 | 17018845 | Renal levels of VEGF and VEGFR-1 proteins and serum creatinine concentrations were significantly higher and renal levels of alpha(3)(IV) collagen and nephrin proteins and endogenous creatinine clearance values were significantly lower in control diabetic than in age-matched nondiabetic (db/m) mice. |
| 4624 | 17027526 | The central theme of this chapter is that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes. |
| 4625 | 17027526 | Human adipocytes secrete at least as much plasminogen activator inhibitor-1 (PAI-1), MCP-1, interleukin-8 (IL-8), and IL-6 in vitro as they do leptin but the nonfat cells of adipose tissue secrete even more of these proteins. |
| 4626 | 17027526 | The amount of serum amyloid A proteins 1 & 2 (SAA 1 & 2), haptoglobin, nerve growth factor (NGF), macrophage migration inhibitory factor (MIF), and PAI-1 secreted by the adipocytes derived from a gram of adipose tissue is 144%, 75%, 72%, 37%, and 23%, respectively, of that by the nonfat cells derived from the same amount of human adipose tissue. |
| 4627 | 17027526 | However, the release of IL-8, MCP-1, vascular endothelial growth factor (VEGF), TGF-beta1, IL-6, PGE(2), TNF-alpha, cathepsin S, hepatocyte growth factor (HGF), IL-1beta, IL-10, resistin, C-reactive protein (CRP), and interleukin-1 receptor antagonist (IL-1Ra) by adipocytes is less than 12% of that by the nonfat cells present in human adipose tissue. |
| 4628 | 17027526 | Obesity markedly elevates the total release of TNF-alpha, IL-6, and IL-8 by adipose tissue but only that of TNF-alpha is enhanced in adipocytes. |
| 4629 | 17027526 | Visceral adipose tissue also releases more VEGF, resistin, IL-6, PAI-1, TGF-beta1, IL-8, and IL-10 per gram of tissue than does abdominal subcutaneous adipose tissue. |
| 4630 | 17027526 | In conclusion, there is an increasing recognition that adipose tissue is an endocrine organ that secretes leptin and adiponectin along with a host of other paracrine and endocrine factors in addition to free fatty acids. |
| 4631 | 17027526 | The central theme of this chapter is that human adipose tissue is a potent source of inflammatory interleukins plus other cytokines and that the majority of this release is due to the nonfat cells in the adipose tissue except for leptin and adiponectin that are primarily secreted by adipocytes. |
| 4632 | 17027526 | Human adipocytes secrete at least as much plasminogen activator inhibitor-1 (PAI-1), MCP-1, interleukin-8 (IL-8), and IL-6 in vitro as they do leptin but the nonfat cells of adipose tissue secrete even more of these proteins. |
| 4633 | 17027526 | The amount of serum amyloid A proteins 1 & 2 (SAA 1 & 2), haptoglobin, nerve growth factor (NGF), macrophage migration inhibitory factor (MIF), and PAI-1 secreted by the adipocytes derived from a gram of adipose tissue is 144%, 75%, 72%, 37%, and 23%, respectively, of that by the nonfat cells derived from the same amount of human adipose tissue. |
| 4634 | 17027526 | However, the release of IL-8, MCP-1, vascular endothelial growth factor (VEGF), TGF-beta1, IL-6, PGE(2), TNF-alpha, cathepsin S, hepatocyte growth factor (HGF), IL-1beta, IL-10, resistin, C-reactive protein (CRP), and interleukin-1 receptor antagonist (IL-1Ra) by adipocytes is less than 12% of that by the nonfat cells present in human adipose tissue. |
| 4635 | 17027526 | Obesity markedly elevates the total release of TNF-alpha, IL-6, and IL-8 by adipose tissue but only that of TNF-alpha is enhanced in adipocytes. |
| 4636 | 17027526 | Visceral adipose tissue also releases more VEGF, resistin, IL-6, PAI-1, TGF-beta1, IL-8, and IL-10 per gram of tissue than does abdominal subcutaneous adipose tissue. |
| 4637 | 17027526 | In conclusion, there is an increasing recognition that adipose tissue is an endocrine organ that secretes leptin and adiponectin along with a host of other paracrine and endocrine factors in addition to free fatty acids. |
| 4638 | 17036509 | Numerous angiogenic and mitogenic factors have been demonstrated to be present in the eye, including transforming growth factor-beta (TGF-beta), insulin-like growth factors, fibroblast growth factor, tumor necrosis factor and vascular endothelial growth factor. |
| 4639 | 17045221 | Predominance of oxidative stress in both obesity and azotemia stimulate synthesis of angiotensin II, which in turn increases TGF-B and plasminogen activator inhibitor-1, thereby propagating glomerular fibrosis. |
| 4640 | 17045221 | Furthermore, local synthesis of angiotensinogen by adipocytes, leptin activation of sympathetic nervous system, and hyperinsulinemia contribute to the development of hypertension in obesity and CKD. |
| 4641 | 17065350 | In wild-type mice, diabetes increased the translocation of PKC-alpha and -beta1 to the membrane, whereas only PKC-alpha was elevated in PKC-beta(-/-) mice. |
| 4642 | 17065350 | Diabetes increased NADPH oxidase activity and the expressions of p47(phox), Nox2, and Nox4 mRNA levels in the renal cortex and were unchanged in diabetic PKC-beta(-/-) mice. |
| 4643 | 17065350 | Increased expression of endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-beta, connective tissue growth factor (CTGF), and collagens IV and VI found in diabetic wild-type mice was attenuated in diabetic PKC-beta(-/-) mice. |
| 4644 | 17065350 | Lack of PKC-beta can protect against diabetes-induced renal dysfunction, fibrosis, and increased expressions of Nox2 and -4, ET-1, VEGF, TGF-beta, CTGF, and oxidant production. |
| 4645 | 17070554 | The overproduction of renal sorbitol, advanced glycation endproducts (AGEs), type IV collagen, and TGF-beta1 mRNA were significantly reduced in magnolol-treated GK rats. |
| 4646 | 17074304 | Rosiglitazone inhibits angiotensin II-induced CTGF expression in vascular smooth muscle cells - role of PPAR-gamma in vascular fibrosis. |
| 4647 | 17074304 | Connective tissue growth factor (CTGF) is a potent profibrotic factor implicated in the Ang II-induced pathologic fibrosis process. |
| 4648 | 17074304 | The present study evaluated the regulation of Ang II-induced CTGF, ECM production and cell growth by rosiglitazone in VSMCs. |
| 4649 | 17074304 | In aorta of Ang II-infused rats, CTGF expression was markedly increased, and type III collagen and fibronectin overexpression was observed. |
| 4650 | 17074304 | In growth-arrested VSMCs, rosiglitazone attenuated the proliferation and apoptosis, increased PPAR-gamma production and activation, and reduced CTGF and ECM production in response to Ang II in a dose-dependent fashion. |
| 4651 | 17074304 | Furthermore, rosiglitazone inhibited Ang II-induced Smad2 production and phosphorylation but had no effect on transforming growth factor-beta(1) (TGF-beta(1)) expression. |
| 4652 | 17074304 | These results suggest that in Ang II-stimulated VSMCs, rosiglitazone caused an antiproliferative, antiapototic effect and reduces ECM production through mechanisms that include reducing CTGF expression, and a crosstalk between PPAR-gamma and Smad may be involved in the inhibitory effects of rosiglitazone. |
| 4653 | 17074304 | This novel finding suggests a role of PPAR-gamma activators in preventing Ang II-induced vascular fibrosis. |
| 4654 | 17082237 | Role of the Akt/FoxO3a pathway in TGF-beta1-mediated mesangial cell dysfunction: a novel mechanism related to diabetic kidney disease. |
| 4655 | 17082237 | TGF-beta is increased in MC under diabetic conditions and in DN and activates key signaling pathways, including the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. |
| 4656 | 17082237 | We tested whether phosphorylation-mediated inactivation of FoxO3a by TGF-beta can mediate MC survival and oxidative stress. |
| 4657 | 17082237 | This FoxO3a inactivation was accompanied by significant decreases in the expression of two key FoxO3a target genes, the proapoptotic Bim and antioxidant manganese superoxide dismutase in MC. |
| 4658 | 17082237 | TGF-beta treatment triggered the nuclear exclusion of FoxO3a, significantly inhibited FoxO3a transcriptional activity, and markedly protected MC from apoptosis. |
| 4659 | 17082237 | A PI3K inhibitor blocked these TGF-beta effects. |
| 4660 | 17082237 | In summary, TGF-beta and diabetes can increase FoxO3a phosphorylation and transcriptional inactivation via PI3K/Akt. |
| 4661 | 17082237 | These new results suggest that Akt/FoxO pathway regulation may be a novel mechanism by which TGF-beta can induce unopposed MC survival and oxidant stress in early DN, thereby accelerating renal disease. |
| 4662 | 17082237 | Role of the Akt/FoxO3a pathway in TGF-beta1-mediated mesangial cell dysfunction: a novel mechanism related to diabetic kidney disease. |
| 4663 | 17082237 | TGF-beta is increased in MC under diabetic conditions and in DN and activates key signaling pathways, including the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. |
| 4664 | 17082237 | We tested whether phosphorylation-mediated inactivation of FoxO3a by TGF-beta can mediate MC survival and oxidative stress. |
| 4665 | 17082237 | This FoxO3a inactivation was accompanied by significant decreases in the expression of two key FoxO3a target genes, the proapoptotic Bim and antioxidant manganese superoxide dismutase in MC. |
| 4666 | 17082237 | TGF-beta treatment triggered the nuclear exclusion of FoxO3a, significantly inhibited FoxO3a transcriptional activity, and markedly protected MC from apoptosis. |
| 4667 | 17082237 | A PI3K inhibitor blocked these TGF-beta effects. |
| 4668 | 17082237 | In summary, TGF-beta and diabetes can increase FoxO3a phosphorylation and transcriptional inactivation via PI3K/Akt. |
| 4669 | 17082237 | These new results suggest that Akt/FoxO pathway regulation may be a novel mechanism by which TGF-beta can induce unopposed MC survival and oxidant stress in early DN, thereby accelerating renal disease. |
| 4670 | 17082237 | Role of the Akt/FoxO3a pathway in TGF-beta1-mediated mesangial cell dysfunction: a novel mechanism related to diabetic kidney disease. |
| 4671 | 17082237 | TGF-beta is increased in MC under diabetic conditions and in DN and activates key signaling pathways, including the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. |
| 4672 | 17082237 | We tested whether phosphorylation-mediated inactivation of FoxO3a by TGF-beta can mediate MC survival and oxidative stress. |
| 4673 | 17082237 | This FoxO3a inactivation was accompanied by significant decreases in the expression of two key FoxO3a target genes, the proapoptotic Bim and antioxidant manganese superoxide dismutase in MC. |
| 4674 | 17082237 | TGF-beta treatment triggered the nuclear exclusion of FoxO3a, significantly inhibited FoxO3a transcriptional activity, and markedly protected MC from apoptosis. |
| 4675 | 17082237 | A PI3K inhibitor blocked these TGF-beta effects. |
| 4676 | 17082237 | In summary, TGF-beta and diabetes can increase FoxO3a phosphorylation and transcriptional inactivation via PI3K/Akt. |
| 4677 | 17082237 | These new results suggest that Akt/FoxO pathway regulation may be a novel mechanism by which TGF-beta can induce unopposed MC survival and oxidant stress in early DN, thereby accelerating renal disease. |
| 4678 | 17082237 | Role of the Akt/FoxO3a pathway in TGF-beta1-mediated mesangial cell dysfunction: a novel mechanism related to diabetic kidney disease. |
| 4679 | 17082237 | TGF-beta is increased in MC under diabetic conditions and in DN and activates key signaling pathways, including the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. |
| 4680 | 17082237 | We tested whether phosphorylation-mediated inactivation of FoxO3a by TGF-beta can mediate MC survival and oxidative stress. |
| 4681 | 17082237 | This FoxO3a inactivation was accompanied by significant decreases in the expression of two key FoxO3a target genes, the proapoptotic Bim and antioxidant manganese superoxide dismutase in MC. |
| 4682 | 17082237 | TGF-beta treatment triggered the nuclear exclusion of FoxO3a, significantly inhibited FoxO3a transcriptional activity, and markedly protected MC from apoptosis. |
| 4683 | 17082237 | A PI3K inhibitor blocked these TGF-beta effects. |
| 4684 | 17082237 | In summary, TGF-beta and diabetes can increase FoxO3a phosphorylation and transcriptional inactivation via PI3K/Akt. |
| 4685 | 17082237 | These new results suggest that Akt/FoxO pathway regulation may be a novel mechanism by which TGF-beta can induce unopposed MC survival and oxidant stress in early DN, thereby accelerating renal disease. |
| 4686 | 17082237 | Role of the Akt/FoxO3a pathway in TGF-beta1-mediated mesangial cell dysfunction: a novel mechanism related to diabetic kidney disease. |
| 4687 | 17082237 | TGF-beta is increased in MC under diabetic conditions and in DN and activates key signaling pathways, including the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. |
| 4688 | 17082237 | We tested whether phosphorylation-mediated inactivation of FoxO3a by TGF-beta can mediate MC survival and oxidative stress. |
| 4689 | 17082237 | This FoxO3a inactivation was accompanied by significant decreases in the expression of two key FoxO3a target genes, the proapoptotic Bim and antioxidant manganese superoxide dismutase in MC. |
| 4690 | 17082237 | TGF-beta treatment triggered the nuclear exclusion of FoxO3a, significantly inhibited FoxO3a transcriptional activity, and markedly protected MC from apoptosis. |
| 4691 | 17082237 | A PI3K inhibitor blocked these TGF-beta effects. |
| 4692 | 17082237 | In summary, TGF-beta and diabetes can increase FoxO3a phosphorylation and transcriptional inactivation via PI3K/Akt. |
| 4693 | 17082237 | These new results suggest that Akt/FoxO pathway regulation may be a novel mechanism by which TGF-beta can induce unopposed MC survival and oxidant stress in early DN, thereby accelerating renal disease. |
| 4694 | 17082237 | Role of the Akt/FoxO3a pathway in TGF-beta1-mediated mesangial cell dysfunction: a novel mechanism related to diabetic kidney disease. |
| 4695 | 17082237 | TGF-beta is increased in MC under diabetic conditions and in DN and activates key signaling pathways, including the phosphoinositide-3-kinase/Akt (PI3K/Akt) pathway. |
| 4696 | 17082237 | We tested whether phosphorylation-mediated inactivation of FoxO3a by TGF-beta can mediate MC survival and oxidative stress. |
| 4697 | 17082237 | This FoxO3a inactivation was accompanied by significant decreases in the expression of two key FoxO3a target genes, the proapoptotic Bim and antioxidant manganese superoxide dismutase in MC. |
| 4698 | 17082237 | TGF-beta treatment triggered the nuclear exclusion of FoxO3a, significantly inhibited FoxO3a transcriptional activity, and markedly protected MC from apoptosis. |
| 4699 | 17082237 | A PI3K inhibitor blocked these TGF-beta effects. |
| 4700 | 17082237 | In summary, TGF-beta and diabetes can increase FoxO3a phosphorylation and transcriptional inactivation via PI3K/Akt. |
| 4701 | 17082237 | These new results suggest that Akt/FoxO pathway regulation may be a novel mechanism by which TGF-beta can induce unopposed MC survival and oxidant stress in early DN, thereby accelerating renal disease. |
| 4702 | 17097041 | Effects of Xiaoke granule on transforming growth factor-beta1 expression and proliferation in rat mesangial cells. |
| 4703 | 17114453 | Using both models, we analyzed CD4+CD25+ and CD4+CD45RC- candidate rat Treg populations. |
| 4704 | 17114453 | In vitro, rat CD4+CD25+ T cells were hyporesponsive and suppressed T cell proliferation in the absence of TGF-beta and IL-10, suggesting that they are natural Tregs. |
| 4705 | 17114453 | Adoptive transfer of purified CD4+CD25+ BBDR T cells to prediabetic BBDP rats prevented diabetes in 80% of recipients. |
| 4706 | 17114453 | The disease-suppressing CD4+CD45RC-CD25- population expressed PD-1 but not Foxp3, which was confined to CD4+CD25+ cells. |
| 4707 | 17114453 | We conclude that CD4+CD25+ cells in the BBDR rat act in vitro and in vivo as natural Tregs. |
| 4708 | 17130203 | Transforming growth factor-beta in human diabetic nephropathy: effects of ACE inhibition. |
| 4709 | 17130491 | Natural CD4(+)CD25(high) regulatory T-cells are derived from thymus, and accordingly human insulin-specific regulatory T-cells should exist. |
| 4710 | 17130491 | The mRNA expression of regulatory T-cell markers (transforming growth factor-beta, Foxp3, cytotoxic T-lymphocyte antigen-4 [CTLA-4], and inducible co-stimulator [ICOS]) or cytokines (gamma-interferon [IFN-gamma], interleukin [IL]-5, IL-4) was measured by quantitative RT-PCR. |
| 4711 | 17130491 | The secretion of IFN-gamma, IL-2, IL-4, IL-5, and IL-10 was also studied. |
| 4712 | 17130491 | The expression of Foxp3, CTLA-4, and ICOS mRNAs in PBMCs stimulated with bovine or human insulin was higher in patients on insulin treatment than in patients studied before starting insulin treatment. |
| 4713 | 17130491 | The insulin-induced Foxp3 protein expression in CD4(+)CD25(high) cells was detectable in flow cytometry. |
| 4714 | 17130491 | Insulin stimulation in vitro induced increased expression of regulatory T-cell markers, Foxp3, CTLA-4, and ICOS only in patients treated with insulin, suggesting that treatment with human insulin activates insulin-specific regulatory T-cells in children with newly diagnosed type 1 diabetes. |
| 4715 | 17130503 | High-sensitivity C-reactive protein (hs-CRP), interleukin (IL)-6, fibrinogen, adhesion molecules, transforming growth factor-beta, and AGE peptides were assessed. |
| 4716 | 17130503 | Changes in IL-6 were associated with changes in albumin excretion (P = 0.04). |
| 4717 | 17142129 | Glomerular macrophage infiltration and expression of monocyte chemoattractant protein 1, malondialdehyde (MDA), nitrotyrosine, transforming growth factor beta1 (TGF-beta1), and type I collagen were evaluated. |
| 4718 | 17142129 | Protein and gene expression levels of monocyte chemoattractant protein 1, TGF-beta1, and type I collagen, which were evaluated by immunohistochemistry and real-time reverse transcriptase-polymerase chain reaction, were down-regulated in the EPA treatment group. |
| 4719 | 17142129 | Glomerular macrophage infiltration and expression of monocyte chemoattractant protein 1, malondialdehyde (MDA), nitrotyrosine, transforming growth factor beta1 (TGF-beta1), and type I collagen were evaluated. |
| 4720 | 17142129 | Protein and gene expression levels of monocyte chemoattractant protein 1, TGF-beta1, and type I collagen, which were evaluated by immunohistochemistry and real-time reverse transcriptase-polymerase chain reaction, were down-regulated in the EPA treatment group. |
| 4721 | 17145658 | Renal expression of transforming growth factor-beta1 (TGF-beta1) were determined by immunochemistry. |
| 4722 | 17161871 | Results showed that CB-SC could significantly inhibit lymphocyte proliferation and reduce tyrosine phosphorylation of STAT5 in both PHA- and IL-2-stimulated lymphocytes, along with the regulation on the phenotypes of CD4+ and CD8+ T cells. |
| 4723 | 17161871 | Additionally, CB-SC also suppressed the proliferation of IL-2-stimulated CD4+CD25+ regulatory T cells. |
| 4724 | 17161871 | Mechanism studies revealed that programmed death receptor-1 ligand 1 (PD-L1) expressed on CB-SC membrane, together with a soluble factor nitric oxide (NO) released by PHA-stimulated CB-SC, not prostaglandin E2 (PGE2) and transforming growth factor-beta1 (TGF-beta1), mainly contributed to the T cell suppression induced by CB-SC, as demonstrated by blocking experiments with a nitric oxide synthase inhibitor (Nomega-nitro-l-arginine, l-NNA) and a neutralizing antibody to PD-L1. |
| 4725 | 17162922 | [The change of transforming growth factor-beta1 in nonproliferation diabetic retinopathy]. |
| 4726 | 17166396 | We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18. |
| 4727 | 17166396 | TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group. |
| 4728 | 17166396 | We examined the expression of genes encoding the cytokines, tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta) and transforming growth factor-beta1 (TGF-beta1) as well as the pan-leukocyte marker CD18. |
| 4729 | 17166396 | TNF-alpha (P<0.05) and TGF-beta1 transcripts (P<0.05) increased over time in the EX group, but these increases did not differ from those in the CON group. |
| 4730 | 17173248 | Glomerular expression of CTGF, TGF-beta 1 and type IV collagen in diabetic nephropathy. |
| 4731 | 17177138 | Blood glucose, triglyceride (TG), cholesterol (CHO), high density lipoprotein (HDL), serum creatinine (Scr), creatinine clearance rate (Ccr), blood urea nitrogen (BUN), urine beta (2)-microglobin (beta (2)-MG), kidney/body weight (K/B) ratio, glomerular area (GA), renal transforming growth factor-beta (1) (TGF-beta (1)) mRNA expression and blood and renal angiotensin II (AngII) expression were determined 8 weeks after the treatment. |
| 4732 | 17177138 | K/B ratio, GA, the excretion of beta (2)-MG, renal TGF-beta (1) mRNA expression and blood and renal AngII expression were significantly increased while the HDL level was decreased 8 week after STZ injection. |
| 4733 | 17177138 | Our results suggest that GQM alleviates the disorder in blood glucose and lipids, protects against the progression of renal nephropathy in diabetic rats, probably by inhibiting the expression of AngII and TGF-beta (1) mRNA. |
| 4734 | 17177138 | Blood glucose, triglyceride (TG), cholesterol (CHO), high density lipoprotein (HDL), serum creatinine (Scr), creatinine clearance rate (Ccr), blood urea nitrogen (BUN), urine beta (2)-microglobin (beta (2)-MG), kidney/body weight (K/B) ratio, glomerular area (GA), renal transforming growth factor-beta (1) (TGF-beta (1)) mRNA expression and blood and renal angiotensin II (AngII) expression were determined 8 weeks after the treatment. |
| 4735 | 17177138 | K/B ratio, GA, the excretion of beta (2)-MG, renal TGF-beta (1) mRNA expression and blood and renal AngII expression were significantly increased while the HDL level was decreased 8 week after STZ injection. |
| 4736 | 17177138 | Our results suggest that GQM alleviates the disorder in blood glucose and lipids, protects against the progression of renal nephropathy in diabetic rats, probably by inhibiting the expression of AngII and TGF-beta (1) mRNA. |
| 4737 | 17177138 | Blood glucose, triglyceride (TG), cholesterol (CHO), high density lipoprotein (HDL), serum creatinine (Scr), creatinine clearance rate (Ccr), blood urea nitrogen (BUN), urine beta (2)-microglobin (beta (2)-MG), kidney/body weight (K/B) ratio, glomerular area (GA), renal transforming growth factor-beta (1) (TGF-beta (1)) mRNA expression and blood and renal angiotensin II (AngII) expression were determined 8 weeks after the treatment. |
| 4738 | 17177138 | K/B ratio, GA, the excretion of beta (2)-MG, renal TGF-beta (1) mRNA expression and blood and renal AngII expression were significantly increased while the HDL level was decreased 8 week after STZ injection. |
| 4739 | 17177138 | Our results suggest that GQM alleviates the disorder in blood glucose and lipids, protects against the progression of renal nephropathy in diabetic rats, probably by inhibiting the expression of AngII and TGF-beta (1) mRNA. |
| 4740 | 17177144 | Serum soluble factors induce the proliferation, alkaline phosphatase activity and transforming growth factor-beta signal in osteoblastic cells in the patient with hepatitis C-associated osteosclerosis. |
| 4741 | 17177144 | We examined the effects of serum of the HCAO patient on the proliferation, alkaline phosphatase (ALP) activity and transforming growth factor (TGF)-beta-Smad signaling in mouse osteoblastic cells. |
| 4742 | 17177144 | The serum from the HCAO patient increased the levels of TGF-beta and Smad3 expression in osteoblastic MC3T3-E1 cells, compared with the control subject. |
| 4743 | 17177144 | Moreover, the serum from the HCAO patient significantly augmented TGF-beta-induced transcriptional activity with luciferase assay using 3TP-Lux with a Smad3-specific responsive element. |
| 4744 | 17177144 | In addition, the serum from the HCAO patient significantly stimulated the MTT intensity, the level of proliferating cell nuclear antigen expression, a proliferation marker, and ALP activity in MC3T3-E1 cells, compared with that from the control subject. |
| 4745 | 17177144 | Serum soluble factors induce the proliferation, alkaline phosphatase activity and transforming growth factor-beta signal in osteoblastic cells in the patient with hepatitis C-associated osteosclerosis. |
| 4746 | 17177144 | We examined the effects of serum of the HCAO patient on the proliferation, alkaline phosphatase (ALP) activity and transforming growth factor (TGF)-beta-Smad signaling in mouse osteoblastic cells. |
| 4747 | 17177144 | The serum from the HCAO patient increased the levels of TGF-beta and Smad3 expression in osteoblastic MC3T3-E1 cells, compared with the control subject. |
| 4748 | 17177144 | Moreover, the serum from the HCAO patient significantly augmented TGF-beta-induced transcriptional activity with luciferase assay using 3TP-Lux with a Smad3-specific responsive element. |
| 4749 | 17177144 | In addition, the serum from the HCAO patient significantly stimulated the MTT intensity, the level of proliferating cell nuclear antigen expression, a proliferation marker, and ALP activity in MC3T3-E1 cells, compared with that from the control subject. |
| 4750 | 17177144 | Serum soluble factors induce the proliferation, alkaline phosphatase activity and transforming growth factor-beta signal in osteoblastic cells in the patient with hepatitis C-associated osteosclerosis. |
| 4751 | 17177144 | We examined the effects of serum of the HCAO patient on the proliferation, alkaline phosphatase (ALP) activity and transforming growth factor (TGF)-beta-Smad signaling in mouse osteoblastic cells. |
| 4752 | 17177144 | The serum from the HCAO patient increased the levels of TGF-beta and Smad3 expression in osteoblastic MC3T3-E1 cells, compared with the control subject. |
| 4753 | 17177144 | Moreover, the serum from the HCAO patient significantly augmented TGF-beta-induced transcriptional activity with luciferase assay using 3TP-Lux with a Smad3-specific responsive element. |
| 4754 | 17177144 | In addition, the serum from the HCAO patient significantly stimulated the MTT intensity, the level of proliferating cell nuclear antigen expression, a proliferation marker, and ALP activity in MC3T3-E1 cells, compared with that from the control subject. |
| 4755 | 17192487 | Transforming growth factor-beta2 and connective tissue growth factor in proliferative vitreoretinal diseases: possible involvement of hyalocytes and therapeutic potential of Rho kinase inhibitor. |
| 4756 | 17192487 | The critical association of connective tissue growth factor (CTGF), which is thought to be one of the downstream mediators of transforming growth factor-beta (TGF-beta), with vitreoretinal diseases remains to be clarified. |
| 4757 | 17192487 | In the current study, we first demonstrated the correlation between the concentrations of TGF-beta2 as well as CTGF in the vitreous and CTGF gene regulation in cultured hyalocytes. |
| 4758 | 17192487 | Concentrations of TGF-beta2 and CTGF in the vitreous from patients with proliferative vitreoretinal diseases were significantly higher than in those with nonproliferative diseases, and there was a positive correlation between their concentrations (r = 0.320, P < 0.01). |
| 4759 | 17192487 | Cultured hyalocytes expressed CTGF mRNA, which was enhanced in the presence of TGF-beta2, associated with nuclear accumulation of Smad4. |
| 4760 | 17192487 | TGF-beta2-dependent Smad4 translocation and CTGF gene expression were mediated through Rho kinase and at least partially via p38 mitogen-activated protein kinase. |
| 4761 | 17192487 | Finally, fasudil, a Rho kinase inhibitor already in clinical use, inhibited both Smad4 translocation and CTGF gene expression. |
| 4762 | 17192487 | In conclusion, combined effects of TGF-beta2 and CTGF appear to be involved in the pathogenesis of proliferative vitreoretinal diseases. |
| 4763 | 17194556 | We also found that KIOM-79 prevented the glomeruli enlargement, overexpression of type IV collagen (p<0.001), PKC protein (p<0.01), TGF-beta mRNA (p<0.05) and VEGF mRNA (p<0.05). |
| 4764 | 17199790 | Troglitazone inhibits synthesis of transforming growth factor-beta1 and reduces matrix production in human peritoneal mesothelial cells. |
| 4765 | 17200159 | The dysregulated spots from the membrane subproteome included binding protein (BiP), calreticulin precursor protein, a 63-kDa transmembrane protein from a ER/Golgi intermediate, and beta-subunit of collagen proline 4-hydroxylase. |
| 4766 | 17200159 | Enolase 1, annexin VI, and gamma(2)-actin were decreased, whereas heat shock protein-70 kDa and calmodulin (CaM) were increased. |
| 4767 | 17200159 | CaM-specific inhibitors blocked glucose transport stimulated by transforming growth factor-beta and insulin in mesangial cells. |
| 4768 | 17200187 | The transforming growth factor (TGF)-beta-inducible integrin alpha v beta6 is preferentially expressed at sites of epithelial remodeling and has been shown to bind and activate latent precursor TGF-beta. |
| 4769 | 17213232 | We investigated the relationship of nine common single-nucleotide polymorphisms (SNPs) in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-10, IL-4 and transforming growth factor (TGF)-beta1 with the atherosclerotic severity in 10 different arteries based on 1503 consecutive autopsies of elderly Japanese subjects registered in the Japanese SNPs for geriatric research (JG-SNP) study. |
| 4770 | 17213232 | The -511T of IL-1beta and the +29T of TGF-beta1 were significant risk factors for atherogenesis in the subclavian and intracranial arteries (OR: 1.35 and 1.48, respectively). |
| 4771 | 17213232 | Functional SNPs in TNF-alpha, IL-1beta and TGF-beta1 genes play a role in atherogenesis, although their influences are less pronounced than those of conventional risk factors and appear to be limited to specific arteries in the Japanese elderly. |
| 4772 | 17213232 | We investigated the relationship of nine common single-nucleotide polymorphisms (SNPs) in tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1beta, IL-10, IL-4 and transforming growth factor (TGF)-beta1 with the atherosclerotic severity in 10 different arteries based on 1503 consecutive autopsies of elderly Japanese subjects registered in the Japanese SNPs for geriatric research (JG-SNP) study. |
| 4773 | 17213232 | The -511T of IL-1beta and the +29T of TGF-beta1 were significant risk factors for atherogenesis in the subclavian and intracranial arteries (OR: 1.35 and 1.48, respectively). |
| 4774 | 17213232 | Functional SNPs in TNF-alpha, IL-1beta and TGF-beta1 genes play a role in atherogenesis, although their influences are less pronounced than those of conventional risk factors and appear to be limited to specific arteries in the Japanese elderly. |
| 4775 | 17215847 | It can be used to deliver protein drugs such as glucagon-like peptide 1 (GLP-1), leptin or transforming growth factor beta (TGF-beta). |
| 4776 | 17217101 | There are two main populations of regulatory T cells - natural regulatory T cells, which form a distinct cellular lineage, develop in thymus and perform their modulatory action through direct intercellular contact, along with the secreted cytokines; and inducible regulatory T cells, which develop in the periphery after contact with the antigen that is presented on the antigen presenting cell, and their primary mode of action is through the interleukin 10 (IL-10) and transforming growth factor beta (TGF-alpha) cytokines. |
| 4777 | 17217101 | Natural regulatory T cells constitutively express surface molecule CD25, but many other surface and intracellular molecules (HLA-DR, CD122, CD45RO, CD62, CTLA-4, GITR, PD-1, Notch, FOXP3, etc.) are being investigated for further phenotypic characterization of these cells. |
| 4778 | 17224327 | The urinary albumin/creatinine ratio (ACR), body weight (BW), levels of fasting and casual blood glucose, blood glycated hemoglobin (HbA(1c)), fasting serum insulin, triglyceride (TG), total cholesterol (T-Cho), and 3-deoxyglucosone (3DG), and systemic blood pressure were measured as biochemical parameters. |
| 4779 | 17224327 | Transforming growth factor beta1 (TGF-beta1) and laminin-beta1 messenger RNA expressions in the kidneys were evaluated by real-time polymerase chain reaction. |
| 4780 | 17224327 | TGF-beta1 and laminin-beta1 messenger RNA expressions in kidneys were significantly lower than those in the controls. |
| 4781 | 17224327 | The urinary albumin/creatinine ratio (ACR), body weight (BW), levels of fasting and casual blood glucose, blood glycated hemoglobin (HbA(1c)), fasting serum insulin, triglyceride (TG), total cholesterol (T-Cho), and 3-deoxyglucosone (3DG), and systemic blood pressure were measured as biochemical parameters. |
| 4782 | 17224327 | Transforming growth factor beta1 (TGF-beta1) and laminin-beta1 messenger RNA expressions in the kidneys were evaluated by real-time polymerase chain reaction. |
| 4783 | 17224327 | TGF-beta1 and laminin-beta1 messenger RNA expressions in kidneys were significantly lower than those in the controls. |
| 4784 | 17229845 | FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults. |
| 4785 | 17229845 | Activin and myostatin are related members of the TGF-beta growth factor superfamily. |
| 4786 | 17229845 | FSTL3 (Follistatin-like 3) is an activin and myostatin antagonist whose physiological role in adults remains to be determined. |
| 4787 | 17229845 | We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients. |
| 4788 | 17229845 | This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist. |
| 4789 | 17229845 | Reduced visceral fat is consistent with a role for increased myostatin action in regulating fat deposition, which, in turn, may be partly responsible for the enhanced glucose tolerance and insulin sensitivity. |
| 4790 | 17229845 | Our results demonstrate that FSTL3 regulation of activin and myostatin is critical for normal adult metabolic homeostasis, suggesting that pharmacological manipulation of FSTL3 activity might simultaneously reduce visceral adiposity, increase beta cell mass, and improve insulin sensitivity. |
| 4791 | 17229845 | FSTL3 deletion reveals roles for TGF-beta family ligands in glucose and fat homeostasis in adults. |
| 4792 | 17229845 | Activin and myostatin are related members of the TGF-beta growth factor superfamily. |
| 4793 | 17229845 | FSTL3 (Follistatin-like 3) is an activin and myostatin antagonist whose physiological role in adults remains to be determined. |
| 4794 | 17229845 | We found that homozygous FSTL3 knockout adults developed a distinct group of metabolic phenotypes, including increased pancreatic islet number and size, beta cell hyperplasia, decreased visceral fat mass, improved glucose tolerance, and enhanced insulin sensitivity, changes that might benefit obese, insulin-resistant patients. |
| 4795 | 17229845 | This combination of phenotypes appears to arise from increased activin and myostatin bioactivity in specific tissues resulting from the absence of the FSTL3 antagonist. |
| 4796 | 17229845 | Reduced visceral fat is consistent with a role for increased myostatin action in regulating fat deposition, which, in turn, may be partly responsible for the enhanced glucose tolerance and insulin sensitivity. |
| 4797 | 17229845 | Our results demonstrate that FSTL3 regulation of activin and myostatin is critical for normal adult metabolic homeostasis, suggesting that pharmacological manipulation of FSTL3 activity might simultaneously reduce visceral adiposity, increase beta cell mass, and improve insulin sensitivity. |
| 4798 | 17237379 | We recently showed that neither iNKT cell protection against diabetes nor iNKT cell inhibition of T cell differentiation in vitro requires cytokines such as IL-4, IL-10, IL-13, and TGF-beta. |
| 4799 | 17259378 | The protein kinase C (PKC)-beta isoform has been implicated to play a pivotal role in the development of diabetic kidney disease. |
| 4800 | 17259378 | After 8 weeks of diabetes, the high-glucose-induced renal and glomerular hypertrophy, as well as the increased expression of extracellular matrix proteins such as collagen and fibronectin, was reduced in PKC-beta(-/-) mice. |
| 4801 | 17259378 | Furthermore, the high-glucose-induced expression of the profibrotic cytokine transforming growth factor (TGF)-beta1 and connective tissue growth factor were significantly diminished in the diabetic PKC-beta(-/-) mice compared with diabetic wild-type mice, suggesting a role of the PKC-beta isoform in the regulation of renal hypertrophy. |
| 4802 | 17259378 | Notably, increased urinary albumin-to-creatinine ratio persisted in the diabetic PKC-beta(-/-) mice. |
| 4803 | 17259378 | The loss of the basement membrane proteoglycan perlecan and the podocyte protein nephrin in the diabetic state was not prevented in the PKC-beta(-/-) mice as previously demonstrated in the nonalbuminuric diabetic PKC-alpha(-/-) mice. |
| 4804 | 17259378 | In summary, the differential effects of PKC-beta deficiency on diabetes-induced renal hypertrophy and albuminuria suggest that PKC-beta contributes to high-glucose-induced TGF-beta1 expression and renal fibrosis, whereas perlecan, as well as nephrin, expression and albuminuria is regulated by other signaling pathways. |
| 4805 | 17259382 | Evidence for a role of transforming growth factor (TGF)-beta1 in the induction of postglomerular albuminuria in diabetic nephropathy: amelioration by soluble TGF-beta type II receptor. |
| 4806 | 17259382 | Here we report for the first time the use of a high-affinity TGF-beta1 binding molecule, the soluble human TGF-beta type II receptor (sTbetaRII.Fc), in the treatment of diabetic nephropathy in 12-week streptozotocin-induced diabetic Sprague-Dawley rats. |
| 4807 | 17259382 | In vitro studies using immortalized rat proximal tubule cells revealed that 50 pmol/l TGF-beta1 disrupted albumin uptake (P < 0.001 vs. control), an inhibition significantly reversed by the use of the sTbetaRII.Fc (1,200 pmol/l). |
| 4808 | 17259382 | This was correlated with an increase in megalin expression (P < 0.05 for diabetic vs. treated) and a reduction in collagen IV expression following sTbetaRII.Fc treatment (P < 0.001 for diabetic vs. treated). |
| 4809 | 17259382 | Evidence for a role of transforming growth factor (TGF)-beta1 in the induction of postglomerular albuminuria in diabetic nephropathy: amelioration by soluble TGF-beta type II receptor. |
| 4810 | 17259382 | Here we report for the first time the use of a high-affinity TGF-beta1 binding molecule, the soluble human TGF-beta type II receptor (sTbetaRII.Fc), in the treatment of diabetic nephropathy in 12-week streptozotocin-induced diabetic Sprague-Dawley rats. |
| 4811 | 17259382 | In vitro studies using immortalized rat proximal tubule cells revealed that 50 pmol/l TGF-beta1 disrupted albumin uptake (P < 0.001 vs. control), an inhibition significantly reversed by the use of the sTbetaRII.Fc (1,200 pmol/l). |
| 4812 | 17259382 | This was correlated with an increase in megalin expression (P < 0.05 for diabetic vs. treated) and a reduction in collagen IV expression following sTbetaRII.Fc treatment (P < 0.001 for diabetic vs. treated). |
| 4813 | 17259382 | Evidence for a role of transforming growth factor (TGF)-beta1 in the induction of postglomerular albuminuria in diabetic nephropathy: amelioration by soluble TGF-beta type II receptor. |
| 4814 | 17259382 | Here we report for the first time the use of a high-affinity TGF-beta1 binding molecule, the soluble human TGF-beta type II receptor (sTbetaRII.Fc), in the treatment of diabetic nephropathy in 12-week streptozotocin-induced diabetic Sprague-Dawley rats. |
| 4815 | 17259382 | In vitro studies using immortalized rat proximal tubule cells revealed that 50 pmol/l TGF-beta1 disrupted albumin uptake (P < 0.001 vs. control), an inhibition significantly reversed by the use of the sTbetaRII.Fc (1,200 pmol/l). |
| 4816 | 17259382 | This was correlated with an increase in megalin expression (P < 0.05 for diabetic vs. treated) and a reduction in collagen IV expression following sTbetaRII.Fc treatment (P < 0.001 for diabetic vs. treated). |
| 4817 | 17259380 | Diabetic SR-A(+/+) mice presented characteristic features of diabetic nephropathy: albuminuria, glomerular hypertrophy, mesangial matrix expansion, and overexpression of transforming growth factor-beta at 6 months after induction of diabetes. |
| 4818 | 17259380 | Moreover, anti-SR-A antibody blocked the attachment of monocytes to type IV collagen substratum but not to endothelial cells. |
| 4819 | 17267584 | Pioglitazone induces apoptosis in human vascular smooth muscle cells from diabetic patients involving the transforming growth factor-beta/activin receptor-like kinase-4/5/7/Smad2 signaling pathway. |
| 4820 | 17267584 | Here, we aimed to study whether pioglitazone was able to induce apoptosis in VSMC from diabetic patients (DP) and, if so, whether the transforming growth factor (TGF)-beta1/Smad-2 pathway was involved. |
| 4821 | 17267584 | This apoptotic effect was inhibited by the activin receptor-like kinase-4/5/7/Smad2 inhibitor 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide (SB-431542), denoting that the TGF-beta1/Smad-2 pathway was involved. |
| 4822 | 17267584 | Pioglitazone rapidly increased the extracellular TGF-beta1 levels and concomitantly induced phosphorylation of Smad2 in VSMC from DP and NDP. |
| 4823 | 17267584 | Pioglitazone induces apoptosis in human vascular smooth muscle cells from diabetic patients involving the transforming growth factor-beta/activin receptor-like kinase-4/5/7/Smad2 signaling pathway. |
| 4824 | 17267584 | Here, we aimed to study whether pioglitazone was able to induce apoptosis in VSMC from diabetic patients (DP) and, if so, whether the transforming growth factor (TGF)-beta1/Smad-2 pathway was involved. |
| 4825 | 17267584 | This apoptotic effect was inhibited by the activin receptor-like kinase-4/5/7/Smad2 inhibitor 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide (SB-431542), denoting that the TGF-beta1/Smad-2 pathway was involved. |
| 4826 | 17267584 | Pioglitazone rapidly increased the extracellular TGF-beta1 levels and concomitantly induced phosphorylation of Smad2 in VSMC from DP and NDP. |
| 4827 | 17267584 | Pioglitazone induces apoptosis in human vascular smooth muscle cells from diabetic patients involving the transforming growth factor-beta/activin receptor-like kinase-4/5/7/Smad2 signaling pathway. |
| 4828 | 17267584 | Here, we aimed to study whether pioglitazone was able to induce apoptosis in VSMC from diabetic patients (DP) and, if so, whether the transforming growth factor (TGF)-beta1/Smad-2 pathway was involved. |
| 4829 | 17267584 | This apoptotic effect was inhibited by the activin receptor-like kinase-4/5/7/Smad2 inhibitor 4-(5-benzo(1,3)dioxol-5-yl-4-pyridin-2-yl-1H-imidazol-2-yl)benzamide (SB-431542), denoting that the TGF-beta1/Smad-2 pathway was involved. |
| 4830 | 17267584 | Pioglitazone rapidly increased the extracellular TGF-beta1 levels and concomitantly induced phosphorylation of Smad2 in VSMC from DP and NDP. |
| 4831 | 17311907 | JT permitted increased expression of mRNA for two isoforms of transforming growth factor-beta and connective tissue growth factor compared with J animals with DM; prior castration did not provide protection in adult-onset DM. |
| 4832 | 17317763 | To define the parameters influencing the efficacy of antigen-specific immunotherapy once diabetes is established, plasmid DNA (pDNA) vaccination was used to suppress autoimmune-mediated destruction of syngeneic islet grafts in diabetic NOD recipients. pDNAs encoding a glutamic acid decarboxylase 65 (GAD65)-Ig molecule (pGAD65), interleukin (IL)-4 (pIL4), and IL-10 (pIL10) significantly delayed the onset of recurrent diabetes compared with pGAD65+pIL10-vaccinated recipients. |
| 4833 | 17317763 | Despite differences in efficacy, a similar frequency of GAD65-specific CD4(+) T-cells secreting IL-4, IL-10, or interferon-gamma were detected in mice treated with pGAD65+pIL4+pIL10 and pGAD65+pIL10. |
| 4834 | 17317763 | However, the frequency of FoxP3-expressing CD4(+)CD25(+)CD62L(hi) T-cells was increased in the renal and pancreatic lymph nodes of diabetic recipients vaccinated with pGAD65+pIL4+pIL10. |
| 4835 | 17317763 | These immunoregulatory CD4(+)CD25(+) T-cells (CD4(+)CD25(+) Treg) exhibited enhanced in vivo and in vitro suppressor activity that partially was transforming growth factor-beta dependent. |
| 4836 | 17317763 | Furthermore, duration of islet graft protection in pGAD65+pIL4+pIL10-vaccinated diabetic recipients correlated with the persistence of CD4(+)CD25(+) Treg. |
| 4837 | 17317763 | These data demonstrate that the frequency and maintenance of FoxP3-expressing CD4(+)CD25(+) Treg influence antigen-induced suppression of ongoing beta-cell autoimmunity in diabetic recipients. |
| 4838 | 17318765 | These altered hemodynamics act independently and in concert with metabolic pathways, to activate intracellular second messengers such as protein kinase C (PKC) and MAP kinase (MAPK), nuclear transcription factors such as nuclear factor-kappaB (NF-kappaB) and various growth factors such as the prosclerotic cytokines, transforming growth factor-beta1 (TGF-beta1), connective tissue growth factor (CTGF) and the angiogenic, permeability enhancing growth factor, vascular endothelial growth factor, VEGF. |
| 4839 | 17319955 | Resequencing of genes for transforming growth factor beta1 (TGFB1) type 1 and 2 receptors (TGFBR1, TGFBR2), and association analysis of variants with diabetic nephropathy. |
| 4840 | 17327431 | The total cardiac collagen content and collagen type 1 and 3 were measured by histochemistry, and MMP-2 activity was measured by gelatin zymography. |
| 4841 | 17327431 | This was accompanied by increased TGFbeta, IL1beta, and fibrosis and decreased MMP-2 activity. |
| 4842 | 17327431 | Treatment with irbesartan attenuated LV dysfunction, IL1beta, TGFbeta, and cardiac fibrosis compared with untreated diabetic animals and normalized MMP activity. |
| 4843 | 17327431 | The total cardiac collagen content and collagen type 1 and 3 were measured by histochemistry, and MMP-2 activity was measured by gelatin zymography. |
| 4844 | 17327431 | This was accompanied by increased TGFbeta, IL1beta, and fibrosis and decreased MMP-2 activity. |
| 4845 | 17327431 | Treatment with irbesartan attenuated LV dysfunction, IL1beta, TGFbeta, and cardiac fibrosis compared with untreated diabetic animals and normalized MMP activity. |
| 4846 | 17327445 | Paradoxically, expression of PGC-1-and nuclear-encoded mitochondrial genes decreased after acipimox, and expression of collagens I and III alpha-subunits (82- and 21-fold increase, respectively, P < 0.05), connective tissue growth factor (2.5-fold increase, P < 0.001), and transforming growth factor-beta1 increased (2.95-fold increase, P < 0.05). |
| 4847 | 17329849 | Treatment with Corni Fructus for 10 d suppressed hyperglycemia, proteinuria, renal AGE formation, and related protein expressions, i.e., receptor for AGEs, nuclear factor-kappaB, transforming growth factor-beta1, and Nepsilon-(carboxymethyl)lysine, in the same way as with aminoguanidine. |
| 4848 | 17331859 | Only one BG, phenformin, caused a concentration-related inhibition of proteoglycan synthesis under basal conditions and in the presence of transforming growth factor-beta1 (TGF-beta1), caused by an inhibition of proteoglycan core protein synthesis secondary to a reduction in total protein synthesis. |
| 4849 | 17331859 | The TZDs--troglitazone (TRO), rosiglitazone (ROS), and pioglitazone (PIO) (10, 30, and 30 micromol/l, respectively)--inhibited proteoglycan biosynthesis and stimulated total proteoglycan core protein synthesis, while TRO alone inhibited overall protein synthesis. |
| 4850 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4851 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4852 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4853 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4854 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4855 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4856 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4857 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4858 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4859 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4860 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4861 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4862 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4863 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4864 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4865 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4866 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4867 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4868 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4869 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4870 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4871 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4872 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4873 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4874 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4875 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4876 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4877 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4878 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4879 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4880 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4881 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4882 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4883 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4884 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4885 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4886 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4887 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4888 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4889 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4890 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4891 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4892 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4893 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4894 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4895 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4896 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4897 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4898 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4899 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4900 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4901 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4902 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4903 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4904 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4905 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4906 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4907 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4908 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4909 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4910 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4911 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4912 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4913 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4914 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4915 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4916 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4917 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4918 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4919 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4920 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4921 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4922 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4923 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4924 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4925 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4926 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4927 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4928 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4929 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4930 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4931 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4932 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4933 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4934 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4935 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4936 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4937 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4938 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4939 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4940 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4941 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4942 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4943 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4944 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4945 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4946 | 17360662 | MicroRNA-192 in diabetic kidney glomeruli and its function in TGF-beta-induced collagen expression via inhibition of E-box repressors. |
| 4947 | 17360662 | Key features of diabetic nephropathy (DN) include the accumulation of extracellular matrix proteins such as collagen 1-alpha 1 and -2 (Col1a1 and -2). |
| 4948 | 17360662 | Transforming growth factor beta1 (TGF-beta), a key regulator of these extracellular matrix genes, is increased in mesangial cells (MC) in DN. |
| 4949 | 17360662 | By microarray profiling, we noted that TGF-beta increased Col1a2 mRNA in mouse MC (MMC) but also decreased mRNA levels of an E-box repressor, deltaEF1. |
| 4950 | 17360662 | TGF-beta treatment or short hairpin RNAs targeting deltaEF1 increased enhancer activity of upstream E-box elements in the Col1a2 gene. |
| 4951 | 17360662 | TGF-beta also decreased the expression of Smad-interacting protein 1 (SIP1), another E-box repressor similar to deltaEF1. |
| 4952 | 17360662 | Interestingly, we noted that SIP1 is a target of microRNA-192 (miR-192), a key miR highly expressed in the kidney. miR-192 levels also were increased by TGF-beta in MMC. |
| 4953 | 17360662 | TGF-beta treatment or transfection with miR-192 decreased endogenous SIP1 expression as well as reporter activity of a SIP1 3' UTR-containing luciferase construct in MMC. |
| 4954 | 17360662 | Conversely, a miR-192 inhibitor enhanced the luciferase activity, confirming SIP1 to be a miR-192 target. |
| 4955 | 17360662 | Furthermore, miR-192 synergized with deltaEF1 short hairpin RNAs to increase Col1a2 E-box-luc activity. |
| 4956 | 17360662 | Importantly, the in vivo relevance was noted by the observation that miR-192 levels were enhanced significantly in glomeruli isolated from streptozotocin-injected diabetic mice as well as diabetic db/db mice relative to corresponding nondiabetic controls, in parallel with increased TGF-beta and Col1a2 levels. |
| 4957 | 17360662 | These results uncover a role for miRs in the kidney and DN in controlling TGF-beta-induced Col1a2 expression by down-regulating E-box repressors. |
| 4958 | 17389382 | Previous results have shown that CD4(+)CD25(+) regulatory T cells (Tregs) control autoimmunity in a spontaneous model of type 1 diabetes, the nonobese diabetic (NOD) mouse. |
| 4959 | 17389382 | This finding contrasts with a large body of work suggesting that CD4(+)CD25(high) Tregs act in a cytokine-independent manner, thus suggesting that another type of Treg is operational in this setting. |
| 4960 | 17389382 | Our present results show that a subset of foxP3(+) cells present within a CD4(+)CD25(low) lymphocyte subset suppresses T cell immunity in spontaneously diabetic NOD mice in a TGF-beta-dependent manner, a functional property typical of "adaptive" regulatory T cells. |
| 4961 | 17389382 | Importantly, in two distinct in vivo models, these TGF-beta-dependent adaptive CD4(+)CD25(low) T cells can be induced from peripheral CD4(+)CD25(-) T lymphocytes by anti-CD3 immunotherapy which correlates with the restoration of self-tolerance. |
| 4962 | 17389681 | In post-OF diabetic mice, mRNA abundance of early growth response-1 (Egr-1), collagen-4alpha1, and matrix metalloproteinase-9 were increased and 3beta-hydroxysteroid dehydrogenase 4 (3beta-HSD4) and transforming growth factor-beta(2) (TGF-beta(2)) were decreased compared with cycling diabetic mice. |
| 4963 | 17389681 | In peri-OF diabetic mice, mRNA abundance of Egr-1 and 3beta-HSD4 were increased, and TGF-beta(2) was decreased compared with cycling diabetic mice. |
| 4964 | 17389681 | In post-OF diabetic mice, mRNA abundance of early growth response-1 (Egr-1), collagen-4alpha1, and matrix metalloproteinase-9 were increased and 3beta-hydroxysteroid dehydrogenase 4 (3beta-HSD4) and transforming growth factor-beta(2) (TGF-beta(2)) were decreased compared with cycling diabetic mice. |
| 4965 | 17389681 | In peri-OF diabetic mice, mRNA abundance of Egr-1 and 3beta-HSD4 were increased, and TGF-beta(2) was decreased compared with cycling diabetic mice. |
| 4966 | 17392166 | BL5923 reduced renal mRNA expression of Ccl2, Ccr1, Ccr2, Ccr5, transforming growth factor-beta1, and collagen I-alpha1 when compared with untreated uninephrectomized male db/db mice of the same age. |
| 4967 | 17401436 | Renal p38 MAP kinase activity in experimental diabetes. |
| 4968 | 17401436 | We examined the p38 pathway in renal cortex of rats with streptozotocin diabetes (4 weeks) with poor (DS), moderate (DM), and intensive (DII) metabolic control, achieved by varying doses of insulin therapy. |
| 4969 | 17401436 | Renal p38 was also studied in 12-month diabetic rats with established nephropathy (DM12) and compared with age-matched controls. p38 activity (in vitro kinase assay and expression of phosphorylated (active) p38 (P-p38)) was increased in DM and DS rats, as compared with non-diabetic controls, and attenuated by intensive insulin treatment. |
| 4970 | 17401436 | Enhanced p38 activity in DS and DM rats was not associated with increases in expression of active mitogen-activated protein kinase 3/6, an activator of p38, but paralleled with increased expression of scaffolding protein transforming growth factor-beta-activated protein kinase 1-binding protein 1. |
| 4971 | 17401436 | Expression of mitogen-activated protein phosphatase-1 (MKP-1), one of the phosphatases involved in inactivation of mitogen-activated protein kinase signaling, was increased in all diabetic groups, irrespective of metabolic control. |
| 4972 | 17401436 | In summary, renal cortical p38 activity was increased in diabetic rats at early and advanced stages of nephropathy, as compared with non-diabetic animals, and attenuated by improved metabolic control. p38 activation in diabetes is likely to occur via multiple pathways and cannot be explained by downregulation of MKP-1. |
| 4973 | 17424908 | Of these, 4-hydroxy-2,3-nonenal (HNE) induces the expression and synthesis of transforming growth factor beta1 (TGFbeta1) and activates nuclear binding of transcription factor activator protein 1 (AP-1) thus stimulating fibrogenesis. |
| 4974 | 17424908 | CR protects the rat aorta from the age-related increase of both oxidative damage and fibrosis; as regards the possible mechanism/s of CR's protection against fibrosclerosis, it is conceivable that, by decreasing oxidative stress, CR reduces HNE levels and consequently TGFbeta1 expression and collagen deposition, likely by down-regulating the activation of Jun-N terminal kinase and of AP-1. |
| 4975 | 17427197 | D-glucose stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and Smad2 requiring functional type II TGF-beta receptors in human umbilical vein endothelium. |
| 4976 | 17427197 | Elevated extracellular D-glucose increases transforming growth factor beta1 (TGF-beta1) release from human umbilical vein endothelium (HUVEC). |
| 4977 | 17427197 | TGF-beta1, via TGF-beta receptors I (TbetaRI) and TbetaRII, activates Smad2 and mitogen-activated protein kinases p44 and p42 (p42/44(mapk)). |
| 4978 | 17427197 | TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. |
| 4979 | 17427197 | TGF-beta1 and high D-glucose increased p42/44(mapk) and Smad2 phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor). |
| 4980 | 17427197 | High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC. |
| 4981 | 17427197 | D-glucose stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and Smad2 requiring functional type II TGF-beta receptors in human umbilical vein endothelium. |
| 4982 | 17427197 | Elevated extracellular D-glucose increases transforming growth factor beta1 (TGF-beta1) release from human umbilical vein endothelium (HUVEC). |
| 4983 | 17427197 | TGF-beta1, via TGF-beta receptors I (TbetaRI) and TbetaRII, activates Smad2 and mitogen-activated protein kinases p44 and p42 (p42/44(mapk)). |
| 4984 | 17427197 | TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. |
| 4985 | 17427197 | TGF-beta1 and high D-glucose increased p42/44(mapk) and Smad2 phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor). |
| 4986 | 17427197 | High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC. |
| 4987 | 17427197 | D-glucose stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and Smad2 requiring functional type II TGF-beta receptors in human umbilical vein endothelium. |
| 4988 | 17427197 | Elevated extracellular D-glucose increases transforming growth factor beta1 (TGF-beta1) release from human umbilical vein endothelium (HUVEC). |
| 4989 | 17427197 | TGF-beta1, via TGF-beta receptors I (TbetaRI) and TbetaRII, activates Smad2 and mitogen-activated protein kinases p44 and p42 (p42/44(mapk)). |
| 4990 | 17427197 | TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. |
| 4991 | 17427197 | TGF-beta1 and high D-glucose increased p42/44(mapk) and Smad2 phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor). |
| 4992 | 17427197 | High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC. |
| 4993 | 17427197 | D-glucose stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and Smad2 requiring functional type II TGF-beta receptors in human umbilical vein endothelium. |
| 4994 | 17427197 | Elevated extracellular D-glucose increases transforming growth factor beta1 (TGF-beta1) release from human umbilical vein endothelium (HUVEC). |
| 4995 | 17427197 | TGF-beta1, via TGF-beta receptors I (TbetaRI) and TbetaRII, activates Smad2 and mitogen-activated protein kinases p44 and p42 (p42/44(mapk)). |
| 4996 | 17427197 | TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. |
| 4997 | 17427197 | TGF-beta1 and high D-glucose increased p42/44(mapk) and Smad2 phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor). |
| 4998 | 17427197 | High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC. |
| 4999 | 17427197 | D-glucose stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and Smad2 requiring functional type II TGF-beta receptors in human umbilical vein endothelium. |
| 5000 | 17427197 | Elevated extracellular D-glucose increases transforming growth factor beta1 (TGF-beta1) release from human umbilical vein endothelium (HUVEC). |
| 5001 | 17427197 | TGF-beta1, via TGF-beta receptors I (TbetaRI) and TbetaRII, activates Smad2 and mitogen-activated protein kinases p44 and p42 (p42/44(mapk)). |
| 5002 | 17427197 | TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. |
| 5003 | 17427197 | TGF-beta1 and high D-glucose increased p42/44(mapk) and Smad2 phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor). |
| 5004 | 17427197 | High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC. |
| 5005 | 17427197 | D-glucose stimulation of L-arginine transport and nitric oxide synthesis results from activation of mitogen-activated protein kinases p42/44 and Smad2 requiring functional type II TGF-beta receptors in human umbilical vein endothelium. |
| 5006 | 17427197 | Elevated extracellular D-glucose increases transforming growth factor beta1 (TGF-beta1) release from human umbilical vein endothelium (HUVEC). |
| 5007 | 17427197 | TGF-beta1, via TGF-beta receptors I (TbetaRI) and TbetaRII, activates Smad2 and mitogen-activated protein kinases p44 and p42 (p42/44(mapk)). |
| 5008 | 17427197 | TGF-beta1 and high D-glucose increased hCAT-1 mRNA expression ( approximately 8-fold) and maximal transport velocity (V(max)), L-[(3)H]citrulline formation from L-[(3)H]arginine (index of NO synthesis) and endothelial NO synthase (eNOS) protein abundance, but did not alter eNOS phosphorylation. |
| 5009 | 17427197 | TGF-beta1 and high D-glucose increased p42/44(mapk) and Smad2 phosphorylation, an effect blocked by PD-98059 (MEK1/2 inhibitor). |
| 5010 | 17427197 | High D-glucose increases L-arginine transport and eNOS expression following TbetaRII activation by TGF-beta1 involving p42/44(mapk) and Smad2 in HUVEC. |
| 5011 | 17437042 | Blood glucose, kidney weight/body weight and 24-hour urine protein in the control and DN rats were examined; the expressions of BMP-7, Smad6 and Smad7 were detected by using immunohistochemical techniques, Western blot and real-time PCR. |
| 5012 | 17437042 | The expressions of BMP-7 and Smad6 proteins in DN rats were elevated, while BMP-7 mRNA expression was increased 2 weeks after STZ injection and decreased 16 weeks after STZ injection. |
| 5013 | 17437042 | In addition, the expressions of transforming growth factor-beta1 (TGF-beta1) and collagen type I (COL-I) mRNA were increased in DN rats. |
| 5014 | 17453245 | MSC-treated wounds also displayed a higher density of CD31(+) vessels and exhibited increases in the production of mRNA for epidermal growth factor, transforming growth factor beta 1, vascular endothelial growth factor, and stromal-derived growth factor 1-alpha. |
| 5015 | 17456374 | [Activation of transforming growth factor-beta1/Smads signal pathway in diabetic cardiomyopathy and effects of valsartan thereon: experiment with rats]. |
| 5016 | 17477023 | This led us to examine TGF-beta1 regulation when the effects of macrophage derived cytokines such as platelet derived growth factor and interleukin-1 are combined with exposure to elevated glucose concentrations. |
| 5017 | 17477023 | In addition, direct interaction between monocyte-macrophage CD18 and PTC cell surface ICAM-1 stimulates TGF-beta1 synthesis. |
| 5018 | 17477023 | We have now identified HA based structures synthesised on the surface of PTC, which act to prevent PTC-macrophage interaction through ICAM-1 thus preventing macrophage driven TGF-beta1 synthesis. |
| 5019 | 17477023 | This led us to examine TGF-beta1 regulation when the effects of macrophage derived cytokines such as platelet derived growth factor and interleukin-1 are combined with exposure to elevated glucose concentrations. |
| 5020 | 17477023 | In addition, direct interaction between monocyte-macrophage CD18 and PTC cell surface ICAM-1 stimulates TGF-beta1 synthesis. |
| 5021 | 17477023 | We have now identified HA based structures synthesised on the surface of PTC, which act to prevent PTC-macrophage interaction through ICAM-1 thus preventing macrophage driven TGF-beta1 synthesis. |
| 5022 | 17477023 | This led us to examine TGF-beta1 regulation when the effects of macrophage derived cytokines such as platelet derived growth factor and interleukin-1 are combined with exposure to elevated glucose concentrations. |
| 5023 | 17477023 | In addition, direct interaction between monocyte-macrophage CD18 and PTC cell surface ICAM-1 stimulates TGF-beta1 synthesis. |
| 5024 | 17477023 | We have now identified HA based structures synthesised on the surface of PTC, which act to prevent PTC-macrophage interaction through ICAM-1 thus preventing macrophage driven TGF-beta1 synthesis. |
| 5025 | 17494090 | We found that, in mesangial cells and renal fibroblasts grown in eight-well chamber slides, transforming growth factor-beta1 (TGF-beta1) disrupted the cell monolayer and induced cell migration into nodules in a dose-, time- and Smad3-dependent manner. |
| 5026 | 17494090 | The nodules contained increased interstitial collagens and showed an increased collagen I:IV ratio. |
| 5027 | 17494090 | Nodules are likely a biological consequence of TGF-beta1-induced matrix overexpression since they were mimicked by addition of collagen I to the cell culture medium. |
| 5028 | 17496904 | Expression of matrix metalloproteinases MMP-2 and MMP-9 is altered during nephrogenesis in fetuses from diabetic rats. |
| 5029 | 17496904 | Recent studies have emphasized the role of matrix metalloproteinases (MMP-2 and MMP-9) in normal mouse nephrogenesis. |
| 5030 | 17496904 | Transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) are known to mediate high glucose effects on matrix degradation. |
| 5031 | 17496904 | The aim of the present study was to address the expression of type IV collagenase and TGF-beta1/CTGF systems in rat kidney during normal development and after in utero exposure to maternal diabetes. |
| 5032 | 17496904 | Both MMP-2 and MMP-9 mRNA metanephric expressions and activities were dramatically downregulated in kidneys issued from diabetic fetuses and in metanephros cultured in the presence of high glucose concentration. |
| 5033 | 17496904 | TGF-beta1 and CTGF expressions were significantly enhanced in diabetic fetal kidneys and in high glucose cultured metanephroi. |
| 5034 | 17496904 | In conclusion, in impaired nephrogenesis resulting from in utero exposure to maternal diabetes, alteration of both type IV collagenase and TGF-beta1/CTGF systems may lead to abnormal remodeling of ECM, which may, in turn, induce defects in ureteral bud branching leading to the observed reduction in the nephron number with consequences later in life: progression of chronic renal disease and hypertension. |
| 5035 | 17496904 | Expression of matrix metalloproteinases MMP-2 and MMP-9 is altered during nephrogenesis in fetuses from diabetic rats. |
| 5036 | 17496904 | Recent studies have emphasized the role of matrix metalloproteinases (MMP-2 and MMP-9) in normal mouse nephrogenesis. |
| 5037 | 17496904 | Transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) are known to mediate high glucose effects on matrix degradation. |
| 5038 | 17496904 | The aim of the present study was to address the expression of type IV collagenase and TGF-beta1/CTGF systems in rat kidney during normal development and after in utero exposure to maternal diabetes. |
| 5039 | 17496904 | Both MMP-2 and MMP-9 mRNA metanephric expressions and activities were dramatically downregulated in kidneys issued from diabetic fetuses and in metanephros cultured in the presence of high glucose concentration. |
| 5040 | 17496904 | TGF-beta1 and CTGF expressions were significantly enhanced in diabetic fetal kidneys and in high glucose cultured metanephroi. |
| 5041 | 17496904 | In conclusion, in impaired nephrogenesis resulting from in utero exposure to maternal diabetes, alteration of both type IV collagenase and TGF-beta1/CTGF systems may lead to abnormal remodeling of ECM, which may, in turn, induce defects in ureteral bud branching leading to the observed reduction in the nephron number with consequences later in life: progression of chronic renal disease and hypertension. |
| 5042 | 17496904 | Expression of matrix metalloproteinases MMP-2 and MMP-9 is altered during nephrogenesis in fetuses from diabetic rats. |
| 5043 | 17496904 | Recent studies have emphasized the role of matrix metalloproteinases (MMP-2 and MMP-9) in normal mouse nephrogenesis. |
| 5044 | 17496904 | Transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) are known to mediate high glucose effects on matrix degradation. |
| 5045 | 17496904 | The aim of the present study was to address the expression of type IV collagenase and TGF-beta1/CTGF systems in rat kidney during normal development and after in utero exposure to maternal diabetes. |
| 5046 | 17496904 | Both MMP-2 and MMP-9 mRNA metanephric expressions and activities were dramatically downregulated in kidneys issued from diabetic fetuses and in metanephros cultured in the presence of high glucose concentration. |
| 5047 | 17496904 | TGF-beta1 and CTGF expressions were significantly enhanced in diabetic fetal kidneys and in high glucose cultured metanephroi. |
| 5048 | 17496904 | In conclusion, in impaired nephrogenesis resulting from in utero exposure to maternal diabetes, alteration of both type IV collagenase and TGF-beta1/CTGF systems may lead to abnormal remodeling of ECM, which may, in turn, induce defects in ureteral bud branching leading to the observed reduction in the nephron number with consequences later in life: progression of chronic renal disease and hypertension. |
| 5049 | 17496904 | Expression of matrix metalloproteinases MMP-2 and MMP-9 is altered during nephrogenesis in fetuses from diabetic rats. |
| 5050 | 17496904 | Recent studies have emphasized the role of matrix metalloproteinases (MMP-2 and MMP-9) in normal mouse nephrogenesis. |
| 5051 | 17496904 | Transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) are known to mediate high glucose effects on matrix degradation. |
| 5052 | 17496904 | The aim of the present study was to address the expression of type IV collagenase and TGF-beta1/CTGF systems in rat kidney during normal development and after in utero exposure to maternal diabetes. |
| 5053 | 17496904 | Both MMP-2 and MMP-9 mRNA metanephric expressions and activities were dramatically downregulated in kidneys issued from diabetic fetuses and in metanephros cultured in the presence of high glucose concentration. |
| 5054 | 17496904 | TGF-beta1 and CTGF expressions were significantly enhanced in diabetic fetal kidneys and in high glucose cultured metanephroi. |
| 5055 | 17496904 | In conclusion, in impaired nephrogenesis resulting from in utero exposure to maternal diabetes, alteration of both type IV collagenase and TGF-beta1/CTGF systems may lead to abnormal remodeling of ECM, which may, in turn, induce defects in ureteral bud branching leading to the observed reduction in the nephron number with consequences later in life: progression of chronic renal disease and hypertension. |
| 5056 | 17498265 | Type 1 diabetes (T1D) is a multifactorial autoimmune disorder where major histocompatibility complex (MHC) genes and the insulin-linked polymorphic region have been shown to play major roles. |
| 5057 | 17498265 | The variants of interferon-gamma (IFN-gamma) (A(+874)T), interleukin (IL)-6 (G(-174)C), IL-10 (A(-1082)G, T(-819)C, C(-592)A) and transforming growth factor (TGF) beta1 (T(cdn10)C, G(cdn25)C) did not show a significant difference between patients and controls. |
| 5058 | 17498265 | However, simultaneous presence of TNF-alpha-308 GA+AA along with both high and low secretor genotypes of IFN-gamma (P < 0.003) was significantly increased in patients. |
| 5059 | 17498265 | Simultaneous presence of TNF-alpha-308 GA + AA along with high secretor genotypes of IL-6 (P < 0.0001, OR = 2.61, 95% CI = 1.5-4.56), IL-10 (P < 0.0001, OR = 4.26, 95% CI = 1.9-10.1) and TGF-beta1 (P < 0.00004, OR = 2.8, 95% CI = 1.6-4.86) was also significantly increased in patients with T1D. |
| 5060 | 17498265 | Low secretor genotype of TNF-alpha-308 GG along with low secretor genotypes of IFN-gamma (P < 0.001, OR = 0.465, 95% CI = 0.28-0.77), high secretor genotypes of IL-6 (P < 0.000004, OR = 0.76, 95% CI = 0.227-0.621) and TGF-beta1 (P < 0.000006, OR = 0.336, 95% CI = 0.198-0.568) was protective. |
| 5061 | 17498265 | The TNF-alpha-308 G allele was in linkage disequilibrium (LD) with the human leukocyte antigen (HLA)-B*0801-DRB1*0301 haplotype, while TNF-alpha-308 A allele was in LD with the HLA-B*5001-DRB1*0301 and B*5801-DRB1*0301 haplotypes, suggesting that the effect of TNF-alpha -308 A allele is not because of its being in LD with any HLA alleles, but because of its functional role and its integrated effect with other cytokines. |
| 5062 | 17498265 | Type 1 diabetes (T1D) is a multifactorial autoimmune disorder where major histocompatibility complex (MHC) genes and the insulin-linked polymorphic region have been shown to play major roles. |
| 5063 | 17498265 | The variants of interferon-gamma (IFN-gamma) (A(+874)T), interleukin (IL)-6 (G(-174)C), IL-10 (A(-1082)G, T(-819)C, C(-592)A) and transforming growth factor (TGF) beta1 (T(cdn10)C, G(cdn25)C) did not show a significant difference between patients and controls. |
| 5064 | 17498265 | However, simultaneous presence of TNF-alpha-308 GA+AA along with both high and low secretor genotypes of IFN-gamma (P < 0.003) was significantly increased in patients. |
| 5065 | 17498265 | Simultaneous presence of TNF-alpha-308 GA + AA along with high secretor genotypes of IL-6 (P < 0.0001, OR = 2.61, 95% CI = 1.5-4.56), IL-10 (P < 0.0001, OR = 4.26, 95% CI = 1.9-10.1) and TGF-beta1 (P < 0.00004, OR = 2.8, 95% CI = 1.6-4.86) was also significantly increased in patients with T1D. |
| 5066 | 17498265 | Low secretor genotype of TNF-alpha-308 GG along with low secretor genotypes of IFN-gamma (P < 0.001, OR = 0.465, 95% CI = 0.28-0.77), high secretor genotypes of IL-6 (P < 0.000004, OR = 0.76, 95% CI = 0.227-0.621) and TGF-beta1 (P < 0.000006, OR = 0.336, 95% CI = 0.198-0.568) was protective. |
| 5067 | 17498265 | The TNF-alpha-308 G allele was in linkage disequilibrium (LD) with the human leukocyte antigen (HLA)-B*0801-DRB1*0301 haplotype, while TNF-alpha-308 A allele was in LD with the HLA-B*5001-DRB1*0301 and B*5801-DRB1*0301 haplotypes, suggesting that the effect of TNF-alpha -308 A allele is not because of its being in LD with any HLA alleles, but because of its functional role and its integrated effect with other cytokines. |
| 5068 | 17511984 | Expression of transforming growth factor-beta (TGF-beta) and connective tissue growth factor (CTGF) mRNA was up-regulated in the renal cortex of diabetic rats, and this was abolished by fasudil as well as statin. |
| 5069 | 17511984 | The present study demonstrates that the Rho/Rho-kinase pathway is involved in up-regulation of TGF-beta, CTGF and NAD(P)H oxidase in diabetic kidney. |
| 5070 | 17511984 | Expression of transforming growth factor-beta (TGF-beta) and connective tissue growth factor (CTGF) mRNA was up-regulated in the renal cortex of diabetic rats, and this was abolished by fasudil as well as statin. |
| 5071 | 17511984 | The present study demonstrates that the Rho/Rho-kinase pathway is involved in up-regulation of TGF-beta, CTGF and NAD(P)H oxidase in diabetic kidney. |
| 5072 | 17533010 | Increased glomerular cyclooxygenase (COX)1 or COX2 expression has been reported in patients with nephritis and in animal models of nephritis. |
| 5073 | 17533010 | Lipoxygenase product 12-hydroxyeicosatetraenoic acid may mediate angiotensin II and transforming growth factor beta-induced mesangial cell abnormality in diabetic nephropathy. |
| 5074 | 17536062 | Peroxisome proliferator-activated receptors (PPARs) are nuclear transcription factors and play a central role in insulin sensitivity, lipid metabolism, and inflammation. |
| 5075 | 17536062 | Treatment with tesaglitazar was associated with reduced plasma insulin and total triglyceride levels and increased plasma adiponectin levels. |
| 5076 | 17536062 | Notably, tesaglitazar markedly attenuated albuminuria and significantly lowered glomerulofibrosis, collagen deposition, and transforming growth factor-beta1 expression in renal tissues of db/db mice. |
| 5077 | 17536062 | In cultured mesangial cells and proximal tubule cells, where both PPARalpha and -gamma were expressed, tesaglitazar treatment abolished high glucose-induced total collagen protein production and type I and IV collagen gene expression. |
| 5078 | 17549301 | Biphasic effect of pioglitazone on isolated human endothelial progenitor cells: involvement of peroxisome proliferator-activated receptor-gamma and transforming growth factor-beta1. |
| 5079 | 17549301 | We evaluated the effects of the anti-diabetic drug pioglitazone on human EPC function and the involvement of PPAR-gamma and TGF-beta1. |
| 5080 | 17549301 | EPCs in culture were characterized at day 7 by the development of colony-forming units (CFUs) and flow cytometry assessment of differentiation marker (DiI-ac-LDL/lectin, KDR and CD31). |
| 5081 | 17549301 | Treatment with pioglitazone for 72 hours increased the number of EPC-CFUs, DiI-ac-LDL(+)/lectin(+), CD31(+) and KDR(+) EPCs at 1 microM but not at 10 microM. |
| 5082 | 17549301 | Indeed, pioglitazone increased EPC adhesion in flow at 1 microM, an effect prevented by PPAR-gamma and beta2-integrin blockade. |
| 5083 | 17549301 | As determined by ELISA, pioglitazone induced a persistent increase in TGF-beta1 secretion only at 10 microM when a significantly elevated expression of endoglin, the accessory receptor for TGF-beta1, was also observed. |
| 5084 | 17549301 | Biphasic effect of pioglitazone on isolated human endothelial progenitor cells: involvement of peroxisome proliferator-activated receptor-gamma and transforming growth factor-beta1. |
| 5085 | 17549301 | We evaluated the effects of the anti-diabetic drug pioglitazone on human EPC function and the involvement of PPAR-gamma and TGF-beta1. |
| 5086 | 17549301 | EPCs in culture were characterized at day 7 by the development of colony-forming units (CFUs) and flow cytometry assessment of differentiation marker (DiI-ac-LDL/lectin, KDR and CD31). |
| 5087 | 17549301 | Treatment with pioglitazone for 72 hours increased the number of EPC-CFUs, DiI-ac-LDL(+)/lectin(+), CD31(+) and KDR(+) EPCs at 1 microM but not at 10 microM. |
| 5088 | 17549301 | Indeed, pioglitazone increased EPC adhesion in flow at 1 microM, an effect prevented by PPAR-gamma and beta2-integrin blockade. |
| 5089 | 17549301 | As determined by ELISA, pioglitazone induced a persistent increase in TGF-beta1 secretion only at 10 microM when a significantly elevated expression of endoglin, the accessory receptor for TGF-beta1, was also observed. |
| 5090 | 17549301 | Biphasic effect of pioglitazone on isolated human endothelial progenitor cells: involvement of peroxisome proliferator-activated receptor-gamma and transforming growth factor-beta1. |
| 5091 | 17549301 | We evaluated the effects of the anti-diabetic drug pioglitazone on human EPC function and the involvement of PPAR-gamma and TGF-beta1. |
| 5092 | 17549301 | EPCs in culture were characterized at day 7 by the development of colony-forming units (CFUs) and flow cytometry assessment of differentiation marker (DiI-ac-LDL/lectin, KDR and CD31). |
| 5093 | 17549301 | Treatment with pioglitazone for 72 hours increased the number of EPC-CFUs, DiI-ac-LDL(+)/lectin(+), CD31(+) and KDR(+) EPCs at 1 microM but not at 10 microM. |
| 5094 | 17549301 | Indeed, pioglitazone increased EPC adhesion in flow at 1 microM, an effect prevented by PPAR-gamma and beta2-integrin blockade. |
| 5095 | 17549301 | As determined by ELISA, pioglitazone induced a persistent increase in TGF-beta1 secretion only at 10 microM when a significantly elevated expression of endoglin, the accessory receptor for TGF-beta1, was also observed. |
| 5096 | 17554073 | Several downstream effects of TGF-beta are mediated by connective tissue growth factor (CTGF), which is up-regulated in several renal cells and secreted in the urine in the diabetic state. |
| 5097 | 17554073 | The ASO also reduced expression of genes involved in matrix expansion such as fibronectin and collagen (I and IV) and an inhibitor of matrix degradation, PAI-1, in the renal cortex, contributing to significant reversal of mesangial expansion in both models of DN. |
| 5098 | 17554073 | Pathway analyses demonstrated that diabetes-induced phosphorylation of p38 MAPK and its downstream target CREB was also inhibited by the ASO. |
| 5099 | 17554150 | Significantly reduced expression of TGF-beta, vascular endothelial growth factor, and collagen IV was found in glomeruli and the tubulointerstitial area with CERA treatment, and these beneficial molecular effects were clearly dosage dependent (both P < 0.05 versus placebo). |
| 5100 | 17554150 | Similarly, CERA treatment caused a dosage-dependent increase in p-Akt, nephrin, and perlecan tissue expression (all P < 0.05 versus placebo). |
| 5101 | 17554258 | Exposure of mesangial cells to AGEs led to a significant reduction in MMP-7, but not MMP-3 or -10. |
| 5102 | 17554258 | MMP-7 expression was normalized by both aminoguanidine, an inhibitor of glycation product formation, or by a neutralizing anti-transforming growth factor-beta (TGF-beta) antibody. |
| 5103 | 17554258 | Our findings suggest that diminished expression of the glycoprotein-degrading enzyme, MMP-7, may play a role in fibronectin accumulation in the diabetic kidney in response to AGEs and/or TGF-beta. |
| 5104 | 17554258 | Exposure of mesangial cells to AGEs led to a significant reduction in MMP-7, but not MMP-3 or -10. |
| 5105 | 17554258 | MMP-7 expression was normalized by both aminoguanidine, an inhibitor of glycation product formation, or by a neutralizing anti-transforming growth factor-beta (TGF-beta) antibody. |
| 5106 | 17554258 | Our findings suggest that diminished expression of the glycoprotein-degrading enzyme, MMP-7, may play a role in fibronectin accumulation in the diabetic kidney in response to AGEs and/or TGF-beta. |
| 5107 | 17566145 | Treatment with breviscapine also significantly decreased lipid peroxidation malondiadehyde levels and increased the activities of antioxidative enzymes such as superoxide dismutase, catalase and glutathione peroxidase in diabetic liver. |
| 5108 | 17566145 | Western blot analysis showed that the expression of transforming growth factor-beta1 in diabetic liver was lowered by breviscapine treatment. |
| 5109 | 17568784 | In this study, we show that statin ameliorates nephropathy in db/db mice, a rodent model of type 2 diabetes, via downregulation of NAD(P)H oxidase NOX4, which is a major source of oxidative stress in the kidney. |
| 5110 | 17568784 | Additionally, 12-week treatment with the statin completely normalized the levels of transforming growth factor-beta1 and fibronectin mRNA as well as the mesangial expansion characteristic of diabetic nephropathy. |
| 5111 | 17570945 | Components of the diabetic milieu (high glucose, accumulation of glycated proteins, high intrarenal angiotensin II (ANG II), and hypertension-induced mechanical stress) result in activation of cytokine systems, the most important of which are transforming growth factor-beta1 (TGF-beta1) and vascular endothelial growth factor-A (VEGF-A). |
| 5112 | 17570945 | ANG II-stimulated podocyte-derived VEGF, through a novel autocrine signaling loop, appears to be a major cause of nephrin downregulation and the development of proteinuria. |
| 5113 | 17574405 | At D30, there was an important increase of laminin whereas fibronectin and collagen V were moderately augmented. |
| 5114 | 17574405 | In contrast, TGFbeta2 levels were significantly higher at D30, concomitant with increased TGFbeta receptor II (TbetaRII), phosphorylated Smads 2 and 3 (pSmads 2-3) and Latent TGFbeta Binding Protein 1 (LTBP1). |
| 5115 | 17582205 | In addition, the expression of Type IV collagen alpha1 chain (Col4A1), Transforming growth factor-beta (TGF-beta), and Txnip were evaluated by real-time polymerase chain reaction. |
| 5116 | 17582205 | The mRNA expression of COL4A1 and TGF-beta was dramatically increased in diabetic mice in comparison with the control mice. |
| 5117 | 17582205 | In addition, the expression of Type IV collagen alpha1 chain (Col4A1), Transforming growth factor-beta (TGF-beta), and Txnip were evaluated by real-time polymerase chain reaction. |
| 5118 | 17582205 | The mRNA expression of COL4A1 and TGF-beta was dramatically increased in diabetic mice in comparison with the control mice. |
| 5119 | 17587828 | Although a number of factors may initiate EMT in the kidney, the most potent is transforming growth factor-beta1 (TGF-beta1). |
| 5120 | 17587828 | Moreover, many other prosclerotic factors have effects on EMT indirectly, via induction of TGF-beta1. |
| 5121 | 17587828 | Signaling events in this pathway include activation of Smad/integrin-linked kinase (ILK) and connective tissue growth factor (CTGF). |
| 5122 | 17587828 | In particular, overexpression of matrix metalloproteinase-2 has a key role in the initiation of EMT, membrane dissolution, and the interstitial transit of transformed mesenchymal cells. |
| 5123 | 17587828 | Although a number of factors may initiate EMT in the kidney, the most potent is transforming growth factor-beta1 (TGF-beta1). |
| 5124 | 17587828 | Moreover, many other prosclerotic factors have effects on EMT indirectly, via induction of TGF-beta1. |
| 5125 | 17587828 | Signaling events in this pathway include activation of Smad/integrin-linked kinase (ILK) and connective tissue growth factor (CTGF). |
| 5126 | 17587828 | In particular, overexpression of matrix metalloproteinase-2 has a key role in the initiation of EMT, membrane dissolution, and the interstitial transit of transformed mesenchymal cells. |
| 5127 | 17593866 | We compared the levels of transforming growth factor beta1 (TGF-beta1), vascular endothelial growth factor (VEGF) and other biochemical parameters in patients with type 1 diabetes mellitus with and without incipient diabetic nephropathy (iDN) and compared them with healthy control subjects. |
| 5128 | 17593866 | Compared with healthy controls, TGF-beta1 levels were increased in both groups of diabetes patients, whereas VEGF was only elevated in patients with iDN. |
| 5129 | 17593866 | Ramipril did not have a significant effect on TGF-beta1 or VEGF levels. |
| 5130 | 17593866 | We compared the levels of transforming growth factor beta1 (TGF-beta1), vascular endothelial growth factor (VEGF) and other biochemical parameters in patients with type 1 diabetes mellitus with and without incipient diabetic nephropathy (iDN) and compared them with healthy control subjects. |
| 5131 | 17593866 | Compared with healthy controls, TGF-beta1 levels were increased in both groups of diabetes patients, whereas VEGF was only elevated in patients with iDN. |
| 5132 | 17593866 | Ramipril did not have a significant effect on TGF-beta1 or VEGF levels. |
| 5133 | 17593866 | We compared the levels of transforming growth factor beta1 (TGF-beta1), vascular endothelial growth factor (VEGF) and other biochemical parameters in patients with type 1 diabetes mellitus with and without incipient diabetic nephropathy (iDN) and compared them with healthy control subjects. |
| 5134 | 17593866 | Compared with healthy controls, TGF-beta1 levels were increased in both groups of diabetes patients, whereas VEGF was only elevated in patients with iDN. |
| 5135 | 17593866 | Ramipril did not have a significant effect on TGF-beta1 or VEGF levels. |
| 5136 | 17596523 | Diabetic nephropathy (DN) is associated with increased oxidative stress, overexpression and activation of growth factor receptors, including those for transforming growth factor-beta1 (TGF-beta-RII), platelet-derived growth factor (PDGF-R), and insulin-like growth factor (IGF1-R). |
| 5137 | 17596523 | The early phase of diabetes was found to be associated with an increase in glomerular expression of IGF1-R, PDGF-R, and TGF-beta-RII and activation of IRS1, Erk 1/2, and Smad 2/3. |
| 5138 | 17597607 | Here, the potential therapeutic effects of PCA in the treatment of diabetic complications were studied by determining this compound's ability to inhibit the formation of advanced glycation end products-bovine serum albumin (BSA) and the expression of receptor for advanced glycation end products and TGF-beta1 in human lens epithelial cells cultured under diabetic conditions. |
| 5139 | 17597607 | Moreover, PCA inhibited high glucose- or S100b-induced TGF-beta1 protein and mRNA expression as well as nuclear accumulation of phosphorylated Smad2/3. |
| 5140 | 17597607 | Here, the potential therapeutic effects of PCA in the treatment of diabetic complications were studied by determining this compound's ability to inhibit the formation of advanced glycation end products-bovine serum albumin (BSA) and the expression of receptor for advanced glycation end products and TGF-beta1 in human lens epithelial cells cultured under diabetic conditions. |
| 5141 | 17597607 | Moreover, PCA inhibited high glucose- or S100b-induced TGF-beta1 protein and mRNA expression as well as nuclear accumulation of phosphorylated Smad2/3. |
| 5142 | 17631805 | [Effects of Chinese herbs for replenishing qi and resolving stagnation on transforming growth factor-beta1 of skin ulcers in rats with diabetes]. |
| 5143 | 17652186 | Inhibin and activin are members of the TGFbeta family that perform mutually antagonistic signaling roles in the anterior pituitary, gonads, and adrenal gland. |
| 5144 | 17652186 | In this study, we demonstrate that Smad3, a key effector of activin signaling, is expressed at high levels and is constitutively activated in tumors from these mice. |
| 5145 | 17652186 | The decrease in cyclinD2 levels in compound knockout mice is related to a reduction in mitogenic signaling through the phosphoinositide-3-kinase (PI3-kinase)/Akt pathway, which is required for normal cell cycle progression in tumor cells. |
| 5146 | 17652186 | Loss of PI3-kinase/Akt signaling cannot be attributed to alterations in IGF expression, suggesting instead that signaling through the FSH receptor is attenuated. |
| 5147 | 17652186 | Gene expression profiling in the ovaries of Madh3-/- and Inha-/-:Madh3-/- compound knockout mice supports this hypothesis and further suggests that Smad3 is specifically required for FSH to activate PI3-kinase/Akt, but not protein kinase A. |
| 5148 | 17652186 | Together these observations imply that activin/Smad3 signaling is necessary for efficient signaling by FSH in Inha-/- tumor cells and that interruption of this pathway uncouples FSH from its intracellular mitogenic effectors. |
| 5149 | 17653209 | Furthermore, podocytes are known to synthesize matrix molecules to the glomerular basement membrane (GBM), including type IV collagen, laminin, entactin, and agrin. |
| 5150 | 17653209 | As a result, many investigations have demonstrated that the diabetic milieu per se, hemodynamic changes, and local growth factors such as transforming growth factor-beta and angiotensin II, which are considered mediators in the pathogenesis of diabetic nephropathy, induce directly and/or indirectly hypertrophy, apoptosis, and structural changes, and increase type IV collagen synthesis in podocytes. |
| 5151 | 17653214 | High glucose upregulates transforming growth factor-beta1 (TGF-beta1) and angiotensin II (Ang II) in renal cells and high glucose, TGF-beta1, and Ang II all generate and signal through ROS. |
| 5152 | 17653214 | Transketolase activators and poly (ADP-ribose) polymerase inhibitors were shown to block major biochemical pathways of hyperglycemic damage. |
| 5153 | 17664181 | High glucose induces macrophage inflammatory protein-3 alpha in renal proximal tubule cells via a transforming growth factor-beta 1 dependent mechanism. |
| 5154 | 17666488 | We investigated FN mRNA, EDB(+)FN mRNA, and transforming growth factor (TGF)-beta mRNA expression, Akt phosphorylation, Akt kinase activity, and NF-kappaB and AP-1 activation in the retina, heart, and kidney. |
| 5155 | 17666488 | Galactose feeding caused significant upregulation of FN, EDB(+)FN, and TGF-beta in all tissues. |
| 5156 | 17666488 | NF-kappaB and AP-1 activation was pronounced in galactose-fed wild-type mice and prevented in the galactose-fed Akt1/PKBalpha-deficient group. |
| 5157 | 17666488 | The data from this study indicate that hyperhexosemia-induced Akt/PKB activation may be an important mechanism leading to NF-kappaB and AP-1 activation and increased ECM protein synthesis in the organs affected by chronic diabetic complications. |
| 5158 | 17675577 | High glucose-induced thioredoxin-interacting protein in renal proximal tubule cells is independent of transforming growth factor-beta1. |
| 5159 | 17675577 | Txnip, heat shock proteins 70 and 90, chemokine (C-C motif) ligand 20, and matrix metalloproteinase-7 were chosen for verification of gene expression. |
| 5160 | 17675577 | The increased protein expression of Txnip, CCL20, and MMP7 were also verified by Western blotting and enzyme-linked immunosorbent assay. |
| 5161 | 17675577 | Subsequent studies focused on the dependence of Txnip expression on up-regulation of transforming growth factor (TGF)-beta1 under high-glucose conditions. |
| 5162 | 17675577 | Overexpression of Txnip and up-regulation of Txnip promoter activity were observed in cells in which the TGF-beta1 gene was silenced in HK-2 cells using short interfering RNA technology. |
| 5163 | 17675577 | High glucose further increased both Txnip expression and its promoter activity in TGF-beta1 silenced cells compared with wild-type cells exposed to high glucose, suggesting that high glucose induced Txnip through a TGF-beta1-indepen-dent pathway. |
| 5164 | 17675577 | High glucose-induced thioredoxin-interacting protein in renal proximal tubule cells is independent of transforming growth factor-beta1. |
| 5165 | 17675577 | Txnip, heat shock proteins 70 and 90, chemokine (C-C motif) ligand 20, and matrix metalloproteinase-7 were chosen for verification of gene expression. |
| 5166 | 17675577 | The increased protein expression of Txnip, CCL20, and MMP7 were also verified by Western blotting and enzyme-linked immunosorbent assay. |
| 5167 | 17675577 | Subsequent studies focused on the dependence of Txnip expression on up-regulation of transforming growth factor (TGF)-beta1 under high-glucose conditions. |
| 5168 | 17675577 | Overexpression of Txnip and up-regulation of Txnip promoter activity were observed in cells in which the TGF-beta1 gene was silenced in HK-2 cells using short interfering RNA technology. |
| 5169 | 17675577 | High glucose further increased both Txnip expression and its promoter activity in TGF-beta1 silenced cells compared with wild-type cells exposed to high glucose, suggesting that high glucose induced Txnip through a TGF-beta1-indepen-dent pathway. |
| 5170 | 17675577 | High glucose-induced thioredoxin-interacting protein in renal proximal tubule cells is independent of transforming growth factor-beta1. |
| 5171 | 17675577 | Txnip, heat shock proteins 70 and 90, chemokine (C-C motif) ligand 20, and matrix metalloproteinase-7 were chosen for verification of gene expression. |
| 5172 | 17675577 | The increased protein expression of Txnip, CCL20, and MMP7 were also verified by Western blotting and enzyme-linked immunosorbent assay. |
| 5173 | 17675577 | Subsequent studies focused on the dependence of Txnip expression on up-regulation of transforming growth factor (TGF)-beta1 under high-glucose conditions. |
| 5174 | 17675577 | Overexpression of Txnip and up-regulation of Txnip promoter activity were observed in cells in which the TGF-beta1 gene was silenced in HK-2 cells using short interfering RNA technology. |
| 5175 | 17675577 | High glucose further increased both Txnip expression and its promoter activity in TGF-beta1 silenced cells compared with wild-type cells exposed to high glucose, suggesting that high glucose induced Txnip through a TGF-beta1-indepen-dent pathway. |
| 5176 | 17679816 | That adipose tissue releases a wide range of adipokines, growth factors, enzymes, and enzyme substrates linked to vascular injury provides a plausible explanation for the role of fat in vascular disease: tumor necrosis factor-alpha, leptin, resistin, interleukin-1, -6, -8, and -18, serum amyloid A, monocyte chemoattractant protein I, macrophage inhibitory factor, aortic carboxypeptidase, hepa-rin-binding epidermal growth factor-like growth factor, vascular endothelial growth factor, transforming growth factor beta, angiotensinogen, cathepsin S, estradiol, cortisol, mineralocorticoid releasing factor, and calcitonin peptides are probable fat-derived prothrombotic, proinflammatory, and proatherosclerotic agents acting in a paracrine and/or endocrine manner. |
| 5177 | 17679816 | Other adipocyte products such as adiponectin, transforming growth factor beta, and interleukin-10 exert some antiatherogenic effects. |
| 5178 | 17679816 | That adipose tissue releases a wide range of adipokines, growth factors, enzymes, and enzyme substrates linked to vascular injury provides a plausible explanation for the role of fat in vascular disease: tumor necrosis factor-alpha, leptin, resistin, interleukin-1, -6, -8, and -18, serum amyloid A, monocyte chemoattractant protein I, macrophage inhibitory factor, aortic carboxypeptidase, hepa-rin-binding epidermal growth factor-like growth factor, vascular endothelial growth factor, transforming growth factor beta, angiotensinogen, cathepsin S, estradiol, cortisol, mineralocorticoid releasing factor, and calcitonin peptides are probable fat-derived prothrombotic, proinflammatory, and proatherosclerotic agents acting in a paracrine and/or endocrine manner. |
| 5179 | 17679816 | Other adipocyte products such as adiponectin, transforming growth factor beta, and interleukin-10 exert some antiatherogenic effects. |
| 5180 | 17686959 | Diabetes was associated with an increase in urine albumin excretion, glomerulosclerosis, tubulointerstitial fibrosis, renal cortical collagen type I and IV, laminin, plasminogen activator inhibitor-1, tissue inhibitors of metalloproteinase-1 and -2, transforming growth factor (TGF)-beta, TGF-beta receptor type I and II, Smad2/3, phosphorylated Smad2/3, and Smad4 protein expression, and CD68-positive cell abundance. |
| 5181 | 17686959 | Decreases in matrix metalloproteinase (MMP)-2 protein expression and activity and decreases in Smad6 and Smad7 protein expression were also associated with diabetes. |
| 5182 | 17697870 | After 5 weeks of diabetes, KO diabetic (D) but not WT-D mice developed marked albuminuria, increases in glomerular content of transforming growth factor beta, collagen alpha1(IV), and nitrotyrosine, and higher glomerular superoxide compared with corresponding values in nondiabetics. |
| 5183 | 17697870 | Treatment of KO-D with the SOD mimetic tempol for 4 weeks suppressed albuminuria, increases in glomerular transforming growth factor beta, collagen alpha1(IV), nitrotyrosine, and glomerular superoxide, and concurrently increased C(In). |
| 5184 | 17697870 | After 5 weeks of diabetes, KO diabetic (D) but not WT-D mice developed marked albuminuria, increases in glomerular content of transforming growth factor beta, collagen alpha1(IV), and nitrotyrosine, and higher glomerular superoxide compared with corresponding values in nondiabetics. |
| 5185 | 17697870 | Treatment of KO-D with the SOD mimetic tempol for 4 weeks suppressed albuminuria, increases in glomerular transforming growth factor beta, collagen alpha1(IV), nitrotyrosine, and glomerular superoxide, and concurrently increased C(In). |
| 5186 | 17709885 | Type 1 diabetes (T1D) results from autoimmune destruction of the insulin-producing beta-cells in the pancreatic islets of Langerhans by autoreactive T helper 1 (Th1) cells characterized by their cytokine secretory products, interleukin-2 (IL-2) and interferon gamma (IFNgamma). |
| 5187 | 17709885 | Th1-type cytokines (IL-2 and IFNgamma) correlate with T1D, whereas Th2 (IL-4 and IL-10), Th3 (transforming growth factor beta [TGFbeta]), and T regulatory cell-type cytokines (IL-10 and TGFbeta) correlate with protection from T1D. |
| 5188 | 17709885 | Paradoxically, however, administrations of Th1-type cytokines (IL-2 and IFNgamma) and immunotherapies that induce Th1-type cytokine responses actually prevent T1D, at least in animal models. |
| 5189 | 17720766 | While tranilast did not affect Smad phosphorylation, it significantly attenuated TGF-beta-induced p44/42 mitogen-activated protein kinase phosphorylation. |
| 5190 | 17724131 | Yet conversion of mature conventional CD4(+) T (T conv) cell lymphocytes can be achieved in several conditions, such as transforming growth factor beta treatment, homeostatic expansion, or chronic exposure to low-dose antigen. |
| 5191 | 17728702 | Mesangial cells (MCs) exposed to high glucose (HG) for short periods have shown that transforming growth factor-beta (TGF-beta) and activated diacylglycerol-dependent protein kinase C (PKC) mediate increased collagen formation. |
| 5192 | 17728702 | In contrast, 8-week exposure to HG resulted in the persistent activation of PKC-delta, did not change PKC-alpha or -beta activity, and decreased PKC-epsilon activity while increasing collagen I and IV gene and protein expression. |
| 5193 | 17728702 | Collagen IV gene expression was completely normalized by TGF-beta neutralization; however, this was associated with plasminogen activator inhibitor-1 (PAI-1) overexpression and a modest reduction in collagen protein. |
| 5194 | 17728702 | Our studies suggest that prolonged exposure to HG results in PKC-delta-driven collagen accumulation by MCs mediated by PAI-1 but independent of TGF-beta. |
| 5195 | 17728702 | Mesangial cells (MCs) exposed to high glucose (HG) for short periods have shown that transforming growth factor-beta (TGF-beta) and activated diacylglycerol-dependent protein kinase C (PKC) mediate increased collagen formation. |
| 5196 | 17728702 | In contrast, 8-week exposure to HG resulted in the persistent activation of PKC-delta, did not change PKC-alpha or -beta activity, and decreased PKC-epsilon activity while increasing collagen I and IV gene and protein expression. |
| 5197 | 17728702 | Collagen IV gene expression was completely normalized by TGF-beta neutralization; however, this was associated with plasminogen activator inhibitor-1 (PAI-1) overexpression and a modest reduction in collagen protein. |
| 5198 | 17728702 | Our studies suggest that prolonged exposure to HG results in PKC-delta-driven collagen accumulation by MCs mediated by PAI-1 but independent of TGF-beta. |
| 5199 | 17728702 | Mesangial cells (MCs) exposed to high glucose (HG) for short periods have shown that transforming growth factor-beta (TGF-beta) and activated diacylglycerol-dependent protein kinase C (PKC) mediate increased collagen formation. |
| 5200 | 17728702 | In contrast, 8-week exposure to HG resulted in the persistent activation of PKC-delta, did not change PKC-alpha or -beta activity, and decreased PKC-epsilon activity while increasing collagen I and IV gene and protein expression. |
| 5201 | 17728702 | Collagen IV gene expression was completely normalized by TGF-beta neutralization; however, this was associated with plasminogen activator inhibitor-1 (PAI-1) overexpression and a modest reduction in collagen protein. |
| 5202 | 17728702 | Our studies suggest that prolonged exposure to HG results in PKC-delta-driven collagen accumulation by MCs mediated by PAI-1 but independent of TGF-beta. |
| 5203 | 17804483 | Interference with TGF-beta signaling by Smad3-knockout in mice limits diabetic glomerulosclerosis without affecting albuminuria. |
| 5204 | 17804483 | To isolate the contribution of one of the signaling pathways of TGF-beta, the Smad3 gene in the mouse was knocked out at exons 2 and 3, and the effect was studied in streptozotocin (STZ)-induced diabetes over a period of 6 wk. |
| 5205 | 17804483 | TGF-beta activity was increased in the diabetic mice but was not able to signal via Smad3 in the knockout (KO) mice. |
| 5206 | 17804483 | The parameters not significantly altered by the Smad3-KO were albuminuria, reduction in podocyte slit pore density, and the increase in vascular endothelial growth factor abundance and activity. |
| 5207 | 17804483 | In conclusion, the effects of the Smad3-KO mirror the effects of anti-TGF-beta therapy in diabetes, suggesting that the chief component of TGF-beta signaling that is relevant to kidney disease is the Smad3 pathway. |
| 5208 | 17804483 | Interference with TGF-beta signaling by Smad3-knockout in mice limits diabetic glomerulosclerosis without affecting albuminuria. |
| 5209 | 17804483 | To isolate the contribution of one of the signaling pathways of TGF-beta, the Smad3 gene in the mouse was knocked out at exons 2 and 3, and the effect was studied in streptozotocin (STZ)-induced diabetes over a period of 6 wk. |
| 5210 | 17804483 | TGF-beta activity was increased in the diabetic mice but was not able to signal via Smad3 in the knockout (KO) mice. |
| 5211 | 17804483 | The parameters not significantly altered by the Smad3-KO were albuminuria, reduction in podocyte slit pore density, and the increase in vascular endothelial growth factor abundance and activity. |
| 5212 | 17804483 | In conclusion, the effects of the Smad3-KO mirror the effects of anti-TGF-beta therapy in diabetes, suggesting that the chief component of TGF-beta signaling that is relevant to kidney disease is the Smad3 pathway. |
| 5213 | 17804483 | Interference with TGF-beta signaling by Smad3-knockout in mice limits diabetic glomerulosclerosis without affecting albuminuria. |
| 5214 | 17804483 | To isolate the contribution of one of the signaling pathways of TGF-beta, the Smad3 gene in the mouse was knocked out at exons 2 and 3, and the effect was studied in streptozotocin (STZ)-induced diabetes over a period of 6 wk. |
| 5215 | 17804483 | TGF-beta activity was increased in the diabetic mice but was not able to signal via Smad3 in the knockout (KO) mice. |
| 5216 | 17804483 | The parameters not significantly altered by the Smad3-KO were albuminuria, reduction in podocyte slit pore density, and the increase in vascular endothelial growth factor abundance and activity. |
| 5217 | 17804483 | In conclusion, the effects of the Smad3-KO mirror the effects of anti-TGF-beta therapy in diabetes, suggesting that the chief component of TGF-beta signaling that is relevant to kidney disease is the Smad3 pathway. |
| 5218 | 17804483 | Interference with TGF-beta signaling by Smad3-knockout in mice limits diabetic glomerulosclerosis without affecting albuminuria. |
| 5219 | 17804483 | To isolate the contribution of one of the signaling pathways of TGF-beta, the Smad3 gene in the mouse was knocked out at exons 2 and 3, and the effect was studied in streptozotocin (STZ)-induced diabetes over a period of 6 wk. |
| 5220 | 17804483 | TGF-beta activity was increased in the diabetic mice but was not able to signal via Smad3 in the knockout (KO) mice. |
| 5221 | 17804483 | The parameters not significantly altered by the Smad3-KO were albuminuria, reduction in podocyte slit pore density, and the increase in vascular endothelial growth factor abundance and activity. |
| 5222 | 17804483 | In conclusion, the effects of the Smad3-KO mirror the effects of anti-TGF-beta therapy in diabetes, suggesting that the chief component of TGF-beta signaling that is relevant to kidney disease is the Smad3 pathway. |
| 5223 | 17804487 | High glucose (HG; 25 mM) induces rounding of differentiated podocytes and changes in the distribution of F-actin but without quantitative changes in E-cadherin and the podocyte markers podocin, CD2AP, Neph1, or synaptopodin. |
| 5224 | 17804487 | In these cells, BMP7 effectively activates smad5 (but not smad1) and raises p38 phosphorylation [which is also increased by transforming growth factor-beta (TGF-beta)]. |
| 5225 | 17804487 | HG as well as TGF-beta raise caspase-3 activity, increase apoptosis, and reduce cell survival which is, in part, blocked by BMP7. |
| 5226 | 17804487 | Knockdown and forced expression studies indicate that smad5 is required as well as sufficient for these actions of BMP7. |
| 5227 | 17804487 | These findings indicate that BMP7 is a differentiation and survival factor for podocytes, requires smad5, and can reduce diabetic podocyte injury. |
| 5228 | 17804487 | High glucose (HG; 25 mM) induces rounding of differentiated podocytes and changes in the distribution of F-actin but without quantitative changes in E-cadherin and the podocyte markers podocin, CD2AP, Neph1, or synaptopodin. |
| 5229 | 17804487 | In these cells, BMP7 effectively activates smad5 (but not smad1) and raises p38 phosphorylation [which is also increased by transforming growth factor-beta (TGF-beta)]. |
| 5230 | 17804487 | HG as well as TGF-beta raise caspase-3 activity, increase apoptosis, and reduce cell survival which is, in part, blocked by BMP7. |
| 5231 | 17804487 | Knockdown and forced expression studies indicate that smad5 is required as well as sufficient for these actions of BMP7. |
| 5232 | 17804487 | These findings indicate that BMP7 is a differentiation and survival factor for podocytes, requires smad5, and can reduce diabetic podocyte injury. |
| 5233 | 17823503 | Although the majority of mechanisms of beta cell destruction remain unclear, many molecules, including proinflammatory cytokines and chemokines such as tumor necrosis factor alpha and monocyte chemoattractant protein-1, are implicated in the development of beta cell damage. |
| 5234 | 17823503 | Development and progression of renal injuries in patients with diabetic nephropathy are also associated with several growth factors and proinflammatory cytokines, including tumor necrosis factor alpha, insulin-like growth factor-1, monocyte chemoattractant protein-1, vascular endothelial growth factor, and transforming growth factor beta. |
| 5235 | 17881461 | Our previous studies demonstrated that the transcription factor, upstream stimulatory factor 2 (USF2), was upregulated by high glucose, which bound to an 18-bp sequence in the thrombospondin 1 (TSP1) gene promoter and regulated high glucose-induced TSP1 expression and TGF-beta activity in mesangial cells, suggesting that USF2 might play a role in the development of diabetic nephropathy. |
| 5236 | 17881461 | At the end of studies, control USF2 (Tg) mice ( approximately 6 mo old) exhibited increased urinary albumin excretion. |
| 5237 | 17881461 | These mice also exhibited glomerular hypertrophy, accompanied by increased TSP1, active TGF-beta, fibronectin accumulation in the glomeruli compared with control WT littermates. |
| 5238 | 17881461 | Type 1 diabetes onset further augmented the urinary albumin excretion and glomerular hypertrophy in the USF2 (Tg) mice. |
| 5239 | 17881461 | Our previous studies demonstrated that the transcription factor, upstream stimulatory factor 2 (USF2), was upregulated by high glucose, which bound to an 18-bp sequence in the thrombospondin 1 (TSP1) gene promoter and regulated high glucose-induced TSP1 expression and TGF-beta activity in mesangial cells, suggesting that USF2 might play a role in the development of diabetic nephropathy. |
| 5240 | 17881461 | At the end of studies, control USF2 (Tg) mice ( approximately 6 mo old) exhibited increased urinary albumin excretion. |
| 5241 | 17881461 | These mice also exhibited glomerular hypertrophy, accompanied by increased TSP1, active TGF-beta, fibronectin accumulation in the glomeruli compared with control WT littermates. |
| 5242 | 17881461 | Type 1 diabetes onset further augmented the urinary albumin excretion and glomerular hypertrophy in the USF2 (Tg) mice. |
| 5243 | 17884968 | Decorin, a proteoglycan that inhibits active transforming growth factor-beta, is increased in diabetic nephropathy; however, its functional significance is unclear. |
| 5244 | 17884968 | In contrast to wild-type diabetic mice, which failed to develop significant nephropathy, the Dcn(-/-) diabetic mice developed a significant increase in albuminuria and plasma creatinine and a concurrent decrease in circulating adiponectin levels. |
| 5245 | 17884968 | By immunohistochemistry, Dcn(-/-) diabetic mice exhibited significant increases in glomerular transforming growth factor-beta, type I collagen, macrophage infiltration, and Nox4. |
| 5246 | 17884968 | Decorin, a proteoglycan that inhibits active transforming growth factor-beta, is increased in diabetic nephropathy; however, its functional significance is unclear. |
| 5247 | 17884968 | In contrast to wild-type diabetic mice, which failed to develop significant nephropathy, the Dcn(-/-) diabetic mice developed a significant increase in albuminuria and plasma creatinine and a concurrent decrease in circulating adiponectin levels. |
| 5248 | 17884968 | By immunohistochemistry, Dcn(-/-) diabetic mice exhibited significant increases in glomerular transforming growth factor-beta, type I collagen, macrophage infiltration, and Nox4. |
| 5249 | 17897750 | Furthermore, renal messenger RNA (mRNA) expression of intercellular adhesion molecule-1 (ICAM-1), cyclooxygenase-2 (COX-2) and transforming growth factor-beta1 (TGF-beta1) was quantified by real-time polymerase chain reaction. |
| 5250 | 17897750 | Treatment with neither FA nor AT had a significant effect on COX-2 or ICAM-1 mRNA expressions. |
| 5251 | 17898696 | In contrast, PGZ but not insulin suppressed enhanced transforming growth factor-beta (TGF-beta) expression. |
| 5252 | 17898696 | We further confirmed in cultured rat proximal tubular cells that insulin enhanced TGF-beta mRNA expression and protein production. |
| 5253 | 17898696 | In contrast, PGZ but not insulin suppressed enhanced transforming growth factor-beta (TGF-beta) expression. |
| 5254 | 17898696 | We further confirmed in cultured rat proximal tubular cells that insulin enhanced TGF-beta mRNA expression and protein production. |
| 5255 | 17899181 | TGF-beta1 induced the phosphorylation of myosin light chains, and Y27632 blocked this activity. |
| 5256 | 17928826 | More fibronectin (FN) and less nephrin were expressed in the VDR knockout mice compared to diabetic wild-type mice. |
| 5257 | 17928826 | In receptor knockout mice, increased renin, angiotensinogen, transforming growth factor-beta (TGF-beta), and connective tissue growth factor accompanied the more severe renal injury. 1,25-Dihydroxyvitmain D3 inhibited high glucose (HG)-induced FN production in cultured mesangial cells and increased nephrin expression in cultured podocytes. 1,25-Dihydroxyvitmain D3 also suppressed HG-induced activation of the RAS and TGF-beta in mesangial and juxtaglomerular cells. |
| 5258 | 17955498 | Reactive oxygen species (ROS) production, the activation of nuclear transcription factors such as nuclear factor kappa B (NFkappaB) and activator protein-1 (AP-1), and the expression/production of transforming growth factor-beta 1 (TGFbeta(1)) and monocyte chemoattractant protein-1 (MCP-1) were evaluated in the presence or absence of ASX. |
| 5259 | 17955662 | Effects of Houttuynia cordata thumb on expression of BMP-7 and TGF-beta1 in the renal tissues of diabetic rats. |
| 5260 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 5261 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 5262 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 5263 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 5264 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 5265 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 5266 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 5267 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 5268 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 5269 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 5270 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 5271 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 5272 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 5273 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 5274 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 5275 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 5276 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 5277 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 5278 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 5279 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 5280 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 5281 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 5282 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 5283 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 5284 | 17971013 | Agent-based model of inflammation and wound healing: insights into diabetic foot ulcer pathology and the role of transforming growth factor-beta1. |
| 5285 | 17971013 | We developed an agent-based model (ABM) capable of reproducing qualitatively much of the literature data on skin wound healing, including changes in relevant cell populations (macrophages, neutrophils, fibroblasts) and their key effector cytokines (tumor necrosis factor-alpha [TNF], interleukin [IL]-1beta, IL-10, and transforming growth factor [TGF]-beta1). |
| 5286 | 17971013 | Studies by others suggest that diabetes and DFU are characterized by elevated TNF and reduced TGF-beta1, although which of these changes is a cause and which one is an effect is unclear. |
| 5287 | 17971013 | Accordingly, we simulated the genesis of DFU in two ways, either by (1) increasing the rate of TNF production fourfold or (2) by decreasing the rate of TGF-beta1 production 67% based on prior literature. |
| 5288 | 17971013 | Both manipulations resulted in increased inflammation (elevated neutrophils, TNF, and tissue damage) and delayed healing (reduced TGF-beta1 and collagen). |
| 5289 | 17971013 | We next simulated the expected effect of administering (1) a neutralizing anti-TNF antibody, (2) an agent that would increase the activation of endogenous latent TGF-beta1, or (3) latent TGF-beta1 (which has a longer half-life than active TGF-beta1), and found that these therapies would have similar effects regardless of the initial assumption of the derangement that underlies DFU (elevated TNF vs. reduced TGF-beta1). |
| 5290 | 17980714 | The Notch ligand Jagged1 and its downstream effector, hairy enhancer of split-1 (Hes1), were identified as genes with significant similarity to Gremlin in terms of promoter structure and predicted microRNA binding elements. |
| 5291 | 17980714 | This led us to discover that transforming growth factor-beta (TGFbeta1), a primary driver of cellular changes in the kidney during nephropathy, increased Gremlin, Jagged1 and Hes1 expression in human kidney epithelial cells. |
| 5292 | 17980714 | Elevated levels of Gremlin, Jagged1 and Hes1 were also detected in extracts from renal biopsies from diabetic nephropathy patients, but not in control living donors. |
| 5293 | 17980714 | In situ hybridization identified specific upregulation and co-expression of Gremlin, Jagged1 and Hes1 in the same tubuli of kidneys from diabetic nephropathy patients, but not controls. |
| 5294 | 17992602 | In this study, we evaluated the effect of BMP-2, BMP-7 and transforming growth factor beta (TGF-beta1) on the secretion and mRNA expression of OPG and its ligands receptor activator of nuclear factor-kappabeta ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL) in HVSMC. |
| 5295 | 17992602 | RANKL mRNA expression declined when treated with TGF-beta1 but were increased by both BMPs. |
| 5296 | 17992602 | TGF-beta1, BMP-2 and BMP-7 exert effects on OPG and its ligands, indicating that these peptides may be involved in the development of vascular calcifications. |
| 5297 | 17992602 | In this study, we evaluated the effect of BMP-2, BMP-7 and transforming growth factor beta (TGF-beta1) on the secretion and mRNA expression of OPG and its ligands receptor activator of nuclear factor-kappabeta ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL) in HVSMC. |
| 5298 | 17992602 | RANKL mRNA expression declined when treated with TGF-beta1 but were increased by both BMPs. |
| 5299 | 17992602 | TGF-beta1, BMP-2 and BMP-7 exert effects on OPG and its ligands, indicating that these peptides may be involved in the development of vascular calcifications. |
| 5300 | 17992602 | In this study, we evaluated the effect of BMP-2, BMP-7 and transforming growth factor beta (TGF-beta1) on the secretion and mRNA expression of OPG and its ligands receptor activator of nuclear factor-kappabeta ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL) in HVSMC. |
| 5301 | 17992602 | RANKL mRNA expression declined when treated with TGF-beta1 but were increased by both BMPs. |
| 5302 | 17992602 | TGF-beta1, BMP-2 and BMP-7 exert effects on OPG and its ligands, indicating that these peptides may be involved in the development of vascular calcifications. |
| 5303 | 18024188 | The CD4(+)CD25(+) lineage of regulatory T (Treg) cells plays a key role in controlling immune and autoimmune responses and is characterized by a unique transcriptional signature. |
| 5304 | 18024188 | We have performed a cross-sectional analysis of the Treg cell signature in Treg-like cells generated under a number of conditions, with or without Foxp3, to delineate the elements that can be ascribed to T cell activation, interleukin-2, transforming growth factor-beta (TGF-beta) signaling, or Foxp3 itself. |
| 5305 | 18029395 | Essential roles of TGF-beta in anti-CD3 antibody therapy: reversal of diabetes in nonobese diabetic mice independent of Foxp3+CD4+ regulatory T cells. |
| 5306 | 18029395 | Furthermore, we found that anti-CD3 treatment did not increase the forkhead box p3+ (Foxp3+)CD4+ regulatory T cells (Tregs). |
| 5307 | 18029395 | Thus, our data showed a dispensable role of Foxp3+CD4+ Tregs in anti-CD3 antibody-reversed diabetes in NOD mice. |
| 5308 | 18030059 | Reverse transcription polymerase chain reaction (RT-PCR) was used to evaluate the receptor of advanced glycation end products (RAGE), nuclear factor-kappaB (NF-kappaB), and transforming growth factor-betal (TGF-betal) gene expression in myocardial tissue. |
| 5309 | 18030059 | After being treated by GSPE, the levels of RAGE, NF-kappaB, and TGF-beta1 mRNA transcription in the myocardial tissue of diabetic rats were reduced (P < 0.05), the number of degenerated mitochondria was decreased, and the preservation of the fine structure of the LV myocardium was improved. |
| 5310 | 18058603 | Comparative quantitative real-time PCR (qRT-PCR) including an expanded sample number of both insulinomas (n=9) and pancreatic islet preparations (n=4) confirmed the decreased TGF-beta1 expression and its target molecules (TGFBI, NNMT, RPN2) in insulinomas. |
| 5311 | 18058603 | However, the consistent down-regulation of the TGF-beta1 targets TGFBI (transforming growth factor, beta-induced), NNMT (nicotinamide N-methyltransferase), RPN2 (ribophorin II) indicates that the parallel up-regulation of TGFBR2 does not compensate for the only marginal TGF-beta1 expression levels in insulinomas. |
| 5312 | 18058603 | Comparative quantitative real-time PCR (qRT-PCR) including an expanded sample number of both insulinomas (n=9) and pancreatic islet preparations (n=4) confirmed the decreased TGF-beta1 expression and its target molecules (TGFBI, NNMT, RPN2) in insulinomas. |
| 5313 | 18058603 | However, the consistent down-regulation of the TGF-beta1 targets TGFBI (transforming growth factor, beta-induced), NNMT (nicotinamide N-methyltransferase), RPN2 (ribophorin II) indicates that the parallel up-regulation of TGFBR2 does not compensate for the only marginal TGF-beta1 expression levels in insulinomas. |
| 5314 | 18064603 | The 24 h urinary transforming growth factor-beta1 (ELISA) was evaluated in diabetic and control rats 15 days after oral treatment with the aqueous LS extract at a dose of 20 mg/kg. |
| 5315 | 18064633 | MIF deficiency resulted in lower proliferation and lymphocyte adhesion, as well as reduced production from the spleens and peritoneal cells of a variety of inflammatory mediators typically associated with development of the disease including IL-12, IL-23, TNF-alpha, and IL-1beta. |
| 5316 | 18064633 | Furthermore, MIF deletion affected the production of IL-18, TNF-alpha, IL-1beta, and iNOS in the islets of Langerhans. |
| 5317 | 18064633 | These data, along with the higher expression of IL-4 and TGF-beta observed in the periphery and in the pancreas of MLD-STZ-challenged MIF(-/-) mice as compared to WT controls suggest that MIF deficiency has induced an immune deviation towards protective type 2/3 response. |
| 5318 | 18156300 | To begin with, there is an obligatory excessive channeling of glucose intermediaries into various metabolic pathways with generation of advanced glycation products (AGEs), activation of protein kinase C (PKC), increased expression of transforming growth factor-beta (TGF-beta), GTP-binding proteins, and generation of reactive oxygen species (ROS). |
| 5319 | 18164317 | The CCCS/FGF provided the most efficiently therapeutic effect among various treatments, showing the shortest healing time (14 days in the CCCS/FGF-treated group as compared to 18~21 days in other treatment groups), the quickest tissue collagen generation, the earliest and highest TGF-beta1 expression and dermal cell proliferation (PCNA expression). |
| 5320 | 18220594 | Moreover, these inhibitors inhibit the activity of VEGF and TGF-beta, two major pathogenic factors of DN. |
| 5321 | 18220619 | Other growth factors or cytokines such as insulin-like growth factor I (IGF-1), hepatocyte growth factor (HGF), basic fibroblast growth factor (b-FGF), platelet derived growth factor (PDGF), pro-inflammatory cytokines and angiopoetins, are also involved in the pathogenesis of PDR. |
| 5322 | 18220619 | The main antiangiogenic factor is the pigment epithelium derived factor (PEDF) but the transforming growth factor beta (TGF-beta), thrombospondin (TSP) and somatostatin are also among the intraocullary synthesized antiangiogenic factors. |
| 5323 | 18220694 | Angiotensin II in turn stimulates podocyte-derived VEGF, suppresses nephrin expression, and induces TGF-beta1 leading to podocyte apoptosis and fostering the development of glomerulosclerosis. |
| 5324 | 18220694 | Besides direct effects of albuminuria on tubular cells, pathophysiological changes in the ultrafiltration barrier lead to an increased tubular filtration of various growth factors (TGF-beta1, insulin-like growth factor I) that may further alter the function of tubular cells. |
| 5325 | 18220694 | In addition, under locally high concentrations of angiotensin II and TGF-beta1, tubular cells may change their phenotype and become fibroblasts by a process called epithelial to mesenchymal transition (EMT) which contributes to interstitial fibrosis and tubular atrophy because of vanishing epithelia cells. |
| 5326 | 18220694 | Angiotensin II in turn stimulates podocyte-derived VEGF, suppresses nephrin expression, and induces TGF-beta1 leading to podocyte apoptosis and fostering the development of glomerulosclerosis. |
| 5327 | 18220694 | Besides direct effects of albuminuria on tubular cells, pathophysiological changes in the ultrafiltration barrier lead to an increased tubular filtration of various growth factors (TGF-beta1, insulin-like growth factor I) that may further alter the function of tubular cells. |
| 5328 | 18220694 | In addition, under locally high concentrations of angiotensin II and TGF-beta1, tubular cells may change their phenotype and become fibroblasts by a process called epithelial to mesenchymal transition (EMT) which contributes to interstitial fibrosis and tubular atrophy because of vanishing epithelia cells. |
| 5329 | 18220694 | Angiotensin II in turn stimulates podocyte-derived VEGF, suppresses nephrin expression, and induces TGF-beta1 leading to podocyte apoptosis and fostering the development of glomerulosclerosis. |
| 5330 | 18220694 | Besides direct effects of albuminuria on tubular cells, pathophysiological changes in the ultrafiltration barrier lead to an increased tubular filtration of various growth factors (TGF-beta1, insulin-like growth factor I) that may further alter the function of tubular cells. |
| 5331 | 18220694 | In addition, under locally high concentrations of angiotensin II and TGF-beta1, tubular cells may change their phenotype and become fibroblasts by a process called epithelial to mesenchymal transition (EMT) which contributes to interstitial fibrosis and tubular atrophy because of vanishing epithelia cells. |
| 5332 | 18223258 | Smad and p38 MAP kinase-mediated signaling of proteoglycan synthesis in vascular smooth muscle. |
| 5333 | 18223258 | This pathway was investigated using the activin receptor-like kinase 5 (ALK5) inhibitor SB431542 and inhibitors of p38 MAP kinase as a possible downstream or alternative mediator. |
| 5334 | 18223258 | TGF-beta stimulated and SB431542 inhibited the phosphorylation of Smad2/3. |
| 5335 | 18223258 | Two different p38 MAP kinase inhibitors, SB203580 and SB202190, but not the inactive analogue SB202474, concentration-dependently blocked TGF-beta-mediated [(35)S]sulfate incorporation. |
| 5336 | 18223258 | TGF-beta increased [(3)H]glucosamine incorporation into glycosaminoglycans by 180% and [(35)S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542. |
| 5337 | 18223258 | Blocking both Smad2/3 and p38 MAP kinase pathways prevented the effect of TGF-beta to increase proteoglycan to LDL binding. |
| 5338 | 18223258 | TGF-beta mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade. |
| 5339 | 18223258 | Smad and p38 MAP kinase-mediated signaling of proteoglycan synthesis in vascular smooth muscle. |
| 5340 | 18223258 | This pathway was investigated using the activin receptor-like kinase 5 (ALK5) inhibitor SB431542 and inhibitors of p38 MAP kinase as a possible downstream or alternative mediator. |
| 5341 | 18223258 | TGF-beta stimulated and SB431542 inhibited the phosphorylation of Smad2/3. |
| 5342 | 18223258 | Two different p38 MAP kinase inhibitors, SB203580 and SB202190, but not the inactive analogue SB202474, concentration-dependently blocked TGF-beta-mediated [(35)S]sulfate incorporation. |
| 5343 | 18223258 | TGF-beta increased [(3)H]glucosamine incorporation into glycosaminoglycans by 180% and [(35)S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542. |
| 5344 | 18223258 | Blocking both Smad2/3 and p38 MAP kinase pathways prevented the effect of TGF-beta to increase proteoglycan to LDL binding. |
| 5345 | 18223258 | TGF-beta mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade. |
| 5346 | 18223258 | Smad and p38 MAP kinase-mediated signaling of proteoglycan synthesis in vascular smooth muscle. |
| 5347 | 18223258 | This pathway was investigated using the activin receptor-like kinase 5 (ALK5) inhibitor SB431542 and inhibitors of p38 MAP kinase as a possible downstream or alternative mediator. |
| 5348 | 18223258 | TGF-beta stimulated and SB431542 inhibited the phosphorylation of Smad2/3. |
| 5349 | 18223258 | Two different p38 MAP kinase inhibitors, SB203580 and SB202190, but not the inactive analogue SB202474, concentration-dependently blocked TGF-beta-mediated [(35)S]sulfate incorporation. |
| 5350 | 18223258 | TGF-beta increased [(3)H]glucosamine incorporation into glycosaminoglycans by 180% and [(35)S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542. |
| 5351 | 18223258 | Blocking both Smad2/3 and p38 MAP kinase pathways prevented the effect of TGF-beta to increase proteoglycan to LDL binding. |
| 5352 | 18223258 | TGF-beta mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade. |
| 5353 | 18223258 | Smad and p38 MAP kinase-mediated signaling of proteoglycan synthesis in vascular smooth muscle. |
| 5354 | 18223258 | This pathway was investigated using the activin receptor-like kinase 5 (ALK5) inhibitor SB431542 and inhibitors of p38 MAP kinase as a possible downstream or alternative mediator. |
| 5355 | 18223258 | TGF-beta stimulated and SB431542 inhibited the phosphorylation of Smad2/3. |
| 5356 | 18223258 | Two different p38 MAP kinase inhibitors, SB203580 and SB202190, but not the inactive analogue SB202474, concentration-dependently blocked TGF-beta-mediated [(35)S]sulfate incorporation. |
| 5357 | 18223258 | TGF-beta increased [(3)H]glucosamine incorporation into glycosaminoglycans by 180% and [(35)S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542. |
| 5358 | 18223258 | Blocking both Smad2/3 and p38 MAP kinase pathways prevented the effect of TGF-beta to increase proteoglycan to LDL binding. |
| 5359 | 18223258 | TGF-beta mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade. |
| 5360 | 18223258 | Smad and p38 MAP kinase-mediated signaling of proteoglycan synthesis in vascular smooth muscle. |
| 5361 | 18223258 | This pathway was investigated using the activin receptor-like kinase 5 (ALK5) inhibitor SB431542 and inhibitors of p38 MAP kinase as a possible downstream or alternative mediator. |
| 5362 | 18223258 | TGF-beta stimulated and SB431542 inhibited the phosphorylation of Smad2/3. |
| 5363 | 18223258 | Two different p38 MAP kinase inhibitors, SB203580 and SB202190, but not the inactive analogue SB202474, concentration-dependently blocked TGF-beta-mediated [(35)S]sulfate incorporation. |
| 5364 | 18223258 | TGF-beta increased [(3)H]glucosamine incorporation into glycosaminoglycans by 180% and [(35)S]Met/Cys incorporation into proteoglycan core proteins by 35% with both effects completely inhibited by SB431542. |
| 5365 | 18223258 | Blocking both Smad2/3 and p38 MAP kinase pathways prevented the effect of TGF-beta to increase proteoglycan to LDL binding. |
| 5366 | 18223258 | TGF-beta mediates its effects on proteoglycan synthesis in VSMCs via the ALK5/Smad2/3 phosphorylation pathway as well as via the p38 MAP kinase signaling cascade. |
| 5367 | 18229460 | Finally, recent research has also identified intracellular pathways such as the diacylglycerol-protein kinase C pathway and several growth factors, such as growth hormone, insulin-like growth factor, transforming growth factor-beta, vascular endothelial growth factor, and platelet derived growth factor as players in diabetic kidney disease. |
| 5368 | 18246672 | Transforming growth factor-beta1 and Smad4 signaling pathway down-regulates renal extracellular matrix degradation in diabetic rats. |
| 5369 | 18259041 | Diabetes was associated with the following increases: 3.2-fold in urine albumin excretion, 6.3-fold in glomerulosclerosis, 6.0-fold in tubulointerstitial fibrosis, 1.6-fold in collagen type I, 1.2-fold in collagen type IV, 1.3-fold in transforming growth factor-beta protein expression, and 32.7-fold in CD68-positive cell abundance. |
| 5370 | 18296490 | We evaluated changes in renal aldosterone content (RAC), aldosterone synthase expression, nuclear factor kappaB (NFkappaB), tumour necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), transforming growth factor beta (TGFbeta), glomerular fibronectin, collagen type IV and urinary albumin extraction (UAE) in response to the aldosterone synthase inhibitor FAD286. |
| 5371 | 18296490 | Compared with control rats, diabetic rats had higher levels of RAC by 488% (P < 0.01), NFkappaB by 293% (P < 0.01), TNFalpha by 356% (P < 0.01), IL-6 by 378% (P < 0.01), TGFbeta by 337% (P < 0.01) and UAE by 1122% (P < 0.01), and increased glomerular fibronectin and collagen type IV immunostaining. |
| 5372 | 18296490 | In diabetic rats, FAD286 reduced RAC (P < 0.01), UAE (P < 0.05), NFkappaB mRNA, TNFalpha mRNA, IL-6 mRNA and TGFbeta mRNA by 51, 41, 41 and 52% and also their proteins and decreased glomerular fibronectin and collagen type IV immunostaining. |
| 5373 | 18296490 | We evaluated changes in renal aldosterone content (RAC), aldosterone synthase expression, nuclear factor kappaB (NFkappaB), tumour necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), transforming growth factor beta (TGFbeta), glomerular fibronectin, collagen type IV and urinary albumin extraction (UAE) in response to the aldosterone synthase inhibitor FAD286. |
| 5374 | 18296490 | Compared with control rats, diabetic rats had higher levels of RAC by 488% (P < 0.01), NFkappaB by 293% (P < 0.01), TNFalpha by 356% (P < 0.01), IL-6 by 378% (P < 0.01), TGFbeta by 337% (P < 0.01) and UAE by 1122% (P < 0.01), and increased glomerular fibronectin and collagen type IV immunostaining. |
| 5375 | 18296490 | In diabetic rats, FAD286 reduced RAC (P < 0.01), UAE (P < 0.05), NFkappaB mRNA, TNFalpha mRNA, IL-6 mRNA and TGFbeta mRNA by 51, 41, 41 and 52% and also their proteins and decreased glomerular fibronectin and collagen type IV immunostaining. |
| 5376 | 18296490 | We evaluated changes in renal aldosterone content (RAC), aldosterone synthase expression, nuclear factor kappaB (NFkappaB), tumour necrosis factor alpha (TNFalpha), interleukin-6 (IL-6), transforming growth factor beta (TGFbeta), glomerular fibronectin, collagen type IV and urinary albumin extraction (UAE) in response to the aldosterone synthase inhibitor FAD286. |
| 5377 | 18296490 | Compared with control rats, diabetic rats had higher levels of RAC by 488% (P < 0.01), NFkappaB by 293% (P < 0.01), TNFalpha by 356% (P < 0.01), IL-6 by 378% (P < 0.01), TGFbeta by 337% (P < 0.01) and UAE by 1122% (P < 0.01), and increased glomerular fibronectin and collagen type IV immunostaining. |
| 5378 | 18296490 | In diabetic rats, FAD286 reduced RAC (P < 0.01), UAE (P < 0.05), NFkappaB mRNA, TNFalpha mRNA, IL-6 mRNA and TGFbeta mRNA by 51, 41, 41 and 52% and also their proteins and decreased glomerular fibronectin and collagen type IV immunostaining. |
| 5379 | 18296558 | ANG II synthesis was catalyzed by renin and angiotensin-converting enzyme (ACE), but not chymase, as determined using specific inhibitors. |
| 5380 | 18296558 | High glucose resulted in increased transforming growth factor-beta and collagen-1 synthesis by cardiac fibroblasts that was partially inhibited by candesartan but completely prevented by renin and ACE inhibitors. |
| 5381 | 18318807 | In vitro, micronized allogenic dermis, when combined with PRP, absorbed nearly 50% of original platelet-derived growth factor, transforming growth factor-beta, vascular endothelial growth factor, and epidermal growth factor from platelets and stimulated fibroblast proliferation. |
| 5382 | 18338624 | [Effect of compound Rhizoma Coptidis capsule on expression of transforming growth factor-beta1 and type IV collagen proteins in renal tissue of diabetic rats with nephropathy]. |
| 5383 | 18365870 | We compared the effect of ET-1 on proliferative transforming growth factor (TGFbeta(1)) expression, fibronectin and laminin release), differentiative [alpha-smooth muscle actin (alpha-SMA) expression] and inflammatory [monocyte chemo-attractant protein (MCP-1) and interleukin-6 (IL-6) expression] responses in skin fibroblasts of healthy subjects (C) and D, testing the relative role of ET(A) and ET(B) receptors in mediating these responses. |
| 5384 | 18365870 | ET-1 did not influence TGFbeta(1), fibronectin or laminin production. alpha-SMA was more abundant and more stimulated in D, as well as MCP-1 and IL-6 expression and release. |
| 5385 | 18365870 | We compared the effect of ET-1 on proliferative transforming growth factor (TGFbeta(1)) expression, fibronectin and laminin release), differentiative [alpha-smooth muscle actin (alpha-SMA) expression] and inflammatory [monocyte chemo-attractant protein (MCP-1) and interleukin-6 (IL-6) expression] responses in skin fibroblasts of healthy subjects (C) and D, testing the relative role of ET(A) and ET(B) receptors in mediating these responses. |
| 5386 | 18365870 | ET-1 did not influence TGFbeta(1), fibronectin or laminin production. alpha-SMA was more abundant and more stimulated in D, as well as MCP-1 and IL-6 expression and release. |
| 5387 | 18367657 | To investigate the impact of bradykinin B(2) receptor (B2R) activation during ACE inhibition, type II diabetic mice (C57BLKS db/db) received for 20 wk: 1) ACEi (ramipril) alone, 2) ACEi + HOE-140 (a specific B2R antagonist), 3) HOE-140 alone, or 4) no treatment. |
| 5388 | 18367657 | Finally, the renal protective effect of ACEi was associated with a marked decrease in glomerular overexpression of insulin-like growth factor-1 (IGF-1) and transforming growth factor-beta pathways, but also in advanced glycation end product receptors and lipid peroxidation assessed by 4-hydroxy-2-nonenal (4-HNE) adducts. |
| 5389 | 18367657 | Concomitant blockade of B2R partly restored glomerular overexpression of IGF-1 receptor beta and 4-HNE complexes. |
| 5390 | 18372234 | Concurrently, we found in D and DS an increase in cardiac beta-myosin heavy chain, atrial natriuretic peptide, skeletal alpha-actin mRNA, type III collagen, and transforming growth factor-beta. |
| 5391 | 18372234 | Myocardial angiotensin-converting enzyme (ACE) mRNA levels were increased while ACE2 mRNA levels were decreased in both D and DS groups. |
| 5392 | 18372234 | Cardiac angiotensin-1 (AT1) receptor protein levels were unchanged but the levels of phosphorylated (p) ERK and Jun-NH(2)-protein kinase (JNK) were increased in D and DS. |
| 5393 | 18372234 | The increase in ACE, the decrease in ACE2, and the increase in cardiac pERK and pJNK suggest an increase in free angiotensin II and AT1R signaling in the diabetic myocardium as a possible mechanism contributing to cardiac remodeling in diabetes. |
| 5394 | 18389287 | High glucose promotes collagen synthesis by cultured cells from rat cervical posterior longitudinal ligament via transforming growth factor-beta1. |
| 5395 | 18389287 | In this in vitro study, we investigated the effect of high glucose on collagen synthesis and transforming growth factor-beta1 (TGF-beta1) production using cells isolated from rat cervical posterior longitudinal ligament. |
| 5396 | 18389287 | Exogenous application of TGF-beta1 was confirmed to increase collagen synthesis of the cells. |
| 5397 | 18389287 | These data suggested that high glucose could promote collagen synthesis in the posterior longitudinal ligament mainly via endogenous TGF-beta1, resulting in hypertrophy of the ligament. |
| 5398 | 18389287 | High glucose promotes collagen synthesis by cultured cells from rat cervical posterior longitudinal ligament via transforming growth factor-beta1. |
| 5399 | 18389287 | In this in vitro study, we investigated the effect of high glucose on collagen synthesis and transforming growth factor-beta1 (TGF-beta1) production using cells isolated from rat cervical posterior longitudinal ligament. |
| 5400 | 18389287 | Exogenous application of TGF-beta1 was confirmed to increase collagen synthesis of the cells. |
| 5401 | 18389287 | These data suggested that high glucose could promote collagen synthesis in the posterior longitudinal ligament mainly via endogenous TGF-beta1, resulting in hypertrophy of the ligament. |
| 5402 | 18389287 | High glucose promotes collagen synthesis by cultured cells from rat cervical posterior longitudinal ligament via transforming growth factor-beta1. |
| 5403 | 18389287 | In this in vitro study, we investigated the effect of high glucose on collagen synthesis and transforming growth factor-beta1 (TGF-beta1) production using cells isolated from rat cervical posterior longitudinal ligament. |
| 5404 | 18389287 | Exogenous application of TGF-beta1 was confirmed to increase collagen synthesis of the cells. |
| 5405 | 18389287 | These data suggested that high glucose could promote collagen synthesis in the posterior longitudinal ligament mainly via endogenous TGF-beta1, resulting in hypertrophy of the ligament. |
| 5406 | 18389287 | High glucose promotes collagen synthesis by cultured cells from rat cervical posterior longitudinal ligament via transforming growth factor-beta1. |
| 5407 | 18389287 | In this in vitro study, we investigated the effect of high glucose on collagen synthesis and transforming growth factor-beta1 (TGF-beta1) production using cells isolated from rat cervical posterior longitudinal ligament. |
| 5408 | 18389287 | Exogenous application of TGF-beta1 was confirmed to increase collagen synthesis of the cells. |
| 5409 | 18389287 | These data suggested that high glucose could promote collagen synthesis in the posterior longitudinal ligament mainly via endogenous TGF-beta1, resulting in hypertrophy of the ligament. |
| 5410 | 18406405 | Transforming growth factor-beta1 (TGF-beta1) has been associated with diabetic nephropathy and retinopathy but not neuropathy. |
| 5411 | 18406405 | In diabetic DRG using quantitative real-time PCR (QRT-PCR), TGF-beta1 and TGF-beta2 mRNA, but not TGF-beta3, was increased at 4 and 12 weeks. |
| 5412 | 18406405 | In high glucose conditions, combination with TGF-beta2>beta1 increases the percent of cleaved caspase-3 compared to high glucose alone and TGF-beta neutralizing antibody inhibits this increase. |
| 5413 | 18406405 | Transforming growth factor-beta1 (TGF-beta1) has been associated with diabetic nephropathy and retinopathy but not neuropathy. |
| 5414 | 18406405 | In diabetic DRG using quantitative real-time PCR (QRT-PCR), TGF-beta1 and TGF-beta2 mRNA, but not TGF-beta3, was increased at 4 and 12 weeks. |
| 5415 | 18406405 | In high glucose conditions, combination with TGF-beta2>beta1 increases the percent of cleaved caspase-3 compared to high glucose alone and TGF-beta neutralizing antibody inhibits this increase. |
| 5416 | 18406405 | Transforming growth factor-beta1 (TGF-beta1) has been associated with diabetic nephropathy and retinopathy but not neuropathy. |
| 5417 | 18406405 | In diabetic DRG using quantitative real-time PCR (QRT-PCR), TGF-beta1 and TGF-beta2 mRNA, but not TGF-beta3, was increased at 4 and 12 weeks. |
| 5418 | 18406405 | In high glucose conditions, combination with TGF-beta2>beta1 increases the percent of cleaved caspase-3 compared to high glucose alone and TGF-beta neutralizing antibody inhibits this increase. |
| 5419 | 18413675 | The mRNA expressions for peroxisome proliferator-activated receptor-alpha, genes for triacylglycerol synthesis, and lipoprotein lipase were increased with diabetes in Wt hearts, whereas this induction was absent in Tg hearts. |
| 5420 | 18413675 | However, Tg hearts displayed no overt fibrosis, concomitant with decreased expression of collagens, transforming growth factor-beta, and matrix metalloproteinase 2. |
| 5421 | 18435801 | Because the role of regulatory T cells in the intestinal inflammation is unknown in coeliac disease (CD) and type 1 diabetes (T1D), the expression of forkhead box P3 (FoxP3), CD25, transforming growth factor-beta, interferon (IFN)-gamma, interleukin (IL)-4, IL-8, IL-10, IL-15 and IL-18 was measured by quantitative reverse transcription-polymerase chain reaction in the small intestinal biopsies from paediatric patients with active or potential CD, T1D and control patients. |
| 5422 | 18435801 | Enhanced intestinal expressions of FoxP3, IL-10 and IFN-gamma mRNAs were found in active CD when compared with controls (P-values < 0.001, 0.004, <0.001). |
| 5423 | 18435801 | The ratio of IFN-gamma to FoxP3-specific mRNA was increased in active and potential CD (P = 0.001 and P = 0.002). |
| 5424 | 18435801 | The increased ratio of IFN-gamma to FoxP3 mRNA in active and potential CD suggests an imbalance between regulatory and effector mechanisms. |
| 5425 | 18453575 | Preferential costimulation by CD80 results in IL-10-dependent TGF-beta1(+) -adaptive regulatory T cell generation. |
| 5426 | 18453575 | Costimulatory ligands CD80 and CD86 have different binding preferences and affinities to their receptors, CD28 and CTLA-4. |
| 5427 | 18453575 | Earlier, we demonstrated that CD80 binds to CTLA-4 with higher affinity and has a role in suppressing T cell response. |
| 5428 | 18453575 | These T cells showed TGF-beta1 on their surface and secreted TGF-beta1 and IL-10 upon restimulation. |
| 5429 | 18453575 | Although blockade of CTLA-4 and neutralization of IL-10 profoundly inhibited the induction of these TGF-beta1(+) T cells, their ability to suppress the effector T cell proliferation was abrogated by neutralization of TGF-beta1 alone. |
| 5430 | 18453575 | Induction of TGF-beta1(+) and IL-10(+) T cells was found to be independent of natural CD4(+)CD25(+) regulatory T cells, demonstrating that preferential ligation of CTLA-4 by CD80 induced IL-10 production by effector T cells, which in turn promoted the secretion of TGF-beta1. |
| 5431 | 18453575 | Treatment of prediabetic NOD mice with islet beta cell Ag-pulsed CD86(-/-) DCs, but not CD80(-/-) DCs, resulted in the induction of TGF-beta1- and IL-10-producing cells, significant suppression of insulitis, and delay of the onset of hyperglycemia. |
| 5432 | 18453575 | These observations demonstrate not only that CD80 preferentially binds to CTLA-4 but also that interaction during Ag presentation can result in IL-10-dependent TGF-beta1(+) regulatory T cell induction, reinstating the potential of approaches to preferentially engage CTLA-4 through CD80 during self-Ag presentation in suppressing autoimmunity. |
| 5433 | 18453575 | Preferential costimulation by CD80 results in IL-10-dependent TGF-beta1(+) -adaptive regulatory T cell generation. |
| 5434 | 18453575 | Costimulatory ligands CD80 and CD86 have different binding preferences and affinities to their receptors, CD28 and CTLA-4. |
| 5435 | 18453575 | Earlier, we demonstrated that CD80 binds to CTLA-4 with higher affinity and has a role in suppressing T cell response. |
| 5436 | 18453575 | These T cells showed TGF-beta1 on their surface and secreted TGF-beta1 and IL-10 upon restimulation. |
| 5437 | 18453575 | Although blockade of CTLA-4 and neutralization of IL-10 profoundly inhibited the induction of these TGF-beta1(+) T cells, their ability to suppress the effector T cell proliferation was abrogated by neutralization of TGF-beta1 alone. |
| 5438 | 18453575 | Induction of TGF-beta1(+) and IL-10(+) T cells was found to be independent of natural CD4(+)CD25(+) regulatory T cells, demonstrating that preferential ligation of CTLA-4 by CD80 induced IL-10 production by effector T cells, which in turn promoted the secretion of TGF-beta1. |
| 5439 | 18453575 | Treatment of prediabetic NOD mice with islet beta cell Ag-pulsed CD86(-/-) DCs, but not CD80(-/-) DCs, resulted in the induction of TGF-beta1- and IL-10-producing cells, significant suppression of insulitis, and delay of the onset of hyperglycemia. |
| 5440 | 18453575 | These observations demonstrate not only that CD80 preferentially binds to CTLA-4 but also that interaction during Ag presentation can result in IL-10-dependent TGF-beta1(+) regulatory T cell induction, reinstating the potential of approaches to preferentially engage CTLA-4 through CD80 during self-Ag presentation in suppressing autoimmunity. |
| 5441 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 5442 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 5443 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 5444 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 5445 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 5446 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 5447 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 5448 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 5449 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 5450 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 5451 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 5452 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 5453 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 5454 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 5455 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 5456 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 5457 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 5458 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 5459 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 5460 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 5461 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 5462 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 5463 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 5464 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 5465 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 5466 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 5467 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 5468 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 5469 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 5470 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 5471 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 5472 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 5473 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 5474 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 5475 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 5476 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 5477 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 5478 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 5479 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 5480 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 5481 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 5482 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 5483 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 5484 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 5485 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 5486 | 18456735 | Microvessel vascular smooth muscle cells contribute to collagen type I deposition through ERK1/2 MAP kinase, alphavbeta3-integrin, and TGF-beta1 in response to ANG II and high glucose. |
| 5487 | 18456735 | This study determines that vascular smooth muscle cell (VSMC) signaling through extracellular signal-regulated kinase (ERK) 1/2-mitogen-activated protein (MAP) kinase, alphavbeta(3)-integrin, and transforming growth factor (TGF)-beta1 dictates collagen type I network induction in mesenteric resistance arteries (MRA) from type 1 diabetic (streptozotocin) or hypertensive (HT; ANG II) mice. |
| 5488 | 18456735 | Pressure-passive-diameter relationship reduction was associated with increased collagen type I deposition in MRA from HT and diabetic mice compared with control. |
| 5489 | 18456735 | Treatment of HT and diabetic mice with neutralizing TGF-beta1 antibody reduced MRA stiffness and collagen type I deposition. |
| 5490 | 18456735 | Cultured VSMC stimulated with HG or ANG II for 5 min increased ERK1/2-MAP kinase phosphorylation, whereas a 48-h stimulation induced latent TGF-beta1, alphavbeta(3)-integrin, and collagen type 1 release in the conditioned media. |
| 5491 | 18456735 | TGF-beta1 bioactivity and Smad2 phosphorylation were alphavbeta(3)-integrin-dependent, since beta(3)-integrin antibody and alphavbeta(3)-integrin inhibitor (SB-223245, 10 microM) significantly prevented TGF-beta1 bioactivity and Smad2 phosphorylation. |
| 5492 | 18456735 | Pretreatment of VSMC with ERK1/2-MAP kinase inhibitor (U-0126, 1 microM) reduced alphavbeta(3)-integrin, TGF-beta1, and collagen type 1 content. |
| 5493 | 18456735 | Additionally, alphavbeta(3)-integrin antibody, SB-223245, TGF-beta1-small-intefering RNA (siRNA), and Smad2-siRNA (40 nM) prevented collagen type I network formation in response to ANG II and HG. |
| 5494 | 18456735 | Together, these data provide evidence that resistance artery fibrosis in type 1 diabetes and hypertension is a consequence of abnormal collagen type I release by VSMC and involves ERK1/2, alphavbeta(3)-integrin, and TGF-beta1 signaling. |
| 5495 | 18483277 | Transforming growth factor beta subverts the immune system into directly promoting tumor growth through interleukin-17. |
| 5496 | 18483277 | Using transplantable models of breast and colon cancer, we made the unexpected finding that CD8+ cells in tumor-bearing animals can directly promote tumorigenesis, by a mechanism that is dependent on TGF-beta. |
| 5497 | 18483277 | We showed that CD8+ splenocytes from tumor-bearing mice expressed elevated interleukin (IL)-17 when compared with naive mice, and that CD8+ T cells could be induced to make IL-17 on addition of TGF-beta and IL-6 in vitro. |
| 5498 | 18483277 | Thus, in addition to suppressing immune surveillance, tumor-induced TGF-beta may actively subvert the CD8+ arm of the immune system into directly promoting tumor growth by an IL-17-dependent mechanism. |
| 5499 | 18483277 | Transforming growth factor beta subverts the immune system into directly promoting tumor growth through interleukin-17. |
| 5500 | 18483277 | Using transplantable models of breast and colon cancer, we made the unexpected finding that CD8+ cells in tumor-bearing animals can directly promote tumorigenesis, by a mechanism that is dependent on TGF-beta. |
| 5501 | 18483277 | We showed that CD8+ splenocytes from tumor-bearing mice expressed elevated interleukin (IL)-17 when compared with naive mice, and that CD8+ T cells could be induced to make IL-17 on addition of TGF-beta and IL-6 in vitro. |
| 5502 | 18483277 | Thus, in addition to suppressing immune surveillance, tumor-induced TGF-beta may actively subvert the CD8+ arm of the immune system into directly promoting tumor growth by an IL-17-dependent mechanism. |
| 5503 | 18483277 | Transforming growth factor beta subverts the immune system into directly promoting tumor growth through interleukin-17. |
| 5504 | 18483277 | Using transplantable models of breast and colon cancer, we made the unexpected finding that CD8+ cells in tumor-bearing animals can directly promote tumorigenesis, by a mechanism that is dependent on TGF-beta. |
| 5505 | 18483277 | We showed that CD8+ splenocytes from tumor-bearing mice expressed elevated interleukin (IL)-17 when compared with naive mice, and that CD8+ T cells could be induced to make IL-17 on addition of TGF-beta and IL-6 in vitro. |
| 5506 | 18483277 | Thus, in addition to suppressing immune surveillance, tumor-induced TGF-beta may actively subvert the CD8+ arm of the immune system into directly promoting tumor growth by an IL-17-dependent mechanism. |
| 5507 | 18483277 | Transforming growth factor beta subverts the immune system into directly promoting tumor growth through interleukin-17. |
| 5508 | 18483277 | Using transplantable models of breast and colon cancer, we made the unexpected finding that CD8+ cells in tumor-bearing animals can directly promote tumorigenesis, by a mechanism that is dependent on TGF-beta. |
| 5509 | 18483277 | We showed that CD8+ splenocytes from tumor-bearing mice expressed elevated interleukin (IL)-17 when compared with naive mice, and that CD8+ T cells could be induced to make IL-17 on addition of TGF-beta and IL-6 in vitro. |
| 5510 | 18483277 | Thus, in addition to suppressing immune surveillance, tumor-induced TGF-beta may actively subvert the CD8+ arm of the immune system into directly promoting tumor growth by an IL-17-dependent mechanism. |
| 5511 | 18490518 | In diabetic TG(mRen-2)27 rats, aliskiren (10 or 30 mg/kg per day, 10 weeks) lowered blood pressure, prevented albuminuria, and suppressed renal transforming growth factor-beta and collagen I expression versus vehicle. |
| 5512 | 18490518 | In human mesangial cells, aliskiren (0.1 micromol/L to 10 micromol/L) did not inhibit binding of (125)I-renin to the (pro)renin receptor, nor did it alter the activation of extracellular signal-regulated kinase 1/2 by renin (20 nmol/L) preincubated with aliskiren (100 nmol/L) or affect gene expression of the (pro)renin receptor. |
| 5513 | 18490518 | The evidence that aliskiren can reduce in vivo gene expression for the (pro)renin receptor and that it may block prorenin-induced angiotensin generation supports the need for additional work to reveal the mechanism of the observed renoprotection by this renin inhibitor. |
| 5514 | 18495798 | We investigated the potential of PKB/Akt to mediate the profibrotic bioactions of TGF-beta1 in kidney. |
| 5515 | 18495798 | Treatment of normal rat kidney epithelial cells (NRK52E) with TGF-beta1 resulted in activation of phosphatidylinositol 3-kinase (PI3K) and PKB/Akt as evidenced by increased Ser473 phosphorylation and GSK-3beta phosphorylation. |
| 5516 | 18495798 | TGF-beta1 also stimulated increased Smad3 phosphorylation in these cells, a response that was insensitive to inhibition of PI3K or PKB/Akt. |
| 5517 | 18495798 | NRK52E cells displayed a loss of zona occludins 1 and E-cadherin and a gain in vimentin and alpha-smooth muscle actin expression, consistent with the fibrotic actions of TGF-beta1. |
| 5518 | 18495798 | These effects were blocked with inhibitors of PI3K and PKB/Akt. |
| 5519 | 18495798 | Furthermore, overexpression of PTEN, the lipid phosphatase regulator of PKB/Akt activation, inhibited TGF-beta1-induced PKB/Akt activation. |
| 5520 | 18495798 | Interestingly, in the Goto-Kakizaki rat model of type 2 diabetes, we also detected increased phosphorylation of PKB/Akt and its downstream target, GSK-3beta, in the tubules, relative to that in control Wistar rats. |
| 5521 | 18495798 | We investigated the potential of PKB/Akt to mediate the profibrotic bioactions of TGF-beta1 in kidney. |
| 5522 | 18495798 | Treatment of normal rat kidney epithelial cells (NRK52E) with TGF-beta1 resulted in activation of phosphatidylinositol 3-kinase (PI3K) and PKB/Akt as evidenced by increased Ser473 phosphorylation and GSK-3beta phosphorylation. |
| 5523 | 18495798 | TGF-beta1 also stimulated increased Smad3 phosphorylation in these cells, a response that was insensitive to inhibition of PI3K or PKB/Akt. |
| 5524 | 18495798 | NRK52E cells displayed a loss of zona occludins 1 and E-cadherin and a gain in vimentin and alpha-smooth muscle actin expression, consistent with the fibrotic actions of TGF-beta1. |
| 5525 | 18495798 | These effects were blocked with inhibitors of PI3K and PKB/Akt. |
| 5526 | 18495798 | Furthermore, overexpression of PTEN, the lipid phosphatase regulator of PKB/Akt activation, inhibited TGF-beta1-induced PKB/Akt activation. |
| 5527 | 18495798 | Interestingly, in the Goto-Kakizaki rat model of type 2 diabetes, we also detected increased phosphorylation of PKB/Akt and its downstream target, GSK-3beta, in the tubules, relative to that in control Wistar rats. |
| 5528 | 18495798 | We investigated the potential of PKB/Akt to mediate the profibrotic bioactions of TGF-beta1 in kidney. |
| 5529 | 18495798 | Treatment of normal rat kidney epithelial cells (NRK52E) with TGF-beta1 resulted in activation of phosphatidylinositol 3-kinase (PI3K) and PKB/Akt as evidenced by increased Ser473 phosphorylation and GSK-3beta phosphorylation. |
| 5530 | 18495798 | TGF-beta1 also stimulated increased Smad3 phosphorylation in these cells, a response that was insensitive to inhibition of PI3K or PKB/Akt. |
| 5531 | 18495798 | NRK52E cells displayed a loss of zona occludins 1 and E-cadherin and a gain in vimentin and alpha-smooth muscle actin expression, consistent with the fibrotic actions of TGF-beta1. |
| 5532 | 18495798 | These effects were blocked with inhibitors of PI3K and PKB/Akt. |
| 5533 | 18495798 | Furthermore, overexpression of PTEN, the lipid phosphatase regulator of PKB/Akt activation, inhibited TGF-beta1-induced PKB/Akt activation. |
| 5534 | 18495798 | Interestingly, in the Goto-Kakizaki rat model of type 2 diabetes, we also detected increased phosphorylation of PKB/Akt and its downstream target, GSK-3beta, in the tubules, relative to that in control Wistar rats. |
| 5535 | 18495798 | We investigated the potential of PKB/Akt to mediate the profibrotic bioactions of TGF-beta1 in kidney. |
| 5536 | 18495798 | Treatment of normal rat kidney epithelial cells (NRK52E) with TGF-beta1 resulted in activation of phosphatidylinositol 3-kinase (PI3K) and PKB/Akt as evidenced by increased Ser473 phosphorylation and GSK-3beta phosphorylation. |
| 5537 | 18495798 | TGF-beta1 also stimulated increased Smad3 phosphorylation in these cells, a response that was insensitive to inhibition of PI3K or PKB/Akt. |
| 5538 | 18495798 | NRK52E cells displayed a loss of zona occludins 1 and E-cadherin and a gain in vimentin and alpha-smooth muscle actin expression, consistent with the fibrotic actions of TGF-beta1. |
| 5539 | 18495798 | These effects were blocked with inhibitors of PI3K and PKB/Akt. |
| 5540 | 18495798 | Furthermore, overexpression of PTEN, the lipid phosphatase regulator of PKB/Akt activation, inhibited TGF-beta1-induced PKB/Akt activation. |
| 5541 | 18495798 | Interestingly, in the Goto-Kakizaki rat model of type 2 diabetes, we also detected increased phosphorylation of PKB/Akt and its downstream target, GSK-3beta, in the tubules, relative to that in control Wistar rats. |
| 5542 | 18497727 | New criteria to define the metabolic syndrome have been proposed, as adipokines, CRP and PAI-1. |
| 5543 | 18497727 | IGFBP-1 is related to hyperinsulinemia/insulin resistance and to the risk of diabetes and fatal ischemic heart disease development. |
| 5544 | 18497727 | The adipose tissue production of adipokines and cytokines (such as IL-6, TNF-alpha and TGF-beta) and the excessive lipid flux towards muscles, heart and liver (Ectopic fat storage syndrome) contribute to the MS genesis and to an increased cardiovascular risk. |
| 5545 | 18508967 | IHG-1 amplifies TGF-beta1 signaling and is increased in renal fibrosis. |
| 5546 | 18508967 | In the diabetic nephropathy specimens, in situ hybridization localized IHG-1 to tubular epithelial cells along with TGF-beta1 and activated Smad3, suggesting a possible role in the development of tubulointerstitial fibrosis. |
| 5547 | 18508967 | In the HK-2 proximal tubule cell line, overexpression of IHG-1 increased TGF-beta1-stimulated expression of connective tissue growth factor and fibronectin. |
| 5548 | 18508967 | IHG-1 was found to amplify TGF-beta1-mediated transcriptional activity by increasing and prolonging phosphorylation of Smad3. |
| 5549 | 18508967 | Conversely, inhibition of endogenous IHG-1 with small interference RNA suppressed transcriptional responses to TGF-beta1. |
| 5550 | 18508967 | In summary, IHG-1, which increases in diabetic nephropathy, may enhance the actions of TGF-beta1 and contribute to the development of tubulointerstitial fibrosis. |
| 5551 | 18508967 | IHG-1 amplifies TGF-beta1 signaling and is increased in renal fibrosis. |
| 5552 | 18508967 | In the diabetic nephropathy specimens, in situ hybridization localized IHG-1 to tubular epithelial cells along with TGF-beta1 and activated Smad3, suggesting a possible role in the development of tubulointerstitial fibrosis. |
| 5553 | 18508967 | In the HK-2 proximal tubule cell line, overexpression of IHG-1 increased TGF-beta1-stimulated expression of connective tissue growth factor and fibronectin. |
| 5554 | 18508967 | IHG-1 was found to amplify TGF-beta1-mediated transcriptional activity by increasing and prolonging phosphorylation of Smad3. |
| 5555 | 18508967 | Conversely, inhibition of endogenous IHG-1 with small interference RNA suppressed transcriptional responses to TGF-beta1. |
| 5556 | 18508967 | In summary, IHG-1, which increases in diabetic nephropathy, may enhance the actions of TGF-beta1 and contribute to the development of tubulointerstitial fibrosis. |
| 5557 | 18508967 | IHG-1 amplifies TGF-beta1 signaling and is increased in renal fibrosis. |
| 5558 | 18508967 | In the diabetic nephropathy specimens, in situ hybridization localized IHG-1 to tubular epithelial cells along with TGF-beta1 and activated Smad3, suggesting a possible role in the development of tubulointerstitial fibrosis. |
| 5559 | 18508967 | In the HK-2 proximal tubule cell line, overexpression of IHG-1 increased TGF-beta1-stimulated expression of connective tissue growth factor and fibronectin. |
| 5560 | 18508967 | IHG-1 was found to amplify TGF-beta1-mediated transcriptional activity by increasing and prolonging phosphorylation of Smad3. |
| 5561 | 18508967 | Conversely, inhibition of endogenous IHG-1 with small interference RNA suppressed transcriptional responses to TGF-beta1. |
| 5562 | 18508967 | In summary, IHG-1, which increases in diabetic nephropathy, may enhance the actions of TGF-beta1 and contribute to the development of tubulointerstitial fibrosis. |
| 5563 | 18508967 | IHG-1 amplifies TGF-beta1 signaling and is increased in renal fibrosis. |
| 5564 | 18508967 | In the diabetic nephropathy specimens, in situ hybridization localized IHG-1 to tubular epithelial cells along with TGF-beta1 and activated Smad3, suggesting a possible role in the development of tubulointerstitial fibrosis. |
| 5565 | 18508967 | In the HK-2 proximal tubule cell line, overexpression of IHG-1 increased TGF-beta1-stimulated expression of connective tissue growth factor and fibronectin. |
| 5566 | 18508967 | IHG-1 was found to amplify TGF-beta1-mediated transcriptional activity by increasing and prolonging phosphorylation of Smad3. |
| 5567 | 18508967 | Conversely, inhibition of endogenous IHG-1 with small interference RNA suppressed transcriptional responses to TGF-beta1. |
| 5568 | 18508967 | In summary, IHG-1, which increases in diabetic nephropathy, may enhance the actions of TGF-beta1 and contribute to the development of tubulointerstitial fibrosis. |
| 5569 | 18511845 | TGFbeta1, TNFalpha, and insulin signaling crosstalk in regulation of the rat cholesterol 7alpha-hydroxylase gene expression. |
| 5570 | 18511845 | Previous studies show that TGFbeta1, TNFalpha, and insulin inhibit cholesterol 7alpha-hydroxylase (CYP7A1) gene transcription and bile acid synthesis in human hepatocytes. |
| 5571 | 18511845 | In this study, we investigated insulin, TGFbeta1, and TNFalpha regulation of rat Cyp7a1 gene transcription. |
| 5572 | 18511845 | Smad3, FoxO1, and HNF4alpha synergistically stimulated rat Cyp7a1 gene transcription. |
| 5573 | 18511845 | Mutations of the Smad3, FoxO1, or HNF4alpha binding site attenuated the rat Cyp7a1 promoter activity. |
| 5574 | 18511845 | Furthermore, TNFalpha and cJun attenuated TGFbeta1 stimulation of rat Cyp7a1. |
| 5575 | 18511845 | Insulin or adenovirus-mediated expression of constitutively active AKT1 inhibited FoxO1 and Smad3 synergy. |
| 5576 | 18511845 | In streptozotocin-induced diabetic rats, Cyp7a1 mRNA expression levels were induced and insulin attenuated CYP7A1 mRNA levels. |
| 5577 | 18511845 | Chromatin immunoprecipitation assay showed that FoxO1 binding to Cyp7a1 chromatin was increased in diabetic rat livers and insulin reduced FoxO1 binding. |
| 5578 | 18511845 | The crosstalk of insulin, TGFbeta and TNFalpha signaling pathways may regulate bile acid synthesis and lipid homeostasis in diabetes, fatty liver disease, and liver fibrosis. |
| 5579 | 18549445 | The proposed cytotoxic lymphocyte antigen 4 (CTLA-4) involvement, together with forkhead box P3 (FoxP3) and transforming growth factor (TGF)-beta are associated with regulatory T cell activity. |
| 5580 | 18549445 | CTLA-4, sCTLA-4, FoxP3 and TGF-beta mRNA transcription was quantified. |
| 5581 | 18549445 | Placebo individuals increased in spontaneous CTLA-4 mRNA (P < 0.05) but decreased in expression after stimulation with GAD(65)-peptide (P < 0.05) and PHA (P < 0.05). |
| 5582 | 18549445 | Spontaneous TGF-beta (P < 0.05) increased whereas PHA- (P < 0.01) and GAD(65)-peptide (P < 0.01)-induced TGF-beta expression decreased in the placebo group, whereas it was maintained in the treated group. |
| 5583 | 18549445 | Without intervention, expression of CTLA-4 and TGF-beta, stimulated with PHA and GAD(65) peptide, decreased with time, with a parallel reduction of GAD(65)-peptide and PHA-stimulated TGF-beta expression. |
| 5584 | 18549445 | The proposed cytotoxic lymphocyte antigen 4 (CTLA-4) involvement, together with forkhead box P3 (FoxP3) and transforming growth factor (TGF)-beta are associated with regulatory T cell activity. |
| 5585 | 18549445 | CTLA-4, sCTLA-4, FoxP3 and TGF-beta mRNA transcription was quantified. |
| 5586 | 18549445 | Placebo individuals increased in spontaneous CTLA-4 mRNA (P < 0.05) but decreased in expression after stimulation with GAD(65)-peptide (P < 0.05) and PHA (P < 0.05). |
| 5587 | 18549445 | Spontaneous TGF-beta (P < 0.05) increased whereas PHA- (P < 0.01) and GAD(65)-peptide (P < 0.01)-induced TGF-beta expression decreased in the placebo group, whereas it was maintained in the treated group. |
| 5588 | 18549445 | Without intervention, expression of CTLA-4 and TGF-beta, stimulated with PHA and GAD(65) peptide, decreased with time, with a parallel reduction of GAD(65)-peptide and PHA-stimulated TGF-beta expression. |
| 5589 | 18549445 | The proposed cytotoxic lymphocyte antigen 4 (CTLA-4) involvement, together with forkhead box P3 (FoxP3) and transforming growth factor (TGF)-beta are associated with regulatory T cell activity. |
| 5590 | 18549445 | CTLA-4, sCTLA-4, FoxP3 and TGF-beta mRNA transcription was quantified. |
| 5591 | 18549445 | Placebo individuals increased in spontaneous CTLA-4 mRNA (P < 0.05) but decreased in expression after stimulation with GAD(65)-peptide (P < 0.05) and PHA (P < 0.05). |
| 5592 | 18549445 | Spontaneous TGF-beta (P < 0.05) increased whereas PHA- (P < 0.01) and GAD(65)-peptide (P < 0.01)-induced TGF-beta expression decreased in the placebo group, whereas it was maintained in the treated group. |
| 5593 | 18549445 | Without intervention, expression of CTLA-4 and TGF-beta, stimulated with PHA and GAD(65) peptide, decreased with time, with a parallel reduction of GAD(65)-peptide and PHA-stimulated TGF-beta expression. |
| 5594 | 18562637 | These effects were associated with lower renal cortical or glomerular levels of profibrotic markers transforming growth factor-beta, connective tissue growth factor, type I and type IV collagens, plasminogen activator inhibitor 1, and fibronectin. |
| 5595 | 18579703 | MCP-1/CCR2 system is involved in high glucose-induced fibronectin and type IV collagen expression in cultured mesangial cells. |
| 5596 | 18579703 | Although previous studies have demonstrated the importance of MCP-1 in the pathogenesis of diabetic nephropathy (DN) in terms of inflammation, the role of MCP-1 and its receptor (C-C chemokine receptor 2; CCR2) in extracellular matrix (ECM) accumulation under diabetic conditions has been largely unexplored. |
| 5597 | 18579703 | This study was undertaken to investigate the functional role of the MCP-1/CCR2 system in high glucose-induced ECM (fibronectin and type IV collagen) protein expression in cultured mesangial cells (MCs). |
| 5598 | 18579703 | To examine the relationship between MCP-1 and transforming growth factor (TGF)-beta1, MCs were also treated with TGF-beta1 (2 ng/ml) with or without mMCP-1 or CCR2 siRNA. |
| 5599 | 18579703 | Cell viability was determined by an MTT assay, mouse and human MCP-1 and TGF-beta1 levels by ELISA, and CCR2 and ECM protein expression by Western blotting. |
| 5600 | 18579703 | HG-induced ECM protein expression and TGF-beta1 levels were significantly attenuated by mMCP-1, CCR2 siRNA, and RS102895 (P < 0.05). |
| 5601 | 18579703 | These results suggest that an interaction between the MCP-1/CCR2 system and TGF-beta1 may contribute to ECM accumulation in DN. |
| 5602 | 18579703 | MCP-1/CCR2 system is involved in high glucose-induced fibronectin and type IV collagen expression in cultured mesangial cells. |
| 5603 | 18579703 | Although previous studies have demonstrated the importance of MCP-1 in the pathogenesis of diabetic nephropathy (DN) in terms of inflammation, the role of MCP-1 and its receptor (C-C chemokine receptor 2; CCR2) in extracellular matrix (ECM) accumulation under diabetic conditions has been largely unexplored. |
| 5604 | 18579703 | This study was undertaken to investigate the functional role of the MCP-1/CCR2 system in high glucose-induced ECM (fibronectin and type IV collagen) protein expression in cultured mesangial cells (MCs). |
| 5605 | 18579703 | To examine the relationship between MCP-1 and transforming growth factor (TGF)-beta1, MCs were also treated with TGF-beta1 (2 ng/ml) with or without mMCP-1 or CCR2 siRNA. |
| 5606 | 18579703 | Cell viability was determined by an MTT assay, mouse and human MCP-1 and TGF-beta1 levels by ELISA, and CCR2 and ECM protein expression by Western blotting. |
| 5607 | 18579703 | HG-induced ECM protein expression and TGF-beta1 levels were significantly attenuated by mMCP-1, CCR2 siRNA, and RS102895 (P < 0.05). |
| 5608 | 18579703 | These results suggest that an interaction between the MCP-1/CCR2 system and TGF-beta1 may contribute to ECM accumulation in DN. |
| 5609 | 18579703 | MCP-1/CCR2 system is involved in high glucose-induced fibronectin and type IV collagen expression in cultured mesangial cells. |
| 5610 | 18579703 | Although previous studies have demonstrated the importance of MCP-1 in the pathogenesis of diabetic nephropathy (DN) in terms of inflammation, the role of MCP-1 and its receptor (C-C chemokine receptor 2; CCR2) in extracellular matrix (ECM) accumulation under diabetic conditions has been largely unexplored. |
| 5611 | 18579703 | This study was undertaken to investigate the functional role of the MCP-1/CCR2 system in high glucose-induced ECM (fibronectin and type IV collagen) protein expression in cultured mesangial cells (MCs). |
| 5612 | 18579703 | To examine the relationship between MCP-1 and transforming growth factor (TGF)-beta1, MCs were also treated with TGF-beta1 (2 ng/ml) with or without mMCP-1 or CCR2 siRNA. |
| 5613 | 18579703 | Cell viability was determined by an MTT assay, mouse and human MCP-1 and TGF-beta1 levels by ELISA, and CCR2 and ECM protein expression by Western blotting. |
| 5614 | 18579703 | HG-induced ECM protein expression and TGF-beta1 levels were significantly attenuated by mMCP-1, CCR2 siRNA, and RS102895 (P < 0.05). |
| 5615 | 18579703 | These results suggest that an interaction between the MCP-1/CCR2 system and TGF-beta1 may contribute to ECM accumulation in DN. |
| 5616 | 18579703 | MCP-1/CCR2 system is involved in high glucose-induced fibronectin and type IV collagen expression in cultured mesangial cells. |
| 5617 | 18579703 | Although previous studies have demonstrated the importance of MCP-1 in the pathogenesis of diabetic nephropathy (DN) in terms of inflammation, the role of MCP-1 and its receptor (C-C chemokine receptor 2; CCR2) in extracellular matrix (ECM) accumulation under diabetic conditions has been largely unexplored. |
| 5618 | 18579703 | This study was undertaken to investigate the functional role of the MCP-1/CCR2 system in high glucose-induced ECM (fibronectin and type IV collagen) protein expression in cultured mesangial cells (MCs). |
| 5619 | 18579703 | To examine the relationship between MCP-1 and transforming growth factor (TGF)-beta1, MCs were also treated with TGF-beta1 (2 ng/ml) with or without mMCP-1 or CCR2 siRNA. |
| 5620 | 18579703 | Cell viability was determined by an MTT assay, mouse and human MCP-1 and TGF-beta1 levels by ELISA, and CCR2 and ECM protein expression by Western blotting. |
| 5621 | 18579703 | HG-induced ECM protein expression and TGF-beta1 levels were significantly attenuated by mMCP-1, CCR2 siRNA, and RS102895 (P < 0.05). |
| 5622 | 18579703 | These results suggest that an interaction between the MCP-1/CCR2 system and TGF-beta1 may contribute to ECM accumulation in DN. |
| 5623 | 18579704 | This degradation pathway is sensitive to metabolic factors responsible for hypertrophy and fibrosis, particularly molecules such as angiotensin II and transforming growth factor-beta1, whose production is stimulated by hyperglycemic and hypertensive environments. |
| 5624 | 18639522 | Furthermore, adiponectin regulated the expression of TGFbeta isoforms in keratinocytes in a dose-dependent manner, which implies that adiponectin modulates other types of cells related to wound repair via secretion of growth factors from keratinocytes. |
| 5625 | 18641317 | CD4 cells induced to express FoxP3, IL-10, and TGF-beta1 in response to TCR signaling and TGF-beta1 can reverse diabetes with clinical restoration of prediabetic serum levels of IL-10. |
| 5626 | 18646321 | Prevalence of diabetes mellitus and correlation of urinary transforming growth factor-beta1 with blood hemoglobin A1C in the Atascosa Diabetes Study. |
| 5627 | 18653620 | These include insulin, hypertonicity, glucose, increased intracellular calcium and transforming growth factor-beta, all of which have been shown to be increased in type II diabetes. |
| 5628 | 18675407 | After TGF-beta blockade, CD4+ T cells differentiated along a route favoring development of Th17, but not Treg cells. |
| 5629 | 18689691 | Transforming growth factor-beta suppresses the activation of CD8+ T-cells when naive but promotes their survival and function once antigen experienced: a two-faced impact on autoimmunity. |
| 5630 | 18713984 | The reprogrammed Tregs cease to express IL-10 and TGFbeta, fail to suppress T cell responses, and gain the ability to produce IFN-gamma, IL-17, and TNF-alpha. |
| 5631 | 18726161 | New concepts about bradykinin, TGF-beta and eNOS signaling as well as JAK/STAT activation and the central role of inflammation in both glomerular and tubulointerstitial fibrosis are discussed. |
| 5632 | 18753303 | Role of Kruppel-like factor 6 in transforming growth factor-beta1-induced epithelial-mesenchymal transition of proximal tubule cells. |
| 5633 | 18753303 | The present study aimed to determine the role of KLF6 and TGF-beta1 in EMT in proximal tubule cells. |
| 5634 | 18753303 | TGF-beta1 was confirmed to induce EMT by morphological change, loss of E-cadherin, and gain in vimentin expression. |
| 5635 | 18753303 | To determine the role of KLF6 in EMT, the above markers of EMT were determined in KLF6-silenced (small interfering RNA) and KLF6-overexpressing proximal tubule cells. |
| 5636 | 18753303 | This increase in KLF6 in response to high glucose was TGF-beta1 mediated. |
| 5637 | 18753303 | Role of Kruppel-like factor 6 in transforming growth factor-beta1-induced epithelial-mesenchymal transition of proximal tubule cells. |
| 5638 | 18753303 | The present study aimed to determine the role of KLF6 and TGF-beta1 in EMT in proximal tubule cells. |
| 5639 | 18753303 | TGF-beta1 was confirmed to induce EMT by morphological change, loss of E-cadherin, and gain in vimentin expression. |
| 5640 | 18753303 | To determine the role of KLF6 in EMT, the above markers of EMT were determined in KLF6-silenced (small interfering RNA) and KLF6-overexpressing proximal tubule cells. |
| 5641 | 18753303 | This increase in KLF6 in response to high glucose was TGF-beta1 mediated. |
| 5642 | 18753303 | Role of Kruppel-like factor 6 in transforming growth factor-beta1-induced epithelial-mesenchymal transition of proximal tubule cells. |
| 5643 | 18753303 | The present study aimed to determine the role of KLF6 and TGF-beta1 in EMT in proximal tubule cells. |
| 5644 | 18753303 | TGF-beta1 was confirmed to induce EMT by morphological change, loss of E-cadherin, and gain in vimentin expression. |
| 5645 | 18753303 | To determine the role of KLF6 in EMT, the above markers of EMT were determined in KLF6-silenced (small interfering RNA) and KLF6-overexpressing proximal tubule cells. |
| 5646 | 18753303 | This increase in KLF6 in response to high glucose was TGF-beta1 mediated. |
| 5647 | 18753303 | Role of Kruppel-like factor 6 in transforming growth factor-beta1-induced epithelial-mesenchymal transition of proximal tubule cells. |
| 5648 | 18753303 | The present study aimed to determine the role of KLF6 and TGF-beta1 in EMT in proximal tubule cells. |
| 5649 | 18753303 | TGF-beta1 was confirmed to induce EMT by morphological change, loss of E-cadherin, and gain in vimentin expression. |
| 5650 | 18753303 | To determine the role of KLF6 in EMT, the above markers of EMT were determined in KLF6-silenced (small interfering RNA) and KLF6-overexpressing proximal tubule cells. |
| 5651 | 18753303 | This increase in KLF6 in response to high glucose was TGF-beta1 mediated. |
| 5652 | 18761006 | PBMC were cultured before and after cryopreservation either with GAD(65) or PHA. |
| 5653 | 18761006 | Secretion of cytokines (IL-5, -6, -10, -12, -13 -17, IFN-gamma and TNF-alpha) and chemokines (IP-10, MCP-1, MIP-1alpha, MIP-1beta and RANTES) was analysed in cell supernatants using multiplex fluorochrome technique (Luminex). |
| 5654 | 18761006 | Expression of FOXP3 and TGF-beta mRNA was detected by multiplex real-time RT-PCR. |
| 5655 | 18761006 | Increased spontaneous secretion of IL-6, -10, -12, -13, IFN-gamma and MCP-1, and mRNA expression of FOXP3 and TGF-beta, was detected after cryopreservation. |
| 5656 | 18761006 | Stimulation with GAD(65) induced higher levels of IL-6, IFN-gamma, TNF-alpha and MIP-1alpha, whereas lower secretion was found for IL-10 and IL-13 in cryopreserved PBMC. |
| 5657 | 18761006 | Stimulation with PHA induced lower secretion of IP-10, MCP-1 and RANTES and FOXP3 mRNA expression after cryopreservation. |
| 5658 | 18761006 | PBMC were cultured before and after cryopreservation either with GAD(65) or PHA. |
| 5659 | 18761006 | Secretion of cytokines (IL-5, -6, -10, -12, -13 -17, IFN-gamma and TNF-alpha) and chemokines (IP-10, MCP-1, MIP-1alpha, MIP-1beta and RANTES) was analysed in cell supernatants using multiplex fluorochrome technique (Luminex). |
| 5660 | 18761006 | Expression of FOXP3 and TGF-beta mRNA was detected by multiplex real-time RT-PCR. |
| 5661 | 18761006 | Increased spontaneous secretion of IL-6, -10, -12, -13, IFN-gamma and MCP-1, and mRNA expression of FOXP3 and TGF-beta, was detected after cryopreservation. |
| 5662 | 18761006 | Stimulation with GAD(65) induced higher levels of IL-6, IFN-gamma, TNF-alpha and MIP-1alpha, whereas lower secretion was found for IL-10 and IL-13 in cryopreserved PBMC. |
| 5663 | 18761006 | Stimulation with PHA induced lower secretion of IP-10, MCP-1 and RANTES and FOXP3 mRNA expression after cryopreservation. |
| 5664 | 18810325 | AMPKalpha, beta, and gamma), and their differential localization in response to stimulation in muscle; (2) the biochemical regulation of AMPK by AMP, protein phosphatases, and its three known upstream kinases, LKB1, Ca2+/calmodulin-dependent protein kinase kinase (CaMKK), and transforming growth factor-beta-activated kinase 1 (TAK1); (3) the pharmacological agents that are currently available for the activation and inhibition of AMPK; (4) the physiological stimuli that activate AMPK in muscle; and (5) the metabolic processes that AMPK regulates in skeletal muscle. |
| 5665 | 18827445 | Normal control and diabetic rats were studied for 2 weeks with and without thiamine, and followings were analyzed; plasma biochemicals (total cholesterol and triglycerides), morphological changes, mRNA abundance relevant to cardiac failure (brain natriuretic peptide) and fibrosis (transforming growth factor-beta1, thrombospondine, fibronectin, plasminogen activator-I and connective tissue growth factor) as well as and matrix metalloproteinase activity were investigated. |
| 5666 | 18838678 | Combination therapy with AT1 blocker and vitamin D analog markedly ameliorates diabetic nephropathy: blockade of compensatory renin increase. |
| 5667 | 18838678 | Here we demonstrated that combination therapy with an AT1 receptor blocker and a vitamin D analog markedly ameliorated renal injury in the streptozotocin (STZ)-induced diabetes model due to the blockade of the compensatory renin rise by the vitamin D analog, leading to more effective RAS inhibition. |
| 5668 | 18838678 | STZ-treated diabetic DBA/2J mice developed progressive albuminuria and glomerulosclerosis within 13 weeks, accompanied by increased intrarenal production of angiotensin (Ang) II, fibronection, TGF-beta, and MCP-1 and decreased expression of slit diaphragm proteins. |
| 5669 | 18838678 | The combined treatment suppressed the induction of fibronection, TGF-beta, and MCP-1 and reversed the decline of slit diaphragm proteins nephrin, Neph-1, ZO-1, and alpha-actinin-4. |
| 5670 | 18838678 | These were accompanied by blockade of intrarenal renin and Ang II accumulation induced by hyperglycemia and losartan. |
| 5671 | 18838678 | Combination therapy with AT1 blocker and vitamin D analog markedly ameliorates diabetic nephropathy: blockade of compensatory renin increase. |
| 5672 | 18838678 | Here we demonstrated that combination therapy with an AT1 receptor blocker and a vitamin D analog markedly ameliorated renal injury in the streptozotocin (STZ)-induced diabetes model due to the blockade of the compensatory renin rise by the vitamin D analog, leading to more effective RAS inhibition. |
| 5673 | 18838678 | STZ-treated diabetic DBA/2J mice developed progressive albuminuria and glomerulosclerosis within 13 weeks, accompanied by increased intrarenal production of angiotensin (Ang) II, fibronection, TGF-beta, and MCP-1 and decreased expression of slit diaphragm proteins. |
| 5674 | 18838678 | The combined treatment suppressed the induction of fibronection, TGF-beta, and MCP-1 and reversed the decline of slit diaphragm proteins nephrin, Neph-1, ZO-1, and alpha-actinin-4. |
| 5675 | 18838678 | These were accompanied by blockade of intrarenal renin and Ang II accumulation induced by hyperglycemia and losartan. |
| 5676 | 18923384 | The inability of mesangial cells to degrade abnormal levels of tenascin-C--along with the increased expression of some growth factors such as platelet-derived growth factor (PDGF) and transforming growth factor-beta (TGF-beta)--is crucial to the pathogenesis of light chain deposition disease (LCDD). |
| 5677 | 18923384 | Mesangial cells incubated with light chains from patients with LCDD show a significant increase in tenascin-C expression, centrally located within newly formed nodules, along with increased expression of PDGF and TGF-betas, compared to mesangial cells incubated with control light chains. |
| 5678 | 18923384 | Addition of active MMP-7 degraded this excess tenascin-C in vitro, a process that could be prevented by an exogenous MMP inhibitor. |
| 5679 | 18931971 | Furthermore, IL-27 up-regulated pro-inflammatory cytokines IFN-gamma and IL-17 and down-regulated anti-inflammatory cytokines IL-4, TGF-beta, and IL-10 secreted by diabetic splenocytes. |
| 5680 | 18977550 | A phase 2 study of PKC-beta inhibition in persons with type 2 diabetes and DKD already treated with angiotensin converting enzyme inhibition and/or angiotensin receptor blockade has been conducted. |
| 5681 | 18977550 | Addition of ruboxistaurin for 1 year reduced urinary albumin, prevented an increase in urinary transforming growth factor-beta, and stabilized estimated glomerular filtration rate. |
| 5682 | 18979373 | Urinary transforming growth factor-beta(1), collagen IV and the effect of insulin in children at diagnosis of diabetes mellitus. |
| 5683 | 18981116 | Furthermore, islet-infiltrating leukocytes in the LTP mice contained Foxp3(+)CD4 T cells. |
| 5684 | 18981116 | The LTP was abolished if mice were treated with either Ab-depleting CD4 T cells or a neutralizing Ab to CTLA-4, in this case, only at a late stage. |
| 5685 | 18981116 | Neutralization of IL-10, TGF-beta, glucocorticoid-induced TNF receptor (GITR), or CD25 had no effect. |
| 5686 | 18981116 | Hence, using monoclonal CD4 T cells, IFN-gamma can have a wide diversity of roles, depending on the setting of the immune process. |
| 5687 | 18990305 | This pathway is sensitive to metabolic factors responsible for hypertrophy and fibrosis, particularly molecules such as angiotensin II and transforming growth factor-beta1, whose production is stimulated by hyperglycemic environments. |
| 5688 | 19003945 | In the presence of high glucose, the levels of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9) and extracellular matrix metalloproteinase inducer (EMMPRIN) were decreased significantly, and the levels of tissue inhibitor of metalloproteinase-2 (TIMP-2), tissue inhibitor of metalloproteinase-1 (TIMP-1) and plasminogen activator inhibitor-1 (PAI-1) were increased significantly. |
| 5689 | 19003945 | GbE lowered the levels of transforming growth factor-beta(1) (TGF-beta(1)), insulin-like growth factor-1 (IGF-1) and connective tissue growth factor (CTGF) of the high glucose group. |
| 5690 | 19003945 | Furthermore, GbE also decreased the expressions of collagen IV and laminin of the high glucose group. |
| 5691 | 19006694 | CD4(+)Foxp3(+) regulatory T (Treg) cells originate primarily from thymic differentiation, but conversion of mature T lymphocytes to Foxp3 positivity can be elicited by several means, including in vitro activation in the presence of TGF-beta. |
| 5692 | 19006694 | We showed here that, rather than enhancing TGF-beta signaling directly in naive CD4(+) T cells, RA negatively regulated an accompanying population of CD4(+) T cells with a CD44(hi) memory and effector phenotype. |
| 5693 | 19006694 | These memory cells actively inhibited the TGF-beta-induced conversion of naive CD4(+) T cells through the synthesis of a set of cytokines (IL-4, IL-21, IFN-gamma) whose expression was coordinately curtailed by RA. |
| 5694 | 19018797 | Furthermore, reactive oxygen species (ROS) in the rat renal cortex were analysed using an H(2)O(2)-based hydroxyl radical-detection assay and the renal content of AGE, RAGE, NADPH oxidase p47phox, nuclear factor (NF)-kappaB p65, phosphorylated (p-) NF-kappaB p65, vascular cell adhesion molecule (VCAM)-1 and transforming growth factor (TGF)-beta1 was determined by immunohistochemistry, quantitative real-time polymerase chain reaction and western blot analysis. 3. |
| 5695 | 19018797 | In addition, benazepril treatment reduced the upregulation of NADPH oxidase p47phox, ROS generation and NF-kappaB p65, p-NF-kappaB p65, VCAM-1 and TGF-beta1 expression in the kidney of SHR compared with both untreated SHR and control WKY rats. 4. |
| 5696 | 19048273 | Sterol regulatory element binding protein-1 (SREBP-1) is transcription factor regulating the synthesis of fatty acid and triglyceride. |
| 5697 | 19048273 | The animal experiment showed that triglyceride and SREBP-1 were up-regulated in proximal tubule of diabetic rats' kidney, which may result in increase of transforming growth factor-beta1 (TGF-beta1) and accumulation of extracellular matrix (ECM). |
| 5698 | 19048273 | The expression of fatty acid synthase (FAS) in HKC cells transfected with specific plasmid for SREBP-1 gene was significantly more than that of the cells transfected with the control plasmid pcDNA3.1 and that of the untransfected cells. |
| 5699 | 19048273 | Simultaneously, up-regulation of TGF-beta1 and fibronectin, an ECM glycoprotein, was evident in HKC cells transfected by specific SREBP-1 plasmid. |
| 5700 | 19048273 | Increasing SREBP-1 plays an important role in the pathogenesis of renal lipid accumulation by up-regulation of FAS and ECM accumulation by inducing TGF-beta1 expression. |
| 5701 | 19048273 | Sterol regulatory element binding protein-1 (SREBP-1) is transcription factor regulating the synthesis of fatty acid and triglyceride. |
| 5702 | 19048273 | The animal experiment showed that triglyceride and SREBP-1 were up-regulated in proximal tubule of diabetic rats' kidney, which may result in increase of transforming growth factor-beta1 (TGF-beta1) and accumulation of extracellular matrix (ECM). |
| 5703 | 19048273 | The expression of fatty acid synthase (FAS) in HKC cells transfected with specific plasmid for SREBP-1 gene was significantly more than that of the cells transfected with the control plasmid pcDNA3.1 and that of the untransfected cells. |
| 5704 | 19048273 | Simultaneously, up-regulation of TGF-beta1 and fibronectin, an ECM glycoprotein, was evident in HKC cells transfected by specific SREBP-1 plasmid. |
| 5705 | 19048273 | Increasing SREBP-1 plays an important role in the pathogenesis of renal lipid accumulation by up-regulation of FAS and ECM accumulation by inducing TGF-beta1 expression. |
| 5706 | 19048273 | Sterol regulatory element binding protein-1 (SREBP-1) is transcription factor regulating the synthesis of fatty acid and triglyceride. |
| 5707 | 19048273 | The animal experiment showed that triglyceride and SREBP-1 were up-regulated in proximal tubule of diabetic rats' kidney, which may result in increase of transforming growth factor-beta1 (TGF-beta1) and accumulation of extracellular matrix (ECM). |
| 5708 | 19048273 | The expression of fatty acid synthase (FAS) in HKC cells transfected with specific plasmid for SREBP-1 gene was significantly more than that of the cells transfected with the control plasmid pcDNA3.1 and that of the untransfected cells. |
| 5709 | 19048273 | Simultaneously, up-regulation of TGF-beta1 and fibronectin, an ECM glycoprotein, was evident in HKC cells transfected by specific SREBP-1 plasmid. |
| 5710 | 19048273 | Increasing SREBP-1 plays an important role in the pathogenesis of renal lipid accumulation by up-regulation of FAS and ECM accumulation by inducing TGF-beta1 expression. |
| 5711 | 19050249 | Exposure of APCs of NOD mice to zymosan, a fungal cell wall component that interacts with TLR2 and dectin 1, resulted in the release of significant amounts of IL-10, TGF-beta1, IL-2, and TNF-alpha. |
| 5712 | 19050249 | Zymosan treatment induced suppression of T1D was associated with an increase in the L-selectin(high) T cell frequencies and enhanced suppressor function of CD4(+)CD25(+) T regulatory cells. |
| 5713 | 19050249 | Further, activation by anti-CD3-Ab induced larger amounts of TGF-beta1 and/or IL-10 production by CD4(+)CD25(+) and CD4(+)CD25(-) T cells from zymosan-treated mice. |
| 5714 | 19052104 | In addition, D+canola attenuated D-associated increase in collagen type I and type IV, IL-6, MCP-1, transforming growth factor-beta, and CD68 expression. |
| 5715 | 19062254 | Autologous bone marrow-derived rat mesenchymal stem cells promote PDX-1 and insulin expression in the islets, alter T cell cytokine pattern and preserve regulatory T cells in the periphery and induce sustained normoglycemia. |
| 5716 | 19062254 | MSC were CD45(-)/CD44(+)/CD54(+)/CD90(+)/CD106(+). |
| 5717 | 19062254 | MSC spontaneously secreted IL-6, HGF, TGF-beta1 and expressed high levels of SDF-1 and low levels of VEGF, IL-1beta and PGE(2), but no EGF, insulin or glucagon. |
| 5718 | 19062254 | Interestingly, immunohistochemistry demonstrated that, the islets from MSC-treated rats expressed high levels of PDX-1 and that these cells were also positive for insulin staining. |
| 5719 | 19062254 | In addition, peripheral T cells from MSC-treated rats exhibited a shift toward IL-10/IL-13 production and higher frequencies of CD4(+)/CD8(+) Foxp3(+) T cells compared to the PBS-treated rats. |
| 5720 | 19066289 | Compared with vehicle-treated diabetic rats, EPS-treated animals displayed a significant decrease in renal macrophage infiltration and overexpression of chemokine (C-C motif) ligand 2 (CCL2) and TGFB1. |
| 5721 | 19075640 | p38 MAP kinase mediated proteoglycan synthesis as a target for the prevention of atherosclerosis. |
| 5722 | 19075640 | It has recently been demonstrated that the actions of transforming growth factor beta on vascular smooth muscle proteoglycan synthesis involves signalling through p38 MAP kinase and inhibition of this pathway reduces binding of lipids. |
| 5723 | 19075640 | Inhibition of p38 MAP kinase will elicit a wide spread anti-inflammatory response which may alleviate some of the deleterious processes in cardiovascular tissues. |
| 5724 | 19075640 | This article explores the potential for the actions of p38 MAP kinase inhibitors directed at proteoglycan synthesis in vascular smooth muscle to contribute to the beneficial outcomes from targeting p38 MAP kinase for the prevention of cardiovascular disease. |
| 5725 | 19082432 | The expressions of p38 MAPK, p-p38 MAPK, Snail1, transforming growth factor-beta1 (TGF-beta1), alpha-smooth muscle actin (alpha-SMA) and E-cadherin protein and mRNA were detected by immunocytochemical staining, Western blot and RT-PCR. |
| 5726 | 19082432 | The p38 MAPK activation was abolished by insulin controlling hyperglycemia to normal level in DM rats and inhibited dramatically by SB202190 in high glucose-cultured PTECs. |
| 5727 | 19091788 | Central to this process is epithelial-mesenchymal transformation (EMT) of proximal tubular epithelial cells driven by maladaptive transforming growth factor-beta1 (TGF-beta1) signaling. |
| 5728 | 19091788 | Changes in cell morphology, TGF-beta1 receptor expression, vimentin, E-cadherin, and phosphorylated Smads were assessed. |
| 5729 | 19091788 | Central to this process is epithelial-mesenchymal transformation (EMT) of proximal tubular epithelial cells driven by maladaptive transforming growth factor-beta1 (TGF-beta1) signaling. |
| 5730 | 19091788 | Changes in cell morphology, TGF-beta1 receptor expression, vimentin, E-cadherin, and phosphorylated Smads were assessed. |
| 5731 | 19120317 | Multiple studies have shown that thymus-derived naturally occurring Tregs constitutively express the forkhead/winged helix transcription factor FoxP3 in addition to high levels of CD25, the negative co-stimulatory molecule CTLA-4, and the glucocorticoid-induced TNF receptor-related protein GITR. |
| 5732 | 19120317 | At variance, adaptive or induced Tregs acquire these phenotypic markers as they differentiate in the periphery, following adequate stimulation in the appropriate environment, together with their capacity to produce immunomodulatory cytokines (mainly, IL-4, IL-10 and TGF-beta) and to display regulatory capacities. |
| 5733 | 19120317 | Moreover, data are presented that simultaneous blockade of CTLA4 and TGF-beta further impairs immunoregulatory circuits that control disease progression. |
| 5734 | 19120317 | Multiple studies have shown that thymus-derived naturally occurring Tregs constitutively express the forkhead/winged helix transcription factor FoxP3 in addition to high levels of CD25, the negative co-stimulatory molecule CTLA-4, and the glucocorticoid-induced TNF receptor-related protein GITR. |
| 5735 | 19120317 | At variance, adaptive or induced Tregs acquire these phenotypic markers as they differentiate in the periphery, following adequate stimulation in the appropriate environment, together with their capacity to produce immunomodulatory cytokines (mainly, IL-4, IL-10 and TGF-beta) and to display regulatory capacities. |
| 5736 | 19120317 | Moreover, data are presented that simultaneous blockade of CTLA4 and TGF-beta further impairs immunoregulatory circuits that control disease progression. |
| 5737 | 19127457 | Recently, another linage of T cells has been described, namely T(H)17, characterized by production of IL-17, that differentiate in response to TGFbeta and IL-6 and participate in the pathogenesis of several autoimmune diseases. |
| 5738 | 19127457 | Using RT-PCR analysis of gene expression, we analyzed the presence of T(H)1 (IL-12 and IFNgamma) and T(H)17 (TGFbeta, IL-6, IL-17A, IL-17F and IL-23) related cytokines in intestinal biopsies from CD patients with active disease compared to remission and from treated patients after acute, in vitro re-exposure to gliadin. |
| 5739 | 19127457 | Recently, another linage of T cells has been described, namely T(H)17, characterized by production of IL-17, that differentiate in response to TGFbeta and IL-6 and participate in the pathogenesis of several autoimmune diseases. |
| 5740 | 19127457 | Using RT-PCR analysis of gene expression, we analyzed the presence of T(H)1 (IL-12 and IFNgamma) and T(H)17 (TGFbeta, IL-6, IL-17A, IL-17F and IL-23) related cytokines in intestinal biopsies from CD patients with active disease compared to remission and from treated patients after acute, in vitro re-exposure to gliadin. |
| 5741 | 19131512 | CTGF is a secreted protein known to modulate several growth factor-signaling pathways including TGF-beta, BMP, and Wnt. |
| 5742 | 19131512 | CTGF is highly expressed in pancreatic ductal epithelium and vascular endothelium, as well as at lower levels in developing insulin(+) cells, but becomes down-regulated in beta-cells soon after birth. |
| 5743 | 19131512 | Pancreata from CTGF null embryos have an increase in glucagon(+) cells with a concomitant decrease in insulin(+) cells, and show defects in islet morphogenesis. |
| 5744 | 19136037 | The effect of CTLA-4 allele and haplotype frequencies on the interferon-gamma, tumor necrosis factor-alpha, and transforming growth factor-beta(1) levels and the presence in serum of GAD65 and IA-2 autoantibodies at the onset of T1D was evaluated. |
| 5745 | 19136037 | On the other hand, higher ketoacidosis at onset, younger age at onset, and higher levels of tumor necrosis factor-alpha and interferon-gamma were observed in T1D patients carriers of G allele in comparison with the carriers of AA genotype. |
| 5746 | 19147827 | The nuclear hormone receptor, peroxisome proliferator-activated receptor (PPAR)-gamma, originally identified as a key mediator of adipogenesis, is expressed widely and implicated in diverse biological responses. |
| 5747 | 19147827 | Both natural and synthetic agonists of PPAR-gamma abrogated the stimulation of collagen synthesis and myofibroblast differentiation induced by transforming growth factor (TGF)-beta in vitro. |
| 5748 | 19147827 | Rosiglitazone treatment reduced the induction of the early-immediate transcription factor Egr-1 in situ without also blocking the activation of Smad2/3. |
| 5749 | 19147827 | In both explanted fibroblasts and skin organ cultures, rosiglitazone prevented the stimulation of collagen gene transcription and cell migration elicited by TGF-beta. |
| 5750 | 19147827 | Rosiglitazone-driven adipogenic differentiation of both fibroblasts and preadipocytes was abrogated in the presence of TGF-beta; this effect was accompanied by the concomitant down-regulation of cellular PPAR-gamma mRNA expression. |
| 5751 | 19147827 | Collectively, these results indicate that rosiglitazone treatment attenuates inflammation, dermal fibrosis, and subcutaneous lipoatrophy via PPAR-gamma in a mouse model of scleroderma and suggest that pharmacological PPAR-gamma ligands, widely used as insulin sensitizers in the treatment of type-2 diabetes mellitus, may be potential therapies for scleroderma. |
| 5752 | 19147827 | The nuclear hormone receptor, peroxisome proliferator-activated receptor (PPAR)-gamma, originally identified as a key mediator of adipogenesis, is expressed widely and implicated in diverse biological responses. |
| 5753 | 19147827 | Both natural and synthetic agonists of PPAR-gamma abrogated the stimulation of collagen synthesis and myofibroblast differentiation induced by transforming growth factor (TGF)-beta in vitro. |
| 5754 | 19147827 | Rosiglitazone treatment reduced the induction of the early-immediate transcription factor Egr-1 in situ without also blocking the activation of Smad2/3. |
| 5755 | 19147827 | In both explanted fibroblasts and skin organ cultures, rosiglitazone prevented the stimulation of collagen gene transcription and cell migration elicited by TGF-beta. |
| 5756 | 19147827 | Rosiglitazone-driven adipogenic differentiation of both fibroblasts and preadipocytes was abrogated in the presence of TGF-beta; this effect was accompanied by the concomitant down-regulation of cellular PPAR-gamma mRNA expression. |
| 5757 | 19147827 | Collectively, these results indicate that rosiglitazone treatment attenuates inflammation, dermal fibrosis, and subcutaneous lipoatrophy via PPAR-gamma in a mouse model of scleroderma and suggest that pharmacological PPAR-gamma ligands, widely used as insulin sensitizers in the treatment of type-2 diabetes mellitus, may be potential therapies for scleroderma. |
| 5758 | 19171978 | Arsenic causes apoptosis via free radical generation, and the cutaneous toxicity is linked to its effect on various cytokines (e.g., IL-8, TGF-beta, TNF-alpha, GM-CSF), growth factors, and transcription factors. |
| 5759 | 19171978 | Increased expression of cytokeratins, keratin-16 (marker for hyperproliferation) and keratin-8 and -18 (marker for less differentiated epithelial cells), can be related to the histopathological findings of hyperkeratosis and dysplastic cells in the arsenicosis skin lesion. |
| 5760 | 19175688 | In this study, we investigated the effect of the xanthine oxidase (XO) inhibitor, allopurinol (ALP), on cardiac dysfunction, oxidative-nitrosative stress, apoptosis, poly(ADP-ribose) polymerase (PARP) activity and fibrosis associated with diabetic cardiomyopathy in mice. |
| 5761 | 19175688 | Myocardial XO, p22(phox), p40(phox), p47(phox), gp91(phox), iNOS, eNOS mRNA and/or protein levels, ROS and nitrotyrosine (NT) formation, caspase3/7 and PARP activity, chromatin fragmentation and various markers of fibrosis (collagen-1, TGF-beta, CTGF, fibronectin) were measured using molecular biology and biochemistry methods or immunohistochemistry. |
| 5762 | 19175688 | Diabetes was characterized by increased myocardial, liver and serum XO activity (but not expression), increased myocardial ROS generation, p22(phox), p40(phox), p47(phox), p91(phox) mRNA expression, iNOS (but not eNOS) expression, NT generation, caspase 3/7 and PARP activity/expression, chromatin fragmentation and fibrosis (enhanced accumulation of collagen, TGF-beta, CTGF and fibronectin), and declined systolic and diastolic myocardial performance. |
| 5763 | 19175688 | ALP attenuated the diabetes-induced increased myocardial, liver and serum XO activity, myocardial ROS, NT generation, iNOS expression, apoptosis, PARP activity and fibrosis, which were accompanied by improved systolic (measured by the evaluation of both load-dependent and independent indices of myocardial contractility) and diastolic performance of the hearts of treated diabetic animals. |
| 5764 | 19182379 | Moreover, advanced glycation end-products (AGEs), angiotensin II (Ang II), transforming growth factor beta(1) (TGF-beta(1)), collagen IV, and monocyte/macrophage (ED-1) either in the serum or kidney were significantly reduced. |
| 5765 | 19211686 | Real-time PCR demonstrated increased glomerular expression of Col4a1, Fn1, and Tgfb1. |
| 5766 | 19214781 | CTGF is also able to interact with receptors on cells, including integrins, tyrosine receptor kinase A (TrkA), low density lipoprotein receptor-related protein (LRP) and heparan sulphate proteoglycans. |
| 5767 | 19214781 | For example, CTGF is often described as an effector of TGF-beta. |
| 5768 | 19214781 | It can promote TGF-beta signalling by binding directly to the growth factor, promoting its interaction with the TGF-beta receptor; by triggering intracellular signalling on binding the TrkA receptor, which leads to the transcriptional repression of Smad7, an inhibitor of the TGF-beta signalling pathway; and by binding to BMP-7 whose own signalling pathway opposing TGF-beta is inhibited, leading to enhanced TGF-beta signalling. |
| 5769 | 19214781 | CTGF is also able to interact with receptors on cells, including integrins, tyrosine receptor kinase A (TrkA), low density lipoprotein receptor-related protein (LRP) and heparan sulphate proteoglycans. |
| 5770 | 19214781 | For example, CTGF is often described as an effector of TGF-beta. |
| 5771 | 19214781 | It can promote TGF-beta signalling by binding directly to the growth factor, promoting its interaction with the TGF-beta receptor; by triggering intracellular signalling on binding the TrkA receptor, which leads to the transcriptional repression of Smad7, an inhibitor of the TGF-beta signalling pathway; and by binding to BMP-7 whose own signalling pathway opposing TGF-beta is inhibited, leading to enhanced TGF-beta signalling. |
| 5772 | 19215684 | The renal protective effects of cilostazol on suppressing pathogenic thrombospondin-1 and transforming growth factor-beta expression in streptozotocin-induced diabetic rats. |
| 5773 | 19215684 | Expression of thrombospondin-1 (TSP-1) and transforming growth factor-beta (TGF-beta) in the kidney was measured by immunohistochemistry and real-time reverse transcription-quantitative polymerase chain reaction analysis in diabetic rats, cilostazol-treated diabetic rats and control rats. |
| 5774 | 19215684 | Four weeks after the induction of diabetes, TSP-1 and TGF-beta expression was significantly increased in the kidneys of diabetic rats compared with the control and was significantly lower in cilostazol-treated diabetic rats than in the untreated diabetic rats. |
| 5775 | 19215684 | In conclusion, this study indicates that cilostazol treatment of diabetic rats effectively prevents pathological kidney changes, possibly via the down-regulation of TSP-1 and TGF-beta expression compared with untreated rats. |
| 5776 | 19215684 | The renal protective effects of cilostazol on suppressing pathogenic thrombospondin-1 and transforming growth factor-beta expression in streptozotocin-induced diabetic rats. |
| 5777 | 19215684 | Expression of thrombospondin-1 (TSP-1) and transforming growth factor-beta (TGF-beta) in the kidney was measured by immunohistochemistry and real-time reverse transcription-quantitative polymerase chain reaction analysis in diabetic rats, cilostazol-treated diabetic rats and control rats. |
| 5778 | 19215684 | Four weeks after the induction of diabetes, TSP-1 and TGF-beta expression was significantly increased in the kidneys of diabetic rats compared with the control and was significantly lower in cilostazol-treated diabetic rats than in the untreated diabetic rats. |
| 5779 | 19215684 | In conclusion, this study indicates that cilostazol treatment of diabetic rats effectively prevents pathological kidney changes, possibly via the down-regulation of TSP-1 and TGF-beta expression compared with untreated rats. |
| 5780 | 19215684 | The renal protective effects of cilostazol on suppressing pathogenic thrombospondin-1 and transforming growth factor-beta expression in streptozotocin-induced diabetic rats. |
| 5781 | 19215684 | Expression of thrombospondin-1 (TSP-1) and transforming growth factor-beta (TGF-beta) in the kidney was measured by immunohistochemistry and real-time reverse transcription-quantitative polymerase chain reaction analysis in diabetic rats, cilostazol-treated diabetic rats and control rats. |
| 5782 | 19215684 | Four weeks after the induction of diabetes, TSP-1 and TGF-beta expression was significantly increased in the kidneys of diabetic rats compared with the control and was significantly lower in cilostazol-treated diabetic rats than in the untreated diabetic rats. |
| 5783 | 19215684 | In conclusion, this study indicates that cilostazol treatment of diabetic rats effectively prevents pathological kidney changes, possibly via the down-regulation of TSP-1 and TGF-beta expression compared with untreated rats. |
| 5784 | 19215684 | The renal protective effects of cilostazol on suppressing pathogenic thrombospondin-1 and transforming growth factor-beta expression in streptozotocin-induced diabetic rats. |
| 5785 | 19215684 | Expression of thrombospondin-1 (TSP-1) and transforming growth factor-beta (TGF-beta) in the kidney was measured by immunohistochemistry and real-time reverse transcription-quantitative polymerase chain reaction analysis in diabetic rats, cilostazol-treated diabetic rats and control rats. |
| 5786 | 19215684 | Four weeks after the induction of diabetes, TSP-1 and TGF-beta expression was significantly increased in the kidneys of diabetic rats compared with the control and was significantly lower in cilostazol-treated diabetic rats than in the untreated diabetic rats. |
| 5787 | 19215684 | In conclusion, this study indicates that cilostazol treatment of diabetic rats effectively prevents pathological kidney changes, possibly via the down-regulation of TSP-1 and TGF-beta expression compared with untreated rats. |
| 5788 | 19246639 | Additionally, hydralazine did not reduce expression levels of either tubulointerstitial thrombospondin-1 or transforming growth factor-beta despite controlling blood pressure. |
| 5789 | 19246639 | On the other hand, the critical role of high glucose levels on the development of tubulointerstitial injury was suggested by the observation that serum glucose levels were correlated with tubulointerstitial injury, as well as with the expression levels of both transforming growth factor-beta and thrombospondin-1. |
| 5790 | 19246639 | These data suggest that glomerular injury is dependent on systemic blood pressure, whereas hyperglycemia may have a more important role in tubulointerstitial injury, possibly due to the stimulation of the thrombospondin-1-transforming growth factor-beta pathway in diabetic eNOSKO mice. |
| 5791 | 19246639 | Additionally, hydralazine did not reduce expression levels of either tubulointerstitial thrombospondin-1 or transforming growth factor-beta despite controlling blood pressure. |
| 5792 | 19246639 | On the other hand, the critical role of high glucose levels on the development of tubulointerstitial injury was suggested by the observation that serum glucose levels were correlated with tubulointerstitial injury, as well as with the expression levels of both transforming growth factor-beta and thrombospondin-1. |
| 5793 | 19246639 | These data suggest that glomerular injury is dependent on systemic blood pressure, whereas hyperglycemia may have a more important role in tubulointerstitial injury, possibly due to the stimulation of the thrombospondin-1-transforming growth factor-beta pathway in diabetic eNOSKO mice. |
| 5794 | 19246639 | Additionally, hydralazine did not reduce expression levels of either tubulointerstitial thrombospondin-1 or transforming growth factor-beta despite controlling blood pressure. |
| 5795 | 19246639 | On the other hand, the critical role of high glucose levels on the development of tubulointerstitial injury was suggested by the observation that serum glucose levels were correlated with tubulointerstitial injury, as well as with the expression levels of both transforming growth factor-beta and thrombospondin-1. |
| 5796 | 19246639 | These data suggest that glomerular injury is dependent on systemic blood pressure, whereas hyperglycemia may have a more important role in tubulointerstitial injury, possibly due to the stimulation of the thrombospondin-1-transforming growth factor-beta pathway in diabetic eNOSKO mice. |
| 5797 | 19275608 | The main pathophysiological mechanisms associated with diabetic nephropathy result from activation of the renin-angiotensin-aldosterone system (RAAS), protein kinase C pathway, pro-inflammatory cytokines and various growth factors. |
| 5798 | 19275608 | Angiotensin II and transforming growth factor-beta (TGF-beta) are two important molecular mediators. |
| 5799 | 19279557 | Circulating transforming growth factor-beta1 levels and the risk for kidney disease in African Americans. |
| 5800 | 19279557 | Transforming growth factor-beta1 (TGF-beta1) is known to induce progression of experimental renal disease. |
| 5801 | 19279557 | Serum TGF-beta1 protein levels were positively and significantly associated with plasma renin activity along with the systolic and diastolic blood pressure in blacks but not whites after controlling for age, gender, and body mass index. |
| 5802 | 19279557 | Circulating transforming growth factor-beta1 levels and the risk for kidney disease in African Americans. |
| 5803 | 19279557 | Transforming growth factor-beta1 (TGF-beta1) is known to induce progression of experimental renal disease. |
| 5804 | 19279557 | Serum TGF-beta1 protein levels were positively and significantly associated with plasma renin activity along with the systolic and diastolic blood pressure in blacks but not whites after controlling for age, gender, and body mass index. |
| 5805 | 19279557 | Circulating transforming growth factor-beta1 levels and the risk for kidney disease in African Americans. |
| 5806 | 19279557 | Transforming growth factor-beta1 (TGF-beta1) is known to induce progression of experimental renal disease. |
| 5807 | 19279557 | Serum TGF-beta1 protein levels were positively and significantly associated with plasma renin activity along with the systolic and diastolic blood pressure in blacks but not whites after controlling for age, gender, and body mass index. |
| 5808 | 19281773 | Besides the expected increases in insulin, glucagon, and duct markers (mucin 6, aquaporin 1 and 5), the beta cell auto-antigen IA-2/phogrin was increased 5-fold in Differentiated. |
| 5809 | 19281773 | In addition, developmentally important pathways, including notch/jagged, Wnt/frizzled, TGFbeta superfamily (follistatin, BMPs, and SMADs), and retinoic acid (COUP-TFI, CRABP1, 2, and RAIG1) were differentially regulated during the expansion/differentiation. |
| 5810 | 19281773 | Two putative markers for islet precursor cells, UCHL1/PGP9.5 and DMBT1, were enhanced during the progression to differentiated cells, but only the latter could be a marker of islet precursor cells. |
| 5811 | 19332876 | Loss of STAT5 causes liver fibrosis and cancer development through increased TGF-{beta} and STAT3 activation. |
| 5812 | 19332876 | Transforming growth factor (TGF)-beta levels and STAT3 activity were elevated in liver tissue from STAT5-LKO mice upon CCl(4) treatment. |
| 5813 | 19332876 | To define the molecular link between STAT5 silencing and TGF-beta up-regulation, as well as STAT3 activation, we examined STAT5-null mouse embryonic fibroblasts and primary hepatocytes. |
| 5814 | 19332876 | Protease inhibitor studies revealed that STAT5 deficiency enhanced the stability of mature TGF-beta. |
| 5815 | 19332876 | Immunoprecipitation and immunohistochemistry analyses demonstrated that STAT5, through its N-terminal sequences, could bind to TGF-beta and that retroviral-mediated overexpression of STAT5 decreased TGF-beta levels. |
| 5816 | 19332876 | To confirm the in vivo significance of the N-terminal domain of STAT5, we treated mice that expressed STAT5 lacking the N terminus (STAT5-DeltaN) with CCl(4). |
| 5817 | 19332876 | In conclusion, loss of STAT5 results in elevated TGF-beta levels and enhanced growth hormone-induced STAT3 activity. |
| 5818 | 19332876 | Loss of STAT5 causes liver fibrosis and cancer development through increased TGF-{beta} and STAT3 activation. |
| 5819 | 19332876 | Transforming growth factor (TGF)-beta levels and STAT3 activity were elevated in liver tissue from STAT5-LKO mice upon CCl(4) treatment. |
| 5820 | 19332876 | To define the molecular link between STAT5 silencing and TGF-beta up-regulation, as well as STAT3 activation, we examined STAT5-null mouse embryonic fibroblasts and primary hepatocytes. |
| 5821 | 19332876 | Protease inhibitor studies revealed that STAT5 deficiency enhanced the stability of mature TGF-beta. |
| 5822 | 19332876 | Immunoprecipitation and immunohistochemistry analyses demonstrated that STAT5, through its N-terminal sequences, could bind to TGF-beta and that retroviral-mediated overexpression of STAT5 decreased TGF-beta levels. |
| 5823 | 19332876 | To confirm the in vivo significance of the N-terminal domain of STAT5, we treated mice that expressed STAT5 lacking the N terminus (STAT5-DeltaN) with CCl(4). |
| 5824 | 19332876 | In conclusion, loss of STAT5 results in elevated TGF-beta levels and enhanced growth hormone-induced STAT3 activity. |
| 5825 | 19332876 | Loss of STAT5 causes liver fibrosis and cancer development through increased TGF-{beta} and STAT3 activation. |
| 5826 | 19332876 | Transforming growth factor (TGF)-beta levels and STAT3 activity were elevated in liver tissue from STAT5-LKO mice upon CCl(4) treatment. |
| 5827 | 19332876 | To define the molecular link between STAT5 silencing and TGF-beta up-regulation, as well as STAT3 activation, we examined STAT5-null mouse embryonic fibroblasts and primary hepatocytes. |
| 5828 | 19332876 | Protease inhibitor studies revealed that STAT5 deficiency enhanced the stability of mature TGF-beta. |
| 5829 | 19332876 | Immunoprecipitation and immunohistochemistry analyses demonstrated that STAT5, through its N-terminal sequences, could bind to TGF-beta and that retroviral-mediated overexpression of STAT5 decreased TGF-beta levels. |
| 5830 | 19332876 | To confirm the in vivo significance of the N-terminal domain of STAT5, we treated mice that expressed STAT5 lacking the N terminus (STAT5-DeltaN) with CCl(4). |
| 5831 | 19332876 | In conclusion, loss of STAT5 results in elevated TGF-beta levels and enhanced growth hormone-induced STAT3 activity. |
| 5832 | 19332876 | Loss of STAT5 causes liver fibrosis and cancer development through increased TGF-{beta} and STAT3 activation. |
| 5833 | 19332876 | Transforming growth factor (TGF)-beta levels and STAT3 activity were elevated in liver tissue from STAT5-LKO mice upon CCl(4) treatment. |
| 5834 | 19332876 | To define the molecular link between STAT5 silencing and TGF-beta up-regulation, as well as STAT3 activation, we examined STAT5-null mouse embryonic fibroblasts and primary hepatocytes. |
| 5835 | 19332876 | Protease inhibitor studies revealed that STAT5 deficiency enhanced the stability of mature TGF-beta. |
| 5836 | 19332876 | Immunoprecipitation and immunohistochemistry analyses demonstrated that STAT5, through its N-terminal sequences, could bind to TGF-beta and that retroviral-mediated overexpression of STAT5 decreased TGF-beta levels. |
| 5837 | 19332876 | To confirm the in vivo significance of the N-terminal domain of STAT5, we treated mice that expressed STAT5 lacking the N terminus (STAT5-DeltaN) with CCl(4). |
| 5838 | 19332876 | In conclusion, loss of STAT5 results in elevated TGF-beta levels and enhanced growth hormone-induced STAT3 activity. |
| 5839 | 19357234 | Smad2 and 3 transcription factors control muscle mass in adulthood. |
| 5840 | 19357234 | Smad2 and Smad3 are the transcription factors downstream of myostatin/TGF-beta and induce an atrophy program that is muscle RING-finger protein 1 (MuRF1) independent. |
| 5841 | 19357234 | Thus myostatin and Akt pathways cross-talk at different levels. |
| 5842 | 19357722 | The expression of inflammatory markers, IL-6, MCP-1, and activated NF-kappaB; type IV collagen, TGF-beta, and ICAM-1 mRNA; or type IV collagen and TGF-beta protein, were all found to be significantly less in glomeruli isolated from diabetic SA/- mice, as compared with diabetic SA/+ mice. |
| 5843 | 19375583 | Effects of alpha-lipoic acid on transforming growth factor beta1-p38 mitogen-activated protein kinase-fibronectin pathway in diabetic nephropathy. |
| 5844 | 19375583 | In diabetic nephropathy, transforming growth factor beta1 (TGFbeta1) is related to p38 mitogen-activated protein kinase (MAPK) that induces production of fibronectin in mesangial cells. |
| 5845 | 19375583 | Phospho-form but not total-form levels as well as fold activations of each protein consisting of p38 MAPK pathway were also attenuated. |
| 5846 | 19375583 | These results suggest that ALA ameliorates proteinuria by attenuating expressions of TGFbeta1 and fibronectin proteins, and these favorable effects are related to inhibition of phosphorylating activation of p38 MAPK pathway in renal cortex of OLETF rats. |
| 5847 | 19375583 | Effects of alpha-lipoic acid on transforming growth factor beta1-p38 mitogen-activated protein kinase-fibronectin pathway in diabetic nephropathy. |
| 5848 | 19375583 | In diabetic nephropathy, transforming growth factor beta1 (TGFbeta1) is related to p38 mitogen-activated protein kinase (MAPK) that induces production of fibronectin in mesangial cells. |
| 5849 | 19375583 | Phospho-form but not total-form levels as well as fold activations of each protein consisting of p38 MAPK pathway were also attenuated. |
| 5850 | 19375583 | These results suggest that ALA ameliorates proteinuria by attenuating expressions of TGFbeta1 and fibronectin proteins, and these favorable effects are related to inhibition of phosphorylating activation of p38 MAPK pathway in renal cortex of OLETF rats. |
| 5851 | 19395281 | Endoglin is an accessory receptor molecule that, in association with transforming growth factor beta (TGF-beta) family receptors Types I and II, binds TGF-beta1, TGF-beta3, activin A, bone morphogenetic protein (BMP)-2 and BMP-7, regulating TGF-beta dependent cellular responses. |
| 5852 | 19452424 | Transforming growth factor beta, connective tissue growth factor, vascular endothelial growth factor, growth hormone and insulin-like growth factors are among those best known and investigated. |
| 5853 | 19452424 | There are also data, even though limited, on the involvement of other two growth factors, epidermal growth factor and platelet derived growth factor, in the pathogenesis of DN. |
| 5854 | 19470878 | Growth-differentiation factor 15 (GDF-15), a stress-responsive transforming growth factor-beta-related cytokine, is emerging as a new risk marker in patients with cardiovascular disease. |
| 5855 | 19472102 | In contrast, IL-10 and IL-5 were decreased in this group. |
| 5856 | 19472102 | We observed different "reactivity pattern" to H.PYLORI within groups with low basal cytokine and chemokine production in healthy H.PYLORI negative controls but with clear specific response in IFN-gamma and TGF-beta production in this group. |
| 5857 | 19493965 | Treatment with 0.75 mg/day DHT attenuated castration-associated increases in urine albumin excretion (DHT(0), 81.2 +/- 18.1; DHT(0.75), 26.57 +/- 5.8 mg/day; P < 0.05), glomerulosclerosis (DHT(0), 1.1 +/- 0.79; DHT(0.75), 0.43 +/- 0.043 arbitrary units; P < 0.001), tubulointerstitial fibrosis (DHT(0), 1.3 +/- 0.12; DHT(0.75), 1.1 +/- 0.096 AU; P < 0.05), collagen type IV [DHT(0), 3.2 +/- 0.11; DHT(0.75), 2.1 +/- 0.070 relative optical density (ROD); P < 0.01], transforming growth factor-beta (DHT(0), 3.2 +/- 0.16; DHT(0.75), 2.1 +/- 0.060 ROD; P < 0.01), IL-6 (DHT(0), 0.37 +/- 0.011; DHT(0.75), 0.27 +/- 0.014 ROD; P < 0.05), and protein expression and reduced CD68-positive cell abundance (DHT(0), 17 +/- 0.86; DHT(0.75), 4.4 +/- 0.55 cells/mm(2); P < 0.001). |
| 5858 | 19543271 | TGF-beta activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. |
| 5859 | 19543271 | Akt kinase is activated by transforming growth factor-beta1 (TGF-beta) in diabetic kidneys, and has important roles in fibrosis, hypertrophy and cell survival in glomerular mesangial cells. |
| 5860 | 19543271 | However, the mechanisms of Akt activation by TGF-beta are not fully understood. |
| 5861 | 19543271 | Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation. |
| 5862 | 19543271 | The RP23 promoter was activated by TGF-beta and miR-192 through E-box-regulated mechanisms, as shown previously. |
| 5863 | 19543271 | Akt activation by these miRs led to glomerular mesangial cell survival and hypertrophy, which were similar to the effects of activation by TGF-beta. |
| 5864 | 19543271 | These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta. |
| 5865 | 19543271 | TGF-beta activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. |
| 5866 | 19543271 | Akt kinase is activated by transforming growth factor-beta1 (TGF-beta) in diabetic kidneys, and has important roles in fibrosis, hypertrophy and cell survival in glomerular mesangial cells. |
| 5867 | 19543271 | However, the mechanisms of Akt activation by TGF-beta are not fully understood. |
| 5868 | 19543271 | Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation. |
| 5869 | 19543271 | The RP23 promoter was activated by TGF-beta and miR-192 through E-box-regulated mechanisms, as shown previously. |
| 5870 | 19543271 | Akt activation by these miRs led to glomerular mesangial cell survival and hypertrophy, which were similar to the effects of activation by TGF-beta. |
| 5871 | 19543271 | These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta. |
| 5872 | 19543271 | TGF-beta activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. |
| 5873 | 19543271 | Akt kinase is activated by transforming growth factor-beta1 (TGF-beta) in diabetic kidneys, and has important roles in fibrosis, hypertrophy and cell survival in glomerular mesangial cells. |
| 5874 | 19543271 | However, the mechanisms of Akt activation by TGF-beta are not fully understood. |
| 5875 | 19543271 | Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation. |
| 5876 | 19543271 | The RP23 promoter was activated by TGF-beta and miR-192 through E-box-regulated mechanisms, as shown previously. |
| 5877 | 19543271 | Akt activation by these miRs led to glomerular mesangial cell survival and hypertrophy, which were similar to the effects of activation by TGF-beta. |
| 5878 | 19543271 | These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta. |
| 5879 | 19543271 | TGF-beta activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. |
| 5880 | 19543271 | Akt kinase is activated by transforming growth factor-beta1 (TGF-beta) in diabetic kidneys, and has important roles in fibrosis, hypertrophy and cell survival in glomerular mesangial cells. |
| 5881 | 19543271 | However, the mechanisms of Akt activation by TGF-beta are not fully understood. |
| 5882 | 19543271 | Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation. |
| 5883 | 19543271 | The RP23 promoter was activated by TGF-beta and miR-192 through E-box-regulated mechanisms, as shown previously. |
| 5884 | 19543271 | Akt activation by these miRs led to glomerular mesangial cell survival and hypertrophy, which were similar to the effects of activation by TGF-beta. |
| 5885 | 19543271 | These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta. |
| 5886 | 19543271 | TGF-beta activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. |
| 5887 | 19543271 | Akt kinase is activated by transforming growth factor-beta1 (TGF-beta) in diabetic kidneys, and has important roles in fibrosis, hypertrophy and cell survival in glomerular mesangial cells. |
| 5888 | 19543271 | However, the mechanisms of Akt activation by TGF-beta are not fully understood. |
| 5889 | 19543271 | Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation. |
| 5890 | 19543271 | The RP23 promoter was activated by TGF-beta and miR-192 through E-box-regulated mechanisms, as shown previously. |
| 5891 | 19543271 | Akt activation by these miRs led to glomerular mesangial cell survival and hypertrophy, which were similar to the effects of activation by TGF-beta. |
| 5892 | 19543271 | These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta. |
| 5893 | 19543271 | TGF-beta activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. |
| 5894 | 19543271 | Akt kinase is activated by transforming growth factor-beta1 (TGF-beta) in diabetic kidneys, and has important roles in fibrosis, hypertrophy and cell survival in glomerular mesangial cells. |
| 5895 | 19543271 | However, the mechanisms of Akt activation by TGF-beta are not fully understood. |
| 5896 | 19543271 | Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation. |
| 5897 | 19543271 | The RP23 promoter was activated by TGF-beta and miR-192 through E-box-regulated mechanisms, as shown previously. |
| 5898 | 19543271 | Akt activation by these miRs led to glomerular mesangial cell survival and hypertrophy, which were similar to the effects of activation by TGF-beta. |
| 5899 | 19543271 | These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta. |
| 5900 | 19543271 | TGF-beta activates Akt kinase through a microRNA-dependent amplifying circuit targeting PTEN. |
| 5901 | 19543271 | Akt kinase is activated by transforming growth factor-beta1 (TGF-beta) in diabetic kidneys, and has important roles in fibrosis, hypertrophy and cell survival in glomerular mesangial cells. |
| 5902 | 19543271 | However, the mechanisms of Akt activation by TGF-beta are not fully understood. |
| 5903 | 19543271 | Here we show that TGF-beta activates Akt in glomerular mesangial cells by inducing the microRNAs (miRNAs) miR-216a and miR-217, both of which target PTEN (phosphatase and tensin homologue), an inhibitor of Akt activation. |
| 5904 | 19543271 | The RP23 promoter was activated by TGF-beta and miR-192 through E-box-regulated mechanisms, as shown previously. |
| 5905 | 19543271 | Akt activation by these miRs led to glomerular mesangial cell survival and hypertrophy, which were similar to the effects of activation by TGF-beta. |
| 5906 | 19543271 | These studies reveal a mechanism of Akt activation through PTEN downregulation by two miRs, which are regulated by upstream miR-192 and TGF-beta. |
| 5907 | 19553350 | Histone deacetylase-2 is a key regulator of diabetes- and transforming growth factor-beta1-induced renal injury. |
| 5908 | 19553350 | This study examined the effect of HDAC inhibition on renal fibrosis induced by diabetes or transforming growth factor (TGF)-beta1 and determined the role of reactive oxygen species (ROS) as mediators of HDAC activation. |
| 5909 | 19553350 | Among the six HDACs tested (HDAC-1 through -5 and HDAC-8), HDAC-2 activity significantly increased in the kidneys of STZ-induced diabetic rats and db/db mice and TGF-beta1-treated NRK52-E cells. |
| 5910 | 19553350 | Levels of mRNA expression of fibronectin and alpha-smooth muscle actin were decreased, whereas E-cadherin mRNA was increased when HDAC-2 was knocked down using RNA interference in NRK52-E cells. |
| 5911 | 19578007 | In mouse mesangial cells, PFD decreased TGF-beta promoter activity, reduced TGF-beta protein secretion, and inhibited TGF-beta-induced Smad2-phosphorylation, 3TP-lux promoter activity, and generation of reactive oxygen species. |
| 5912 | 19580379 | We have investigated the role of transcription and translation on the GAG hyper-elongation effect of platelet-derived growth factor (PDGF) in human vascular smooth muscle cells (VSMCs). |
| 5913 | 19580379 | To determine if the response involves specific signalling pathways or the process of GAG hyper-elongation we have also investigated the effects of epidermal growth factor (EGF), transforming growth factor-beta (TGF-beta) and thrombin. |
| 5914 | 19582775 | Role of Smad3, acting independently of transforming growth factor-beta, in the early induction of Wnt-beta-catenin signaling by parathyroid hormone in mouse osteoblastic cells. |
| 5915 | 19582775 | We showed previously that PTH interacts with the canonical Wnt-beta-catenin signaling pathway via the transforming growth factor (TGF)-beta signaling molecule, Smad3, to modulate osteoblast differentiation and apoptosis. |
| 5916 | 19582775 | Here, we examined which actions of Smad3 are TGF-beta-independent in stimulating the osteoblast phenotype and PTH-induced Wnt-beta-catenin signaling. |
| 5917 | 19582775 | For this, the TGF-beta receptor type 1 [activin receptor-like kinase (ALK5)] inhibitor (SB431542), and a Smad3 mutant in which the site normally phosphorylated by ALK5 is mutated from SSVS to AAVA, was used. |
| 5918 | 19582775 | PTH induced total beta-catenin and reduced phosphorylated beta-catenin levels at 1, 6, and 24 h in mouse osteoblastic MC3T3-E1 cells. |
| 5919 | 19582775 | Transient transfection of Smad3AAVA inhibited the PTH induction of total beta-catenin and reduction of phosphorylated beta-catenin levels at 6 and 24 h, but not at 1 h, indicating that the early effects occur independently of TGF-beta receptor signaling. |
| 5920 | 19582775 | On the other hand, MC3T3-E1 cell clones in which Smad3AAVA was stably expressed demonstrated elevated beta-catenin levels, although alkaline phosphatase (ALP) activity and mineralization were unaltered. |
| 5921 | 19582775 | In contrast, MC3T3-E1 cell clones in which wild-type Smad3 was stably expressed exhibited increased ALP activity and mineralization that were decreased by the ALK5 inhibitor, SB431542, although the beta-catenin levels induced in these cells were not modulated. |
| 5922 | 19582775 | In conclusion, the present study indicates that PTH induces osteoblast beta-catenin levels via Smad3 independently of, and dependently on, TGF-beta in the early and later induction phases, respectively. |
| 5923 | 19582775 | Role of Smad3, acting independently of transforming growth factor-beta, in the early induction of Wnt-beta-catenin signaling by parathyroid hormone in mouse osteoblastic cells. |
| 5924 | 19582775 | We showed previously that PTH interacts with the canonical Wnt-beta-catenin signaling pathway via the transforming growth factor (TGF)-beta signaling molecule, Smad3, to modulate osteoblast differentiation and apoptosis. |
| 5925 | 19582775 | Here, we examined which actions of Smad3 are TGF-beta-independent in stimulating the osteoblast phenotype and PTH-induced Wnt-beta-catenin signaling. |
| 5926 | 19582775 | For this, the TGF-beta receptor type 1 [activin receptor-like kinase (ALK5)] inhibitor (SB431542), and a Smad3 mutant in which the site normally phosphorylated by ALK5 is mutated from SSVS to AAVA, was used. |
| 5927 | 19582775 | PTH induced total beta-catenin and reduced phosphorylated beta-catenin levels at 1, 6, and 24 h in mouse osteoblastic MC3T3-E1 cells. |
| 5928 | 19582775 | Transient transfection of Smad3AAVA inhibited the PTH induction of total beta-catenin and reduction of phosphorylated beta-catenin levels at 6 and 24 h, but not at 1 h, indicating that the early effects occur independently of TGF-beta receptor signaling. |
| 5929 | 19582775 | On the other hand, MC3T3-E1 cell clones in which Smad3AAVA was stably expressed demonstrated elevated beta-catenin levels, although alkaline phosphatase (ALP) activity and mineralization were unaltered. |
| 5930 | 19582775 | In contrast, MC3T3-E1 cell clones in which wild-type Smad3 was stably expressed exhibited increased ALP activity and mineralization that were decreased by the ALK5 inhibitor, SB431542, although the beta-catenin levels induced in these cells were not modulated. |
| 5931 | 19582775 | In conclusion, the present study indicates that PTH induces osteoblast beta-catenin levels via Smad3 independently of, and dependently on, TGF-beta in the early and later induction phases, respectively. |
| 5932 | 19582775 | Role of Smad3, acting independently of transforming growth factor-beta, in the early induction of Wnt-beta-catenin signaling by parathyroid hormone in mouse osteoblastic cells. |
| 5933 | 19582775 | We showed previously that PTH interacts with the canonical Wnt-beta-catenin signaling pathway via the transforming growth factor (TGF)-beta signaling molecule, Smad3, to modulate osteoblast differentiation and apoptosis. |
| 5934 | 19582775 | Here, we examined which actions of Smad3 are TGF-beta-independent in stimulating the osteoblast phenotype and PTH-induced Wnt-beta-catenin signaling. |
| 5935 | 19582775 | For this, the TGF-beta receptor type 1 [activin receptor-like kinase (ALK5)] inhibitor (SB431542), and a Smad3 mutant in which the site normally phosphorylated by ALK5 is mutated from SSVS to AAVA, was used. |
| 5936 | 19582775 | PTH induced total beta-catenin and reduced phosphorylated beta-catenin levels at 1, 6, and 24 h in mouse osteoblastic MC3T3-E1 cells. |
| 5937 | 19582775 | Transient transfection of Smad3AAVA inhibited the PTH induction of total beta-catenin and reduction of phosphorylated beta-catenin levels at 6 and 24 h, but not at 1 h, indicating that the early effects occur independently of TGF-beta receptor signaling. |
| 5938 | 19582775 | On the other hand, MC3T3-E1 cell clones in which Smad3AAVA was stably expressed demonstrated elevated beta-catenin levels, although alkaline phosphatase (ALP) activity and mineralization were unaltered. |
| 5939 | 19582775 | In contrast, MC3T3-E1 cell clones in which wild-type Smad3 was stably expressed exhibited increased ALP activity and mineralization that were decreased by the ALK5 inhibitor, SB431542, although the beta-catenin levels induced in these cells were not modulated. |
| 5940 | 19582775 | In conclusion, the present study indicates that PTH induces osteoblast beta-catenin levels via Smad3 independently of, and dependently on, TGF-beta in the early and later induction phases, respectively. |
| 5941 | 19582775 | Role of Smad3, acting independently of transforming growth factor-beta, in the early induction of Wnt-beta-catenin signaling by parathyroid hormone in mouse osteoblastic cells. |
| 5942 | 19582775 | We showed previously that PTH interacts with the canonical Wnt-beta-catenin signaling pathway via the transforming growth factor (TGF)-beta signaling molecule, Smad3, to modulate osteoblast differentiation and apoptosis. |
| 5943 | 19582775 | Here, we examined which actions of Smad3 are TGF-beta-independent in stimulating the osteoblast phenotype and PTH-induced Wnt-beta-catenin signaling. |
| 5944 | 19582775 | For this, the TGF-beta receptor type 1 [activin receptor-like kinase (ALK5)] inhibitor (SB431542), and a Smad3 mutant in which the site normally phosphorylated by ALK5 is mutated from SSVS to AAVA, was used. |
| 5945 | 19582775 | PTH induced total beta-catenin and reduced phosphorylated beta-catenin levels at 1, 6, and 24 h in mouse osteoblastic MC3T3-E1 cells. |
| 5946 | 19582775 | Transient transfection of Smad3AAVA inhibited the PTH induction of total beta-catenin and reduction of phosphorylated beta-catenin levels at 6 and 24 h, but not at 1 h, indicating that the early effects occur independently of TGF-beta receptor signaling. |
| 5947 | 19582775 | On the other hand, MC3T3-E1 cell clones in which Smad3AAVA was stably expressed demonstrated elevated beta-catenin levels, although alkaline phosphatase (ALP) activity and mineralization were unaltered. |
| 5948 | 19582775 | In contrast, MC3T3-E1 cell clones in which wild-type Smad3 was stably expressed exhibited increased ALP activity and mineralization that were decreased by the ALK5 inhibitor, SB431542, although the beta-catenin levels induced in these cells were not modulated. |
| 5949 | 19582775 | In conclusion, the present study indicates that PTH induces osteoblast beta-catenin levels via Smad3 independently of, and dependently on, TGF-beta in the early and later induction phases, respectively. |
| 5950 | 19586629 | Cilostazol inhibits high glucose- and angiotensin II-induced type 1 plasminogen activator inhibitor expression in artery wall and neointimal region after vascular injury. |
| 5951 | 19586629 | We found that cilostazol effectively inhibits angiotensin II-, high glucose- and TGF-beta-stimulated PAI-1 expression in vivo and in vitro. |
| 5952 | 19586629 | Cilostazol inhibited PAI-1 expression by multiple mechanisms including downregulation of TGF-beta, JNK and p38 signaling pathways. |
| 5953 | 19586629 | Cilostazol also inhibited transactivating activity at the PAI-1 promoter by Smad3, leading to a suppression of PAI-1 gene transcription. |
| 5954 | 19592635 | Transforming growth factor-beta1 and incident type 2 diabetes: results from the MONICA/KORA case-cohort study, 1984-2002. |
| 5955 | 19605553 | Body and kidney weight, blood glucose, glycated hemoglobin, urinary albumin and creatinine excretions were monitored. |
| 5956 | 19605553 | Kidney histopathology, collagen accumulation, fibrinogen and transforming growth factor-beta 1 (TGF-β1) expression were also examined. |
| 5957 | 19605949 | Real time PCR was used to investigate the expression of transforming growth factor beta1 (TGFbeta1) and atrial natriuretic peptide. |
| 5958 | 19617014 | Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist inhibits transforming growth factor-beta1 and matrix production in human dermal fibroblasts. |
| 5959 | 19617014 | The mRNA expressions of TGF-beta1, collagen I (Col I) and fibronectin (FN) were determined by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). |
| 5960 | 19617014 | The protein of transforming growth factor-beta1 (TGF-beta1) was determined by enzyme-linked immunosorbent assay (ELISA) and proteins of Col I and FN were determined by Western blotting. |
| 5961 | 19617014 | Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist inhibits transforming growth factor-beta1 and matrix production in human dermal fibroblasts. |
| 5962 | 19617014 | The mRNA expressions of TGF-beta1, collagen I (Col I) and fibronectin (FN) were determined by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). |
| 5963 | 19617014 | The protein of transforming growth factor-beta1 (TGF-beta1) was determined by enzyme-linked immunosorbent assay (ELISA) and proteins of Col I and FN were determined by Western blotting. |
| 5964 | 19617014 | Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) agonist inhibits transforming growth factor-beta1 and matrix production in human dermal fibroblasts. |
| 5965 | 19617014 | The mRNA expressions of TGF-beta1, collagen I (Col I) and fibronectin (FN) were determined by quantitative real-time reverse transcription polymerase chain reaction (RT-PCR). |
| 5966 | 19617014 | The protein of transforming growth factor-beta1 (TGF-beta1) was determined by enzyme-linked immunosorbent assay (ELISA) and proteins of Col I and FN were determined by Western blotting. |
| 5967 | 19617408 | The p38 mitogen-activated protein kinase (MAPK) is activated during heart diseases that might be associated with myocardial damage and cardiac remodeling process. |
| 5968 | 19617408 | The purpose of this study was to investigate the role of p38alpha MAPK after experimental diabetes by using transgenic (TG) mice with cardiac-specific expression of a dominant-negative mutant form of p38alpha MAPK. |
| 5969 | 19617408 | In addition, diabetic TG mice had reduced cardiac myocyte diameter, content of cardiac fibrosis, LV tissue expressions of atrial natriuretic peptide, transforming growth factor beta1, and collagen III compared with diabetic NTG mice. |
| 5970 | 19617408 | Moreover, LV expression of NADPH oxidase subunits, p22(phox), p67(phox), gp91(phox), and Nox4, reactive oxygen species and lipid peroxidation levels were significantly increased in diabetic NTG mice, but not in diabetic TG mice. |
| 5971 | 19617408 | Furthermore, myocardial apoptosis, the number of caspase-3-positive cells, and the downregulation of antiapoptotic protein Bcl-X(L) were less in diabetic TG mice compared with diabetic NTG mice. |
| 5972 | 19617408 | In conclusion, our data establish that p38alpha MAPK activity is required for cardiac remodeling after diabetes induction and suggest that p38alpha MAPK may promote cardiomyocyte apoptosis by downregulation of Bcl-X(L). |
| 5973 | 19639539 | The more powerful effects of rhein on decreasing transforming growth factor-beta1 (TGF-beta1) and fibronectin immunohistochemistry expression in renal tissue were also observed. |
| 5974 | 19639539 | And the plasma levels of cholesterol (Chol), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and ApoE all decreased in both the rhein and the simvastatin groups. |
| 5975 | 19644810 | Results showed that astilbin inhibited high glucose stimulated HK-2 cell production of transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) in vitro, especially CTGF; analogic results was also found in vivo. |
| 5976 | 19644810 | Astilbin can exert an early renal protective role to DN, inhibit production of TGF-beta1 and especially of CTGF. |
| 5977 | 19644810 | Results showed that astilbin inhibited high glucose stimulated HK-2 cell production of transforming growth factor-beta1 (TGF-beta1) and connective tissue growth factor (CTGF) in vitro, especially CTGF; analogic results was also found in vivo. |
| 5978 | 19644810 | Astilbin can exert an early renal protective role to DN, inhibit production of TGF-beta1 and especially of CTGF. |
| 5979 | 19652382 | Losartan treatment also down-regulated transforming growth factor-beta1 expression and attenuated the increased expression levels of p22(phox) and Nox4. |
| 5980 | 19657322 | Transforming growth factor-beta2 upregulates sphingosine kinase-1 activity, which in turn attenuates the fibrotic response to TGF-beta2 by impeding CTGF expression. |
| 5981 | 19657322 | Transforming growth factor-beta2 (TGF-beta2) stimulates the expression of pro-fibrotic connective tissue growth factor (CTGF) during the course of renal disease. |
| 5982 | 19657322 | Because sphingosine kinase-1 (SK-1) activity is also upregulated by TGF-beta, we studied its effect on CTGF expression and on the development of renal fibrosis. |
| 5983 | 19657322 | Over-expression of SK-1 reduced CTGF induction, an effect mediated by intracellular sphingosine-1-phosphate. |
| 5984 | 19657322 | Similarly, in a mouse model of streptozotocin-induced diabetic nephropathy, SK-1 and CTGF were upregulated in podocytes. |
| 5985 | 19690518 | Efficacy was associated with an expansion of bystander suppressor regulatory T cells (Tregs) recognizing the C-terminal region of GAD65 and secreting interleukin-10 (IL-10), transforming growth factor-beta (TGF-beta), and interferon-gamma (IFN-gamma). |
| 5986 | 19690518 | In addition, we found that frequency and epitope specificity of GAD65-reactive CD4(+) T cells during antigen priming at diabetes onset and Tregs detected after CT correlated. |
| 5987 | 19690518 | Consequently, NOD mice harbored significantly lower levels of GAD65-reactive CD4(+) T cells than RIP-LCMV-GP before and after treatment. |
| 5988 | 19786738 | Positive feedback loop between plasminogen activator inhibitor-1 and transforming growth factor-beta1 during renal fibrosis in diabetes. |
| 5989 | 19816015 | Calcium-phosphate product (Ca x P), body mass index (BMI), fetuin-A, osteoprotegerin (OPG), osteopontin, transforming growth factor-beta1 (TGF-beta1), fibroblast growth factor-23 (FGF-23) and matrix Gla protein (MGP) were considered. |
| 5990 | 19816015 | Multivariate regression analysis, adjusted for age and for dialysis vintage, showed that TGF-beta1, OPG and days with Ca x P >55 mg/dl are independent predictors of CAC, while MGP was shown to be a protective factor. |
| 5991 | 19816015 | Calcium-phosphate product (Ca x P), body mass index (BMI), fetuin-A, osteoprotegerin (OPG), osteopontin, transforming growth factor-beta1 (TGF-beta1), fibroblast growth factor-23 (FGF-23) and matrix Gla protein (MGP) were considered. |
| 5992 | 19816015 | Multivariate regression analysis, adjusted for age and for dialysis vintage, showed that TGF-beta1, OPG and days with Ca x P >55 mg/dl are independent predictors of CAC, while MGP was shown to be a protective factor. |
| 5993 | 19820199 | The expression of profibrotic factors, transforming growth factor-beta (TGF-beta1), connective tissue growth factor, and matrix proteins was increased, and the TGF-beta1-linked transcription factors phospho-Smad3/4 and activator protein-1 were activated in the DM1 myocardium. |
| 5994 | 19820199 | Proapoptotic molecules FasL, Fas, Bax, and cleaved caspase-3 were also augmented. |
| 5995 | 19820199 | In addition, hypertension was associated with activation of NF-kappaB, increased inflammatory cell infiltrate, and expression of the mediators [interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, monocyte chemoattractant protein 1, vascular cell adhesion molecule 1, angiotensinogen, and oxidants], which were absent in long-term DM1. |
| 5996 | 19820199 | In cultured cardiomyocytes, IL-10, TGF-beta1, and catalase blocked the glucose-stimulated expression of proinflammatory genes. |
| 5997 | 19820199 | The expression of profibrotic factors, transforming growth factor-beta (TGF-beta1), connective tissue growth factor, and matrix proteins was increased, and the TGF-beta1-linked transcription factors phospho-Smad3/4 and activator protein-1 were activated in the DM1 myocardium. |
| 5998 | 19820199 | Proapoptotic molecules FasL, Fas, Bax, and cleaved caspase-3 were also augmented. |
| 5999 | 19820199 | In addition, hypertension was associated with activation of NF-kappaB, increased inflammatory cell infiltrate, and expression of the mediators [interleukin-1beta (IL-1beta), tumor necrosis factor-alpha, monocyte chemoattractant protein 1, vascular cell adhesion molecule 1, angiotensinogen, and oxidants], which were absent in long-term DM1. |
| 6000 | 19820199 | In cultured cardiomyocytes, IL-10, TGF-beta1, and catalase blocked the glucose-stimulated expression of proinflammatory genes. |
| 6001 | 19836472 | Thus, indicating a potential novel role for GRAP in TGF-beta-induced tubule injury in diabetic kidney disease. |
| 6002 | 19854869 | Renal concentrations of TGF-beta(1), vascular endothelial growth factor, endothelin-1, TNF-alpha, monocyte chemoattractant protein-1, lipid peroxidation products, and nitrotyrosine were increased in diabetic rats, and all these changes as well as an increase in urinary TNF-alpha excretion were completely or partially prevented by ISO and GPI-15427. |
| 6003 | 19858036 | Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. |
| 6004 | 19858036 | This study was undertaken to test the hypothesis that the preventive effects of HGF may result from interventions in TGF-beta1-mediated signaling and collagen III secretion. |
| 6005 | 19858036 | We examined the expression of HGF/HGF receptor (c-Met) and TGF-beta1 in renal fibroblasts at multiple time points. |
| 6006 | 19858036 | The effects of recombinant human HGF on TGF-beta1 expression were studied by RT-PCR and Western blotting, and the levels of collagen III were measured by ELISA. |
| 6007 | 19858036 | In the high-glucose condition, the expression of HGF and c-Met in renal fibroblasts was detected as early as 6 hours following cell culture while the level of TGF-beta1 peaked at 96 hours. |
| 6008 | 19858036 | The addition of recombinant human HGF to the culture media dose-dependently inhibited TGF-beta1 mRNA expression and reduced collagen III secretion by 34%. |
| 6009 | 19858036 | These results indicate that, during hyperglycemia, HGF inhibits TGF-beta1 signaling and type III collagen activation in interstitial fibroblasts. |
| 6010 | 19858036 | Furthermore, we should recognize that changes in the balance between HGF and TGF-beta1 might be decisive in the pathogenesis of chronic renal fibrosis. |
| 6011 | 19858036 | Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. |
| 6012 | 19858036 | This study was undertaken to test the hypothesis that the preventive effects of HGF may result from interventions in TGF-beta1-mediated signaling and collagen III secretion. |
| 6013 | 19858036 | We examined the expression of HGF/HGF receptor (c-Met) and TGF-beta1 in renal fibroblasts at multiple time points. |
| 6014 | 19858036 | The effects of recombinant human HGF on TGF-beta1 expression were studied by RT-PCR and Western blotting, and the levels of collagen III were measured by ELISA. |
| 6015 | 19858036 | In the high-glucose condition, the expression of HGF and c-Met in renal fibroblasts was detected as early as 6 hours following cell culture while the level of TGF-beta1 peaked at 96 hours. |
| 6016 | 19858036 | The addition of recombinant human HGF to the culture media dose-dependently inhibited TGF-beta1 mRNA expression and reduced collagen III secretion by 34%. |
| 6017 | 19858036 | These results indicate that, during hyperglycemia, HGF inhibits TGF-beta1 signaling and type III collagen activation in interstitial fibroblasts. |
| 6018 | 19858036 | Furthermore, we should recognize that changes in the balance between HGF and TGF-beta1 might be decisive in the pathogenesis of chronic renal fibrosis. |
| 6019 | 19858036 | Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. |
| 6020 | 19858036 | This study was undertaken to test the hypothesis that the preventive effects of HGF may result from interventions in TGF-beta1-mediated signaling and collagen III secretion. |
| 6021 | 19858036 | We examined the expression of HGF/HGF receptor (c-Met) and TGF-beta1 in renal fibroblasts at multiple time points. |
| 6022 | 19858036 | The effects of recombinant human HGF on TGF-beta1 expression were studied by RT-PCR and Western blotting, and the levels of collagen III were measured by ELISA. |
| 6023 | 19858036 | In the high-glucose condition, the expression of HGF and c-Met in renal fibroblasts was detected as early as 6 hours following cell culture while the level of TGF-beta1 peaked at 96 hours. |
| 6024 | 19858036 | The addition of recombinant human HGF to the culture media dose-dependently inhibited TGF-beta1 mRNA expression and reduced collagen III secretion by 34%. |
| 6025 | 19858036 | These results indicate that, during hyperglycemia, HGF inhibits TGF-beta1 signaling and type III collagen activation in interstitial fibroblasts. |
| 6026 | 19858036 | Furthermore, we should recognize that changes in the balance between HGF and TGF-beta1 might be decisive in the pathogenesis of chronic renal fibrosis. |
| 6027 | 19858036 | Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. |
| 6028 | 19858036 | This study was undertaken to test the hypothesis that the preventive effects of HGF may result from interventions in TGF-beta1-mediated signaling and collagen III secretion. |
| 6029 | 19858036 | We examined the expression of HGF/HGF receptor (c-Met) and TGF-beta1 in renal fibroblasts at multiple time points. |
| 6030 | 19858036 | The effects of recombinant human HGF on TGF-beta1 expression were studied by RT-PCR and Western blotting, and the levels of collagen III were measured by ELISA. |
| 6031 | 19858036 | In the high-glucose condition, the expression of HGF and c-Met in renal fibroblasts was detected as early as 6 hours following cell culture while the level of TGF-beta1 peaked at 96 hours. |
| 6032 | 19858036 | The addition of recombinant human HGF to the culture media dose-dependently inhibited TGF-beta1 mRNA expression and reduced collagen III secretion by 34%. |
| 6033 | 19858036 | These results indicate that, during hyperglycemia, HGF inhibits TGF-beta1 signaling and type III collagen activation in interstitial fibroblasts. |
| 6034 | 19858036 | Furthermore, we should recognize that changes in the balance between HGF and TGF-beta1 might be decisive in the pathogenesis of chronic renal fibrosis. |
| 6035 | 19858036 | Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. |
| 6036 | 19858036 | This study was undertaken to test the hypothesis that the preventive effects of HGF may result from interventions in TGF-beta1-mediated signaling and collagen III secretion. |
| 6037 | 19858036 | We examined the expression of HGF/HGF receptor (c-Met) and TGF-beta1 in renal fibroblasts at multiple time points. |
| 6038 | 19858036 | The effects of recombinant human HGF on TGF-beta1 expression were studied by RT-PCR and Western blotting, and the levels of collagen III were measured by ELISA. |
| 6039 | 19858036 | In the high-glucose condition, the expression of HGF and c-Met in renal fibroblasts was detected as early as 6 hours following cell culture while the level of TGF-beta1 peaked at 96 hours. |
| 6040 | 19858036 | The addition of recombinant human HGF to the culture media dose-dependently inhibited TGF-beta1 mRNA expression and reduced collagen III secretion by 34%. |
| 6041 | 19858036 | These results indicate that, during hyperglycemia, HGF inhibits TGF-beta1 signaling and type III collagen activation in interstitial fibroblasts. |
| 6042 | 19858036 | Furthermore, we should recognize that changes in the balance between HGF and TGF-beta1 might be decisive in the pathogenesis of chronic renal fibrosis. |
| 6043 | 19858036 | Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. |
| 6044 | 19858036 | This study was undertaken to test the hypothesis that the preventive effects of HGF may result from interventions in TGF-beta1-mediated signaling and collagen III secretion. |
| 6045 | 19858036 | We examined the expression of HGF/HGF receptor (c-Met) and TGF-beta1 in renal fibroblasts at multiple time points. |
| 6046 | 19858036 | The effects of recombinant human HGF on TGF-beta1 expression were studied by RT-PCR and Western blotting, and the levels of collagen III were measured by ELISA. |
| 6047 | 19858036 | In the high-glucose condition, the expression of HGF and c-Met in renal fibroblasts was detected as early as 6 hours following cell culture while the level of TGF-beta1 peaked at 96 hours. |
| 6048 | 19858036 | The addition of recombinant human HGF to the culture media dose-dependently inhibited TGF-beta1 mRNA expression and reduced collagen III secretion by 34%. |
| 6049 | 19858036 | These results indicate that, during hyperglycemia, HGF inhibits TGF-beta1 signaling and type III collagen activation in interstitial fibroblasts. |
| 6050 | 19858036 | Furthermore, we should recognize that changes in the balance between HGF and TGF-beta1 might be decisive in the pathogenesis of chronic renal fibrosis. |
| 6051 | 19858036 | Hepatocyte growth factor suppresses transforming growth factor-beta-1 and type III collagen in human primary renal fibroblasts. |
| 6052 | 19858036 | This study was undertaken to test the hypothesis that the preventive effects of HGF may result from interventions in TGF-beta1-mediated signaling and collagen III secretion. |
| 6053 | 19858036 | We examined the expression of HGF/HGF receptor (c-Met) and TGF-beta1 in renal fibroblasts at multiple time points. |
| 6054 | 19858036 | The effects of recombinant human HGF on TGF-beta1 expression were studied by RT-PCR and Western blotting, and the levels of collagen III were measured by ELISA. |
| 6055 | 19858036 | In the high-glucose condition, the expression of HGF and c-Met in renal fibroblasts was detected as early as 6 hours following cell culture while the level of TGF-beta1 peaked at 96 hours. |
| 6056 | 19858036 | The addition of recombinant human HGF to the culture media dose-dependently inhibited TGF-beta1 mRNA expression and reduced collagen III secretion by 34%. |
| 6057 | 19858036 | These results indicate that, during hyperglycemia, HGF inhibits TGF-beta1 signaling and type III collagen activation in interstitial fibroblasts. |
| 6058 | 19858036 | Furthermore, we should recognize that changes in the balance between HGF and TGF-beta1 might be decisive in the pathogenesis of chronic renal fibrosis. |
| 6059 | 19917393 | Herein we have shown that interleukin-6 (IL-6), vascular endothelial growth factor-A (VEGF-A), hepatocyte growth factor (HGF), and transforming growth factor-beta (TGF-beta) were significantly increased as measured by enzyme-linked immunosorbent assay (ELISA) in MSCs-cultured medium, factors that have been shown to improve the survival, function, and angiogenesis/revascularization of islets. |
| 6060 | 19933924 | The favorable effects of the peroxisome proliferator-activated receptor-gamma ligand pioglitazone on glucose metabolism are associated with an increase in the fat-derived hormone adiponectin in the bloodstream. |
| 6061 | 19933924 | Here we investigated the effect of pioglitazone on angiotensin II (Ang II)-induced cardiac hypertrophy and assessed the potential contribution of adiponectin to the action of pioglitazone on the heart. |
| 6062 | 19933924 | Wild-type or adiponectin-deficient mice were treated with pioglitazone as food admixture at a concentration of 0.01% for 1 week followed by 2 weeks of infusion with Ang II at 3.2 mg/kg per day. |
| 6063 | 19933924 | Ang II infusion in wild-type mice resulted in exacerbated myocyte hypertrophy and increased interstitial fibrosis, which were accompanied by elevated phosphorylation of extracellular signal-regulated kinase and expression of transforming growth factor-beta1 in the heart. |
| 6064 | 19933924 | Treatment of wild-type mice with pioglitazone attenuated cardiac hypertrophy and fibrosis, extracellular signal-regulated kinase phosphorylation, and transforming growth factor-beta1 expression in response to Ang II. |
| 6065 | 19933924 | Pioglitazone also increased the plasma adiponectin level and phosphorylation of cardiac AMP-activated protein kinase in wild-type mice in the presence of Ang II. |
| 6066 | 19933924 | The suppressive effects of pioglitazone on Ang II-induced cardiac hypertrophy and fibrosis were diminished in adiponectin-deficient mice. |
| 6067 | 19933924 | Furthermore, pioglitazone had no effects on the phosphorylation of extracellular signal-regulated kinase and AMP-activated protein kinase in the Ang II-infused heart of adiponectin-deficient mice. |
| 6068 | 19933924 | These data provide direct evidence that pioglitazone protects against Ang II-induced pathological cardiac remodeling via an adiponectin-dependent mechanism. |
| 6069 | 19933924 | The favorable effects of the peroxisome proliferator-activated receptor-gamma ligand pioglitazone on glucose metabolism are associated with an increase in the fat-derived hormone adiponectin in the bloodstream. |
| 6070 | 19933924 | Here we investigated the effect of pioglitazone on angiotensin II (Ang II)-induced cardiac hypertrophy and assessed the potential contribution of adiponectin to the action of pioglitazone on the heart. |
| 6071 | 19933924 | Wild-type or adiponectin-deficient mice were treated with pioglitazone as food admixture at a concentration of 0.01% for 1 week followed by 2 weeks of infusion with Ang II at 3.2 mg/kg per day. |
| 6072 | 19933924 | Ang II infusion in wild-type mice resulted in exacerbated myocyte hypertrophy and increased interstitial fibrosis, which were accompanied by elevated phosphorylation of extracellular signal-regulated kinase and expression of transforming growth factor-beta1 in the heart. |
| 6073 | 19933924 | Treatment of wild-type mice with pioglitazone attenuated cardiac hypertrophy and fibrosis, extracellular signal-regulated kinase phosphorylation, and transforming growth factor-beta1 expression in response to Ang II. |
| 6074 | 19933924 | Pioglitazone also increased the plasma adiponectin level and phosphorylation of cardiac AMP-activated protein kinase in wild-type mice in the presence of Ang II. |
| 6075 | 19933924 | The suppressive effects of pioglitazone on Ang II-induced cardiac hypertrophy and fibrosis were diminished in adiponectin-deficient mice. |
| 6076 | 19933924 | Furthermore, pioglitazone had no effects on the phosphorylation of extracellular signal-regulated kinase and AMP-activated protein kinase in the Ang II-infused heart of adiponectin-deficient mice. |
| 6077 | 19933924 | These data provide direct evidence that pioglitazone protects against Ang II-induced pathological cardiac remodeling via an adiponectin-dependent mechanism. |
| 6078 | 19945439 | Urinary albumin, isoprostane, and 8-hydroxy-2'-deoxyguanosine excretion, and renal concentrations of transforming growth factor-beta(1), vascular endothelial growth factor, soluble intercellular adhesion molecule-1, fibronectin, and nitrotyrosine were evaluated by ELISA, and urinary creatinine and renal lipid peroxidation products by colorimetric assays. |
| 6079 | 19945439 | PARP inhibition counteracted diabetes-induced renal transforming growth factor-beta(1), vascular endothelial growth factor, and fibronectin, but not soluble intercellular adhesion molecule-1 and nitrotyrosine, accumulations. |
| 6080 | 19945439 | Urinary albumin, isoprostane, and 8-hydroxy-2'-deoxyguanosine excretion, and renal concentrations of transforming growth factor-beta(1), vascular endothelial growth factor, soluble intercellular adhesion molecule-1, fibronectin, and nitrotyrosine were evaluated by ELISA, and urinary creatinine and renal lipid peroxidation products by colorimetric assays. |
| 6081 | 19945439 | PARP inhibition counteracted diabetes-induced renal transforming growth factor-beta(1), vascular endothelial growth factor, and fibronectin, but not soluble intercellular adhesion molecule-1 and nitrotyrosine, accumulations. |
| 6082 | 19959647 | TGF-beta, a multipotent cytokine acting through its receptors ALK5 and -1, has been postulated to be involved in this phenomenon. |
| 6083 | 19959647 | Bovine retinal endothelial cells and pericytes were stimulated with TGF-beta1 in the presence or absence of SD-208, a specific inhibitor of the TGF-beta type I receptor ALK5, or ALK5 small interfering (si)RNA. |
| 6084 | 19959647 | TGF-beta-signaling pathways were characterized by analysis of phosphorylated Smad2 or -1/5/8 proteins and TGF-beta target genes (PAI-1, fibronectin, CTGF, Smad7, and Id1) and protein (fibronectin). |
| 6085 | 19959647 | ALK5 was expressed in both cell types, whereas ALK1 was exclusively expressed in endothelial cells. |
| 6086 | 19959647 | In endothelial cells, TGF-beta induced Smad2 phosphorylation at high concentrations, which was efficiently blocked by ALK5 inhibition. |
| 6087 | 19959647 | In contrast, in pericytes, Smad2 phosphorylation was rapidly induced at low concentrations of TGF-beta. |
| 6088 | 19959647 | The ALK1-Smad1/5/8 pathway was activated by TGF-beta in endothelial cells only. |
| 6089 | 19959647 | TGF-beta caused ALK5-mediated upregulation of PAI-1, Smad7, and fibronectin and in pericytes at lower TGF-beta concentrations than in endothelial cells. |
| 6090 | 19959647 | TGF-beta, a multipotent cytokine acting through its receptors ALK5 and -1, has been postulated to be involved in this phenomenon. |
| 6091 | 19959647 | Bovine retinal endothelial cells and pericytes were stimulated with TGF-beta1 in the presence or absence of SD-208, a specific inhibitor of the TGF-beta type I receptor ALK5, or ALK5 small interfering (si)RNA. |
| 6092 | 19959647 | TGF-beta-signaling pathways were characterized by analysis of phosphorylated Smad2 or -1/5/8 proteins and TGF-beta target genes (PAI-1, fibronectin, CTGF, Smad7, and Id1) and protein (fibronectin). |
| 6093 | 19959647 | ALK5 was expressed in both cell types, whereas ALK1 was exclusively expressed in endothelial cells. |
| 6094 | 19959647 | In endothelial cells, TGF-beta induced Smad2 phosphorylation at high concentrations, which was efficiently blocked by ALK5 inhibition. |
| 6095 | 19959647 | In contrast, in pericytes, Smad2 phosphorylation was rapidly induced at low concentrations of TGF-beta. |
| 6096 | 19959647 | The ALK1-Smad1/5/8 pathway was activated by TGF-beta in endothelial cells only. |
| 6097 | 19959647 | TGF-beta caused ALK5-mediated upregulation of PAI-1, Smad7, and fibronectin and in pericytes at lower TGF-beta concentrations than in endothelial cells. |
| 6098 | 19959647 | TGF-beta, a multipotent cytokine acting through its receptors ALK5 and -1, has been postulated to be involved in this phenomenon. |
| 6099 | 19959647 | Bovine retinal endothelial cells and pericytes were stimulated with TGF-beta1 in the presence or absence of SD-208, a specific inhibitor of the TGF-beta type I receptor ALK5, or ALK5 small interfering (si)RNA. |
| 6100 | 19959647 | TGF-beta-signaling pathways were characterized by analysis of phosphorylated Smad2 or -1/5/8 proteins and TGF-beta target genes (PAI-1, fibronectin, CTGF, Smad7, and Id1) and protein (fibronectin). |
| 6101 | 19959647 | ALK5 was expressed in both cell types, whereas ALK1 was exclusively expressed in endothelial cells. |
| 6102 | 19959647 | In endothelial cells, TGF-beta induced Smad2 phosphorylation at high concentrations, which was efficiently blocked by ALK5 inhibition. |
| 6103 | 19959647 | In contrast, in pericytes, Smad2 phosphorylation was rapidly induced at low concentrations of TGF-beta. |
| 6104 | 19959647 | The ALK1-Smad1/5/8 pathway was activated by TGF-beta in endothelial cells only. |
| 6105 | 19959647 | TGF-beta caused ALK5-mediated upregulation of PAI-1, Smad7, and fibronectin and in pericytes at lower TGF-beta concentrations than in endothelial cells. |
| 6106 | 19959647 | TGF-beta, a multipotent cytokine acting through its receptors ALK5 and -1, has been postulated to be involved in this phenomenon. |
| 6107 | 19959647 | Bovine retinal endothelial cells and pericytes were stimulated with TGF-beta1 in the presence or absence of SD-208, a specific inhibitor of the TGF-beta type I receptor ALK5, or ALK5 small interfering (si)RNA. |
| 6108 | 19959647 | TGF-beta-signaling pathways were characterized by analysis of phosphorylated Smad2 or -1/5/8 proteins and TGF-beta target genes (PAI-1, fibronectin, CTGF, Smad7, and Id1) and protein (fibronectin). |
| 6109 | 19959647 | ALK5 was expressed in both cell types, whereas ALK1 was exclusively expressed in endothelial cells. |
| 6110 | 19959647 | In endothelial cells, TGF-beta induced Smad2 phosphorylation at high concentrations, which was efficiently blocked by ALK5 inhibition. |
| 6111 | 19959647 | In contrast, in pericytes, Smad2 phosphorylation was rapidly induced at low concentrations of TGF-beta. |
| 6112 | 19959647 | The ALK1-Smad1/5/8 pathway was activated by TGF-beta in endothelial cells only. |
| 6113 | 19959647 | TGF-beta caused ALK5-mediated upregulation of PAI-1, Smad7, and fibronectin and in pericytes at lower TGF-beta concentrations than in endothelial cells. |
| 6114 | 19959647 | TGF-beta, a multipotent cytokine acting through its receptors ALK5 and -1, has been postulated to be involved in this phenomenon. |
| 6115 | 19959647 | Bovine retinal endothelial cells and pericytes were stimulated with TGF-beta1 in the presence or absence of SD-208, a specific inhibitor of the TGF-beta type I receptor ALK5, or ALK5 small interfering (si)RNA. |
| 6116 | 19959647 | TGF-beta-signaling pathways were characterized by analysis of phosphorylated Smad2 or -1/5/8 proteins and TGF-beta target genes (PAI-1, fibronectin, CTGF, Smad7, and Id1) and protein (fibronectin). |
| 6117 | 19959647 | ALK5 was expressed in both cell types, whereas ALK1 was exclusively expressed in endothelial cells. |
| 6118 | 19959647 | In endothelial cells, TGF-beta induced Smad2 phosphorylation at high concentrations, which was efficiently blocked by ALK5 inhibition. |
| 6119 | 19959647 | In contrast, in pericytes, Smad2 phosphorylation was rapidly induced at low concentrations of TGF-beta. |
| 6120 | 19959647 | The ALK1-Smad1/5/8 pathway was activated by TGF-beta in endothelial cells only. |
| 6121 | 19959647 | TGF-beta caused ALK5-mediated upregulation of PAI-1, Smad7, and fibronectin and in pericytes at lower TGF-beta concentrations than in endothelial cells. |
| 6122 | 19959647 | TGF-beta, a multipotent cytokine acting through its receptors ALK5 and -1, has been postulated to be involved in this phenomenon. |
| 6123 | 19959647 | Bovine retinal endothelial cells and pericytes were stimulated with TGF-beta1 in the presence or absence of SD-208, a specific inhibitor of the TGF-beta type I receptor ALK5, or ALK5 small interfering (si)RNA. |
| 6124 | 19959647 | TGF-beta-signaling pathways were characterized by analysis of phosphorylated Smad2 or -1/5/8 proteins and TGF-beta target genes (PAI-1, fibronectin, CTGF, Smad7, and Id1) and protein (fibronectin). |
| 6125 | 19959647 | ALK5 was expressed in both cell types, whereas ALK1 was exclusively expressed in endothelial cells. |
| 6126 | 19959647 | In endothelial cells, TGF-beta induced Smad2 phosphorylation at high concentrations, which was efficiently blocked by ALK5 inhibition. |
| 6127 | 19959647 | In contrast, in pericytes, Smad2 phosphorylation was rapidly induced at low concentrations of TGF-beta. |
| 6128 | 19959647 | The ALK1-Smad1/5/8 pathway was activated by TGF-beta in endothelial cells only. |
| 6129 | 19959647 | TGF-beta caused ALK5-mediated upregulation of PAI-1, Smad7, and fibronectin and in pericytes at lower TGF-beta concentrations than in endothelial cells. |
| 6130 | 19959647 | TGF-beta, a multipotent cytokine acting through its receptors ALK5 and -1, has been postulated to be involved in this phenomenon. |
| 6131 | 19959647 | Bovine retinal endothelial cells and pericytes were stimulated with TGF-beta1 in the presence or absence of SD-208, a specific inhibitor of the TGF-beta type I receptor ALK5, or ALK5 small interfering (si)RNA. |
| 6132 | 19959647 | TGF-beta-signaling pathways were characterized by analysis of phosphorylated Smad2 or -1/5/8 proteins and TGF-beta target genes (PAI-1, fibronectin, CTGF, Smad7, and Id1) and protein (fibronectin). |
| 6133 | 19959647 | ALK5 was expressed in both cell types, whereas ALK1 was exclusively expressed in endothelial cells. |
| 6134 | 19959647 | In endothelial cells, TGF-beta induced Smad2 phosphorylation at high concentrations, which was efficiently blocked by ALK5 inhibition. |
| 6135 | 19959647 | In contrast, in pericytes, Smad2 phosphorylation was rapidly induced at low concentrations of TGF-beta. |
| 6136 | 19959647 | The ALK1-Smad1/5/8 pathway was activated by TGF-beta in endothelial cells only. |
| 6137 | 19959647 | TGF-beta caused ALK5-mediated upregulation of PAI-1, Smad7, and fibronectin and in pericytes at lower TGF-beta concentrations than in endothelial cells. |
| 6138 | 20019166 | Wnt/beta-catenin signaling mediates renal fibrosis in several model systems including diabetic nephropathy. |
| 6139 | 20019166 | Dickkopf-1 (DKK-1) is an endogenous inhibitor of Wnt/beta-catenin signaling, but whether DKK-1 modulates diabetic nephropathy is unknown. |
| 6140 | 20019166 | In vitro, HG increased expression of DKK1, receptor Kremen-2, TGF-beta1, and fibronectin in mesangial cells. |
| 6141 | 20019166 | Loss and gain of DKK1 function modulated HG-mediated c-Jun, TGF-beta1, and fibronectin expression. |
| 6142 | 20019166 | DKK1 mediated HG-induced phosphorylation of Ser45-beta-catenin and reduction of nuclear beta-catenin levels, but not phosphorylation of ERK kinase. |
| 6143 | 20019166 | Wnt3a protein and the beta-catenin (Delta45) mutation increased nuclear beta-catenin but abrogated HG-induced DKK1 and fibronectin expression. |
| 6144 | 20019166 | Taken together, DKK1 mediates HG-induced destabilization of beta-catenin and matrix accumulation in mesangial cells. |
| 6145 | 20034431 | In addition, paeoniflorin treatment effectively suppressed glomerular hypertrophy; blood glucose; the expression of transforming growth factor beta, type IV collagen, and intercellular adhesion molecule 1; and renal infiltration of macrophages compared with levels in untreated DM rats. |
| 6146 | 20035397 | Since overexpression of the extracellular matrix (ECM) components (type IV collagen and fibronectin) and transforming growth factor beta (TGF-beta) have been previously implicated in the development of the renal glomerulus damage of diabetic nephropathy, we included these substances in our study. |
| 6147 | 20035397 | The results showed that high concentration of glucose (450 mg.dl(-1)) stimulated the synthesis of type IV collagen and fibronectin and the secretion of TGF-beta. |
| 6148 | 20035397 | Since overexpression of the extracellular matrix (ECM) components (type IV collagen and fibronectin) and transforming growth factor beta (TGF-beta) have been previously implicated in the development of the renal glomerulus damage of diabetic nephropathy, we included these substances in our study. |
| 6149 | 20035397 | The results showed that high concentration of glucose (450 mg.dl(-1)) stimulated the synthesis of type IV collagen and fibronectin and the secretion of TGF-beta. |
| 6150 | 20039009 | The glomerular hypertrophy and mesangial matrix expansion seen in early diabetes can be reduced or prevented by C-peptide administration, possibly via interference with TGF-beta1 and TNFalpha signaling. |
| 6151 | 20039825 | Significant correlation between association of polymorphism in codon 10 of transforming growth factor-beta1 T (29) C with type 1 diabetes and patients with nephropathy disorder. |
| 6152 | 20039825 | In order to investigate the immunosuppressive action of transforming growth factor-beta1 (TGF-beta1) in type 1 diabetes, 388 patients with type 1 diabetes and 229 normal controls were genotyped for the TGF-beta1 T (29) C gene polymorphism. |
| 6153 | 20039825 | Significant correlation between association of polymorphism in codon 10 of transforming growth factor-beta1 T (29) C with type 1 diabetes and patients with nephropathy disorder. |
| 6154 | 20039825 | In order to investigate the immunosuppressive action of transforming growth factor-beta1 (TGF-beta1) in type 1 diabetes, 388 patients with type 1 diabetes and 229 normal controls were genotyped for the TGF-beta1 T (29) C gene polymorphism. |
| 6155 | 20045460 | Renal pathology, levels of oxidative stress, and the expressions of angiotensinogen (AGT), monocyte chemoattractant protein-1 (MCP-1) and transforming growth factor beta 1 (Tgf-beta1) mRNA were investigated. |
| 6156 | 20045460 | In diabetic mice without treatment, renal AGT and MCP-1 mRNA were increased, while they were effectively suppressed by syn-BMT. |
| 6157 | 20045460 | These preventive effects could be partly via maintaining oxidative stress and expression of AGT and MCP-1 in kidney in streptozotocin-diabetic mice. |
| 6158 | 20130530 | The thiazolidinedione (TZD) insulin sensitizers decrease albuminuria in diabetic nephropathy (DN) and reduce OPN expression in vascular and cardiac tissue. |
| 6159 | 20130530 | To examine whether OPN is a critical mediator of DN we treated db/db mice with insulin, rosiglitazone, or pioglitazone to achieve similar fasting plasma glucose levels. |
| 6160 | 20130530 | The urine albumin-to-creatinine ratio and glomerular OPN expression were increased in diabetic mice, but both were reduced by the TZDs more than by insulin. |
| 6161 | 20130530 | In each case, OPN deletion decreased albuminuria, mesangial area, and glomerular collagen IV, fibronectin and transforming growth factor (TGF)-beta in the diabetic mice compared with their respective controls. |
| 6162 | 20130530 | In cultured mouse mesangial cells, TZDs but not insulin decreased angiotensin II-induced OPN expression, while recombinant OPN upregulated TGF-beta, ERK/MAPK, and JNK/MAPK signaling. |
| 6163 | 20130530 | These studies show that OPN expression in DN mouse models enhances glomerular damage, likely through the expression of TGF-beta, while its deletion protects against disease progression, suggesting that OPN might serve as a therapeutic target. |
| 6164 | 20130530 | The thiazolidinedione (TZD) insulin sensitizers decrease albuminuria in diabetic nephropathy (DN) and reduce OPN expression in vascular and cardiac tissue. |
| 6165 | 20130530 | To examine whether OPN is a critical mediator of DN we treated db/db mice with insulin, rosiglitazone, or pioglitazone to achieve similar fasting plasma glucose levels. |
| 6166 | 20130530 | The urine albumin-to-creatinine ratio and glomerular OPN expression were increased in diabetic mice, but both were reduced by the TZDs more than by insulin. |
| 6167 | 20130530 | In each case, OPN deletion decreased albuminuria, mesangial area, and glomerular collagen IV, fibronectin and transforming growth factor (TGF)-beta in the diabetic mice compared with their respective controls. |
| 6168 | 20130530 | In cultured mouse mesangial cells, TZDs but not insulin decreased angiotensin II-induced OPN expression, while recombinant OPN upregulated TGF-beta, ERK/MAPK, and JNK/MAPK signaling. |
| 6169 | 20130530 | These studies show that OPN expression in DN mouse models enhances glomerular damage, likely through the expression of TGF-beta, while its deletion protects against disease progression, suggesting that OPN might serve as a therapeutic target. |
| 6170 | 20136517 | Recombinant decorin ameliorates the pulmonary structure alterations by down-regulating transforming growth factor-beta1/SMADS signaling in the diabetic rats. |
| 6171 | 20136517 | This study investigated the role of transforming growth factor-beta1 (TGF-beta1)/Smads signaling in the alterations of lung structure and the effect of the exogenous decorin on lung structure modification in streptozotocin (STZ)-induced diabetic rats. |
| 6172 | 20136517 | At 8, 16, and 28 weeks after STZ treatment, haematoxylin-eosin (H&E) and Masson's trichrome staining were performed to investigate the histological changes of diabetic lungs; Expressions of TGF-beta1 and collagen type IV in the diabetic lung were measured by Western blot and immunohistochemistry. |
| 6173 | 20136517 | Phosphorylated Smad2 (P-Smad2), one of the major TGF-beta1 receptor substrates, was also detected using Western blot. |
| 6174 | 20136517 | Exogenous decorin effectively suppressed the increased activities of TGF-beta1/Smads signaling and partly attenuated collagen deposits in the alveolar septum. |
| 6175 | 20136517 | Increased activity of TGF-beta1/Smads signaling might play a critical role in the accumulation of collagen in the diabetic lung. |
| 6176 | 20136517 | The protective effect of decorin in the diabetic lung is at least partly because of the down-regulation of the TGF-beta1/Smads signaling. |
| 6177 | 20136517 | Recombinant decorin ameliorates the pulmonary structure alterations by down-regulating transforming growth factor-beta1/SMADS signaling in the diabetic rats. |
| 6178 | 20136517 | This study investigated the role of transforming growth factor-beta1 (TGF-beta1)/Smads signaling in the alterations of lung structure and the effect of the exogenous decorin on lung structure modification in streptozotocin (STZ)-induced diabetic rats. |
| 6179 | 20136517 | At 8, 16, and 28 weeks after STZ treatment, haematoxylin-eosin (H&E) and Masson's trichrome staining were performed to investigate the histological changes of diabetic lungs; Expressions of TGF-beta1 and collagen type IV in the diabetic lung were measured by Western blot and immunohistochemistry. |
| 6180 | 20136517 | Phosphorylated Smad2 (P-Smad2), one of the major TGF-beta1 receptor substrates, was also detected using Western blot. |
| 6181 | 20136517 | Exogenous decorin effectively suppressed the increased activities of TGF-beta1/Smads signaling and partly attenuated collagen deposits in the alveolar septum. |
| 6182 | 20136517 | Increased activity of TGF-beta1/Smads signaling might play a critical role in the accumulation of collagen in the diabetic lung. |
| 6183 | 20136517 | The protective effect of decorin in the diabetic lung is at least partly because of the down-regulation of the TGF-beta1/Smads signaling. |
| 6184 | 20136517 | Recombinant decorin ameliorates the pulmonary structure alterations by down-regulating transforming growth factor-beta1/SMADS signaling in the diabetic rats. |
| 6185 | 20136517 | This study investigated the role of transforming growth factor-beta1 (TGF-beta1)/Smads signaling in the alterations of lung structure and the effect of the exogenous decorin on lung structure modification in streptozotocin (STZ)-induced diabetic rats. |
| 6186 | 20136517 | At 8, 16, and 28 weeks after STZ treatment, haematoxylin-eosin (H&E) and Masson's trichrome staining were performed to investigate the histological changes of diabetic lungs; Expressions of TGF-beta1 and collagen type IV in the diabetic lung were measured by Western blot and immunohistochemistry. |
| 6187 | 20136517 | Phosphorylated Smad2 (P-Smad2), one of the major TGF-beta1 receptor substrates, was also detected using Western blot. |
| 6188 | 20136517 | Exogenous decorin effectively suppressed the increased activities of TGF-beta1/Smads signaling and partly attenuated collagen deposits in the alveolar septum. |
| 6189 | 20136517 | Increased activity of TGF-beta1/Smads signaling might play a critical role in the accumulation of collagen in the diabetic lung. |
| 6190 | 20136517 | The protective effect of decorin in the diabetic lung is at least partly because of the down-regulation of the TGF-beta1/Smads signaling. |
| 6191 | 20136517 | Recombinant decorin ameliorates the pulmonary structure alterations by down-regulating transforming growth factor-beta1/SMADS signaling in the diabetic rats. |
| 6192 | 20136517 | This study investigated the role of transforming growth factor-beta1 (TGF-beta1)/Smads signaling in the alterations of lung structure and the effect of the exogenous decorin on lung structure modification in streptozotocin (STZ)-induced diabetic rats. |
| 6193 | 20136517 | At 8, 16, and 28 weeks after STZ treatment, haematoxylin-eosin (H&E) and Masson's trichrome staining were performed to investigate the histological changes of diabetic lungs; Expressions of TGF-beta1 and collagen type IV in the diabetic lung were measured by Western blot and immunohistochemistry. |
| 6194 | 20136517 | Phosphorylated Smad2 (P-Smad2), one of the major TGF-beta1 receptor substrates, was also detected using Western blot. |
| 6195 | 20136517 | Exogenous decorin effectively suppressed the increased activities of TGF-beta1/Smads signaling and partly attenuated collagen deposits in the alveolar septum. |
| 6196 | 20136517 | Increased activity of TGF-beta1/Smads signaling might play a critical role in the accumulation of collagen in the diabetic lung. |
| 6197 | 20136517 | The protective effect of decorin in the diabetic lung is at least partly because of the down-regulation of the TGF-beta1/Smads signaling. |
| 6198 | 20136517 | Recombinant decorin ameliorates the pulmonary structure alterations by down-regulating transforming growth factor-beta1/SMADS signaling in the diabetic rats. |
| 6199 | 20136517 | This study investigated the role of transforming growth factor-beta1 (TGF-beta1)/Smads signaling in the alterations of lung structure and the effect of the exogenous decorin on lung structure modification in streptozotocin (STZ)-induced diabetic rats. |
| 6200 | 20136517 | At 8, 16, and 28 weeks after STZ treatment, haematoxylin-eosin (H&E) and Masson's trichrome staining were performed to investigate the histological changes of diabetic lungs; Expressions of TGF-beta1 and collagen type IV in the diabetic lung were measured by Western blot and immunohistochemistry. |
| 6201 | 20136517 | Phosphorylated Smad2 (P-Smad2), one of the major TGF-beta1 receptor substrates, was also detected using Western blot. |
| 6202 | 20136517 | Exogenous decorin effectively suppressed the increased activities of TGF-beta1/Smads signaling and partly attenuated collagen deposits in the alveolar septum. |
| 6203 | 20136517 | Increased activity of TGF-beta1/Smads signaling might play a critical role in the accumulation of collagen in the diabetic lung. |
| 6204 | 20136517 | The protective effect of decorin in the diabetic lung is at least partly because of the down-regulation of the TGF-beta1/Smads signaling. |
| 6205 | 20136517 | Recombinant decorin ameliorates the pulmonary structure alterations by down-regulating transforming growth factor-beta1/SMADS signaling in the diabetic rats. |
| 6206 | 20136517 | This study investigated the role of transforming growth factor-beta1 (TGF-beta1)/Smads signaling in the alterations of lung structure and the effect of the exogenous decorin on lung structure modification in streptozotocin (STZ)-induced diabetic rats. |
| 6207 | 20136517 | At 8, 16, and 28 weeks after STZ treatment, haematoxylin-eosin (H&E) and Masson's trichrome staining were performed to investigate the histological changes of diabetic lungs; Expressions of TGF-beta1 and collagen type IV in the diabetic lung were measured by Western blot and immunohistochemistry. |
| 6208 | 20136517 | Phosphorylated Smad2 (P-Smad2), one of the major TGF-beta1 receptor substrates, was also detected using Western blot. |
| 6209 | 20136517 | Exogenous decorin effectively suppressed the increased activities of TGF-beta1/Smads signaling and partly attenuated collagen deposits in the alveolar septum. |
| 6210 | 20136517 | Increased activity of TGF-beta1/Smads signaling might play a critical role in the accumulation of collagen in the diabetic lung. |
| 6211 | 20136517 | The protective effect of decorin in the diabetic lung is at least partly because of the down-regulation of the TGF-beta1/Smads signaling. |
| 6212 | 20136517 | Recombinant decorin ameliorates the pulmonary structure alterations by down-regulating transforming growth factor-beta1/SMADS signaling in the diabetic rats. |
| 6213 | 20136517 | This study investigated the role of transforming growth factor-beta1 (TGF-beta1)/Smads signaling in the alterations of lung structure and the effect of the exogenous decorin on lung structure modification in streptozotocin (STZ)-induced diabetic rats. |
| 6214 | 20136517 | At 8, 16, and 28 weeks after STZ treatment, haematoxylin-eosin (H&E) and Masson's trichrome staining were performed to investigate the histological changes of diabetic lungs; Expressions of TGF-beta1 and collagen type IV in the diabetic lung were measured by Western blot and immunohistochemistry. |
| 6215 | 20136517 | Phosphorylated Smad2 (P-Smad2), one of the major TGF-beta1 receptor substrates, was also detected using Western blot. |
| 6216 | 20136517 | Exogenous decorin effectively suppressed the increased activities of TGF-beta1/Smads signaling and partly attenuated collagen deposits in the alveolar septum. |
| 6217 | 20136517 | Increased activity of TGF-beta1/Smads signaling might play a critical role in the accumulation of collagen in the diabetic lung. |
| 6218 | 20136517 | The protective effect of decorin in the diabetic lung is at least partly because of the down-regulation of the TGF-beta1/Smads signaling. |
| 6219 | 20143240 | CD4+CD25+(high) regulatory T cells (Tregs) play a pivotal role in the control of the immune response. |
| 6220 | 20143240 | We showed that iTregs from RO T1D subjects had increased expression of Foxp3, E3 ubiquitin ligase (ITCH) and TGF-beta-inducible early gene 1 (TIEG1) compared with control and LS T1D subjects. |
| 6221 | 20146476 | Enhanced expression and secretion of connective tissue growth factor (CTGF) play an important role in the expansion of glomerular mesangial matrix mostly composed of type IV collagen. |
| 6222 | 20146476 | The present study was to investigate whether nontoxic isoliquiritigenin inhibited high glucose (HG)-induced mesangial fibrosis by retarding formation of type IV collagen as well as CTGF in human mesangial cells (HRMC). |
| 6223 | 20146476 | Exposure of cells to HG caused marked increases in collagen secretion and CTGF expression, which was dose-dependently reversed by isoliquiritigenin at the transcriptional levels. |
| 6224 | 20146476 | Additionally, isoliquiritigenin boosted HG-plummeted type matrix metalloproteinase-1 (MT-1 MMP) expression and dampened HG-elevated tissue inhibitor of MMP-2 (TIMP-2) expression, facilitating the degradation of mesangial matrix. |
| 6225 | 20146476 | Isoliquiritigenin inhibited HG-upregulated CTGF and TIMP-2 expression via disturbing TGF-beta1 signaling in HRMC, as evidenced by TGF-beta receptor I kinase (TGF-beta RI) inhibitor. |
| 6226 | 20146476 | HG-activated SMAD2 through autocrine TGF-beta signaling was repealed by > or =10 microM isoliquiritigenin. |
| 6227 | 20146476 | HG induced SMAD4 expression of HRMC and obliterated antagonistic SMAD7, whereas isoliquiritigenin suppressed induction of TGF-beta RII and TGF-beta RI with blunting their downstream SMAD signaling. |
| 6228 | 20146476 | Enhanced expression and secretion of connective tissue growth factor (CTGF) play an important role in the expansion of glomerular mesangial matrix mostly composed of type IV collagen. |
| 6229 | 20146476 | The present study was to investigate whether nontoxic isoliquiritigenin inhibited high glucose (HG)-induced mesangial fibrosis by retarding formation of type IV collagen as well as CTGF in human mesangial cells (HRMC). |
| 6230 | 20146476 | Exposure of cells to HG caused marked increases in collagen secretion and CTGF expression, which was dose-dependently reversed by isoliquiritigenin at the transcriptional levels. |
| 6231 | 20146476 | Additionally, isoliquiritigenin boosted HG-plummeted type matrix metalloproteinase-1 (MT-1 MMP) expression and dampened HG-elevated tissue inhibitor of MMP-2 (TIMP-2) expression, facilitating the degradation of mesangial matrix. |
| 6232 | 20146476 | Isoliquiritigenin inhibited HG-upregulated CTGF and TIMP-2 expression via disturbing TGF-beta1 signaling in HRMC, as evidenced by TGF-beta receptor I kinase (TGF-beta RI) inhibitor. |
| 6233 | 20146476 | HG-activated SMAD2 through autocrine TGF-beta signaling was repealed by > or =10 microM isoliquiritigenin. |
| 6234 | 20146476 | HG induced SMAD4 expression of HRMC and obliterated antagonistic SMAD7, whereas isoliquiritigenin suppressed induction of TGF-beta RII and TGF-beta RI with blunting their downstream SMAD signaling. |
| 6235 | 20146476 | Enhanced expression and secretion of connective tissue growth factor (CTGF) play an important role in the expansion of glomerular mesangial matrix mostly composed of type IV collagen. |
| 6236 | 20146476 | The present study was to investigate whether nontoxic isoliquiritigenin inhibited high glucose (HG)-induced mesangial fibrosis by retarding formation of type IV collagen as well as CTGF in human mesangial cells (HRMC). |
| 6237 | 20146476 | Exposure of cells to HG caused marked increases in collagen secretion and CTGF expression, which was dose-dependently reversed by isoliquiritigenin at the transcriptional levels. |
| 6238 | 20146476 | Additionally, isoliquiritigenin boosted HG-plummeted type matrix metalloproteinase-1 (MT-1 MMP) expression and dampened HG-elevated tissue inhibitor of MMP-2 (TIMP-2) expression, facilitating the degradation of mesangial matrix. |
| 6239 | 20146476 | Isoliquiritigenin inhibited HG-upregulated CTGF and TIMP-2 expression via disturbing TGF-beta1 signaling in HRMC, as evidenced by TGF-beta receptor I kinase (TGF-beta RI) inhibitor. |
| 6240 | 20146476 | HG-activated SMAD2 through autocrine TGF-beta signaling was repealed by > or =10 microM isoliquiritigenin. |
| 6241 | 20146476 | HG induced SMAD4 expression of HRMC and obliterated antagonistic SMAD7, whereas isoliquiritigenin suppressed induction of TGF-beta RII and TGF-beta RI with blunting their downstream SMAD signaling. |
| 6242 | 20157598 | TGF-beta antagonists exert anti-tumor effects through #1 activating effector cells such as NK cells and cytotoxic CD8(+) T cells (CTLs), #2 inhibiting regulatory/suppressor cell populations, #3 making tumor cells visible to immune cells, #4 inhibiting the production of tumor growth factors. |
| 6243 | 20164378 | It is well established that thrombospondin1 (TSP1) is a major regulator of TGF-beta activation in renal and cardiac complications of diabetes. |
| 6244 | 20164378 | In the present study, we investigated whether high glucose regulation of PKG protein and activity in VSMCs similarly regulates TSP1 expression and downstream TGF-beta activity. |
| 6245 | 20164378 | These studies showed that high glucose stimulates both TSP1 expression and TGF-beta bioactivity in primary murine aortic smooth muscle cells (VSMCs). |
| 6246 | 20164378 | TSP1 is responsible for the increased TGF-beta bioactivity under high glucose conditions, because treatment with anti-TSP1 antibody, small interfering RNA-TSP1, or an inhibitory peptide blocked glucose-mediated increases in TGF-beta activity and extracellular matrix protein (fibronectin) expression. |
| 6247 | 20164378 | Overexpression of constitutively active PKG, but not the PKG-I protein, inhibited glucose-induced TSP1 expression and TGF-beta bioactivity, suggesting that PKG protein expression is insufficient to regulate TSP1 expression. |
| 6248 | 20164378 | Together, these data establish that glucose-mediated downregulation of PKG levels stimulates TSP1 expression and enhances TGF-beta activity and matrix protein expression, which can contribute to vascular remodeling in diabetes. |
| 6249 | 20164378 | It is well established that thrombospondin1 (TSP1) is a major regulator of TGF-beta activation in renal and cardiac complications of diabetes. |
| 6250 | 20164378 | In the present study, we investigated whether high glucose regulation of PKG protein and activity in VSMCs similarly regulates TSP1 expression and downstream TGF-beta activity. |
| 6251 | 20164378 | These studies showed that high glucose stimulates both TSP1 expression and TGF-beta bioactivity in primary murine aortic smooth muscle cells (VSMCs). |
| 6252 | 20164378 | TSP1 is responsible for the increased TGF-beta bioactivity under high glucose conditions, because treatment with anti-TSP1 antibody, small interfering RNA-TSP1, or an inhibitory peptide blocked glucose-mediated increases in TGF-beta activity and extracellular matrix protein (fibronectin) expression. |
| 6253 | 20164378 | Overexpression of constitutively active PKG, but not the PKG-I protein, inhibited glucose-induced TSP1 expression and TGF-beta bioactivity, suggesting that PKG protein expression is insufficient to regulate TSP1 expression. |
| 6254 | 20164378 | Together, these data establish that glucose-mediated downregulation of PKG levels stimulates TSP1 expression and enhances TGF-beta activity and matrix protein expression, which can contribute to vascular remodeling in diabetes. |
| 6255 | 20164378 | It is well established that thrombospondin1 (TSP1) is a major regulator of TGF-beta activation in renal and cardiac complications of diabetes. |
| 6256 | 20164378 | In the present study, we investigated whether high glucose regulation of PKG protein and activity in VSMCs similarly regulates TSP1 expression and downstream TGF-beta activity. |
| 6257 | 20164378 | These studies showed that high glucose stimulates both TSP1 expression and TGF-beta bioactivity in primary murine aortic smooth muscle cells (VSMCs). |
| 6258 | 20164378 | TSP1 is responsible for the increased TGF-beta bioactivity under high glucose conditions, because treatment with anti-TSP1 antibody, small interfering RNA-TSP1, or an inhibitory peptide blocked glucose-mediated increases in TGF-beta activity and extracellular matrix protein (fibronectin) expression. |
| 6259 | 20164378 | Overexpression of constitutively active PKG, but not the PKG-I protein, inhibited glucose-induced TSP1 expression and TGF-beta bioactivity, suggesting that PKG protein expression is insufficient to regulate TSP1 expression. |
| 6260 | 20164378 | Together, these data establish that glucose-mediated downregulation of PKG levels stimulates TSP1 expression and enhances TGF-beta activity and matrix protein expression, which can contribute to vascular remodeling in diabetes. |
| 6261 | 20164378 | It is well established that thrombospondin1 (TSP1) is a major regulator of TGF-beta activation in renal and cardiac complications of diabetes. |
| 6262 | 20164378 | In the present study, we investigated whether high glucose regulation of PKG protein and activity in VSMCs similarly regulates TSP1 expression and downstream TGF-beta activity. |
| 6263 | 20164378 | These studies showed that high glucose stimulates both TSP1 expression and TGF-beta bioactivity in primary murine aortic smooth muscle cells (VSMCs). |
| 6264 | 20164378 | TSP1 is responsible for the increased TGF-beta bioactivity under high glucose conditions, because treatment with anti-TSP1 antibody, small interfering RNA-TSP1, or an inhibitory peptide blocked glucose-mediated increases in TGF-beta activity and extracellular matrix protein (fibronectin) expression. |
| 6265 | 20164378 | Overexpression of constitutively active PKG, but not the PKG-I protein, inhibited glucose-induced TSP1 expression and TGF-beta bioactivity, suggesting that PKG protein expression is insufficient to regulate TSP1 expression. |
| 6266 | 20164378 | Together, these data establish that glucose-mediated downregulation of PKG levels stimulates TSP1 expression and enhances TGF-beta activity and matrix protein expression, which can contribute to vascular remodeling in diabetes. |
| 6267 | 20164378 | It is well established that thrombospondin1 (TSP1) is a major regulator of TGF-beta activation in renal and cardiac complications of diabetes. |
| 6268 | 20164378 | In the present study, we investigated whether high glucose regulation of PKG protein and activity in VSMCs similarly regulates TSP1 expression and downstream TGF-beta activity. |
| 6269 | 20164378 | These studies showed that high glucose stimulates both TSP1 expression and TGF-beta bioactivity in primary murine aortic smooth muscle cells (VSMCs). |
| 6270 | 20164378 | TSP1 is responsible for the increased TGF-beta bioactivity under high glucose conditions, because treatment with anti-TSP1 antibody, small interfering RNA-TSP1, or an inhibitory peptide blocked glucose-mediated increases in TGF-beta activity and extracellular matrix protein (fibronectin) expression. |
| 6271 | 20164378 | Overexpression of constitutively active PKG, but not the PKG-I protein, inhibited glucose-induced TSP1 expression and TGF-beta bioactivity, suggesting that PKG protein expression is insufficient to regulate TSP1 expression. |
| 6272 | 20164378 | Together, these data establish that glucose-mediated downregulation of PKG levels stimulates TSP1 expression and enhances TGF-beta activity and matrix protein expression, which can contribute to vascular remodeling in diabetes. |
| 6273 | 20164378 | It is well established that thrombospondin1 (TSP1) is a major regulator of TGF-beta activation in renal and cardiac complications of diabetes. |
| 6274 | 20164378 | In the present study, we investigated whether high glucose regulation of PKG protein and activity in VSMCs similarly regulates TSP1 expression and downstream TGF-beta activity. |
| 6275 | 20164378 | These studies showed that high glucose stimulates both TSP1 expression and TGF-beta bioactivity in primary murine aortic smooth muscle cells (VSMCs). |
| 6276 | 20164378 | TSP1 is responsible for the increased TGF-beta bioactivity under high glucose conditions, because treatment with anti-TSP1 antibody, small interfering RNA-TSP1, or an inhibitory peptide blocked glucose-mediated increases in TGF-beta activity and extracellular matrix protein (fibronectin) expression. |
| 6277 | 20164378 | Overexpression of constitutively active PKG, but not the PKG-I protein, inhibited glucose-induced TSP1 expression and TGF-beta bioactivity, suggesting that PKG protein expression is insufficient to regulate TSP1 expression. |
| 6278 | 20164378 | Together, these data establish that glucose-mediated downregulation of PKG levels stimulates TSP1 expression and enhances TGF-beta activity and matrix protein expression, which can contribute to vascular remodeling in diabetes. |
| 6279 | 20170650 | Continuous high glucose exposure for 2-12 days significantly elevated gene expressions and protein concentrations of IL-1 beta, NF-kB, VEGF, TNF-alpha, TGF-beta and ICAM-1 in retinal pericytes. |
| 6280 | 20175453 | Menin function is related to transcriptional regulation and cell cycle control and it physically and functionally interacts with osteotropic transcription factors, such as Smad1/5, Smad3, Runx2 and JunD. |
| 6281 | 20175453 | Menin promotes the commitment of pluripotent mesenchymal stem cells to the osteoblast lineage, mediated by interactions between menin and the BMP signaling molecules, Smad1/5, or Runx2. |
| 6282 | 20175453 | On the other hand, in mature osteoblasts the interaction of menin and the TGF-beta/Smad3 pathway counteracts the BMP-2/Smad1/5- and Runx2-induced transcriptional activities leading to inhibition of late stage osteoblast differentiation. |
| 6283 | 20182412 | Further, there was increased glomerular expression of extracellular matrix proteins, monocyte chemoattractant protein-1 and transforming growth factor-beta. |
| 6284 | 20182412 | These effects were accompanied by blockade of the compensatory increase of renin production and angiotensin I/II accumulation in the kidney. |
| 6285 | 20191437 | Fibrosis of the thyroid tissue was assessed, based on the expression levels of fibrosis-associated genes (COL1A1 and COL3A1) in thyroid FNAB samples, on the FNAB specimen cellularity and other features of the tissue fibrosis assessed during cytological examination, as well as on the size of thyroid gland and its function. |
| 6286 | 20191437 | Following routine cytological examination, 63 thyroid FNAB specimens, received from patients with Hashimoto's thyroiditis (HT, n=30) and non-toxic goitre (NTG, n=33), were quantitatively evaluated regarding TGFB1, COL1A1 and COL3A1 expression level by real-time PCR in the ABI PRISM 7500 Sequence Detection System. |
| 6287 | 20191437 | The obtained results showed statistically significant differences regarding the expression level (RQ) of TGFB1 and of COL1A1 genes between the groups with HT and with NTG (higher expression in HT group). |
| 6288 | 20191437 | In HT group statistically significant correlation was found between TGFB1 gene and COL3A1 gene expression levels (p<0.05). |
| 6289 | 20191437 | Fibrosis of the thyroid tissue was assessed, based on the expression levels of fibrosis-associated genes (COL1A1 and COL3A1) in thyroid FNAB samples, on the FNAB specimen cellularity and other features of the tissue fibrosis assessed during cytological examination, as well as on the size of thyroid gland and its function. |
| 6290 | 20191437 | Following routine cytological examination, 63 thyroid FNAB specimens, received from patients with Hashimoto's thyroiditis (HT, n=30) and non-toxic goitre (NTG, n=33), were quantitatively evaluated regarding TGFB1, COL1A1 and COL3A1 expression level by real-time PCR in the ABI PRISM 7500 Sequence Detection System. |
| 6291 | 20191437 | The obtained results showed statistically significant differences regarding the expression level (RQ) of TGFB1 and of COL1A1 genes between the groups with HT and with NTG (higher expression in HT group). |
| 6292 | 20191437 | In HT group statistically significant correlation was found between TGFB1 gene and COL3A1 gene expression levels (p<0.05). |
| 6293 | 20191437 | Fibrosis of the thyroid tissue was assessed, based on the expression levels of fibrosis-associated genes (COL1A1 and COL3A1) in thyroid FNAB samples, on the FNAB specimen cellularity and other features of the tissue fibrosis assessed during cytological examination, as well as on the size of thyroid gland and its function. |
| 6294 | 20191437 | Following routine cytological examination, 63 thyroid FNAB specimens, received from patients with Hashimoto's thyroiditis (HT, n=30) and non-toxic goitre (NTG, n=33), were quantitatively evaluated regarding TGFB1, COL1A1 and COL3A1 expression level by real-time PCR in the ABI PRISM 7500 Sequence Detection System. |
| 6295 | 20191437 | The obtained results showed statistically significant differences regarding the expression level (RQ) of TGFB1 and of COL1A1 genes between the groups with HT and with NTG (higher expression in HT group). |
| 6296 | 20191437 | In HT group statistically significant correlation was found between TGFB1 gene and COL3A1 gene expression levels (p<0.05). |
| 6297 | 20197308 | Proinsulin C-peptide antagonizes the profibrotic effects of TGF-beta1 via up-regulation of retinoic acid and HGF-related signaling pathways. |
| 6298 | 20197308 | Expression of retinoic acid receptor beta (RARbeta), hepatocyte growth factor (HGF), cellular retinoic acid-binding protein II (CRABPII), vimentin, E-cadherin, Snail, and beta-catenin was assessed by immunoblotting. |
| 6299 | 20197308 | The cellular localization of vimentin and beta-catenin was determined by immunocytochemistry. |
| 6300 | 20197308 | Immunoblotting demonstrated that C-peptide increased RARbeta, CRABPII, and HGF. |
| 6301 | 20197308 | Further, effects of TGF-beta1 on Snail and E-cadherin expression were blocked by HGF, and inhibitory effects of C-peptide were removed by blockade of HGF activity. |
| 6302 | 20197308 | Proinsulin C-peptide antagonizes the profibrotic effects of TGF-beta1 via up-regulation of retinoic acid and HGF-related signaling pathways. |
| 6303 | 20197308 | Expression of retinoic acid receptor beta (RARbeta), hepatocyte growth factor (HGF), cellular retinoic acid-binding protein II (CRABPII), vimentin, E-cadherin, Snail, and beta-catenin was assessed by immunoblotting. |
| 6304 | 20197308 | The cellular localization of vimentin and beta-catenin was determined by immunocytochemistry. |
| 6305 | 20197308 | Immunoblotting demonstrated that C-peptide increased RARbeta, CRABPII, and HGF. |
| 6306 | 20197308 | Further, effects of TGF-beta1 on Snail and E-cadherin expression were blocked by HGF, and inhibitory effects of C-peptide were removed by blockade of HGF activity. |
| 6307 | 20200004 | Parathyroid hormone-related protein induces hypertrophy in podocytes via TGF-beta(1) and p27(Kip1): implications for diabetic nephropathy. |
| 6308 | 20213272 | TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2. |
| 6309 | 20213272 | Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains. |
| 6310 | 20213272 | TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L). |
| 6311 | 20213272 | Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect. |
| 6312 | 20213272 | Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L. |
| 6313 | 20213272 | Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells. |
| 6314 | 20213272 | TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2. |
| 6315 | 20213272 | Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains. |
| 6316 | 20213272 | TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L). |
| 6317 | 20213272 | Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect. |
| 6318 | 20213272 | Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L. |
| 6319 | 20213272 | Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells. |
| 6320 | 20213272 | TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2. |
| 6321 | 20213272 | Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains. |
| 6322 | 20213272 | TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L). |
| 6323 | 20213272 | Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect. |
| 6324 | 20213272 | Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L. |
| 6325 | 20213272 | Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells. |
| 6326 | 20213272 | TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2. |
| 6327 | 20213272 | Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains. |
| 6328 | 20213272 | TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L). |
| 6329 | 20213272 | Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect. |
| 6330 | 20213272 | Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L. |
| 6331 | 20213272 | Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells. |
| 6332 | 20213272 | TGF-beta stimulates biglycan synthesis via p38 and ERK phosphorylation of the linker region of Smad2. |
| 6333 | 20213272 | Transforming growth factor (TGF)-beta treatment of human vascular smooth-muscle cells increases the expression of biglycan and causes marked elongation of its glycosaminoglycan (GAG) chains. |
| 6334 | 20213272 | TGF-beta-stimulated phosphorylation of p38, ERK, and JNK as well as Smad2 at both its carboxy terminal (phospho-Smad2C) and in the linker region (phospho-Smad2L). |
| 6335 | 20213272 | Pharmacological inhibition of ERK and p38 blocked TGF-beta-mediated GAG elongation and expression of biglycan whereas inhibition of JNK had no effect. |
| 6336 | 20213272 | Inhibition of ERK and p38 but not JNK attenuated the effect of TGF-beta to increase phospho-Smad2L. |
| 6337 | 20213272 | Thus, MAP kinase signaling through ERK and p38 and via phosphorylation of the linker region of Smad2 mediates the effects of TGF-beta on biglycan synthesis in vascular smooth-muscle cells. |
| 6338 | 20215829 | Expression changes of transforming growth factor-beta1 and thrombospondin-1 in cavernous tissues of diabetic rats. |
| 6339 | 20222150 | In particular, biomarkers of renal dysfunction such as transferrin, type IV collagen and N-acetyl-beta-D-glucosaminidase might prove to be more sensitive than urinary albumin, the current gold standard, in the detection of incipient nephropathy and risk assessment of cardiovascular disease. |
| 6340 | 20222150 | Inflammatory markers including orosomucoid, tumour necrosis factor-alpha, transforming growth factor-beta, vascular endothelial growth factor and monocyte chemoattractant protein-1, as well as oxidative stress markers such as 8-hydroxy-2'deoxyguanosine may also be useful biomarkers for diagnosis or monitoring of diabetic complications, particularly kidney disease. |
| 6341 | 20231436 | Treg cells from the gut proved dissimilar to cells elicited by exposure to TGFbeta in vitro, but instead they resembled a CD103(+)Klrg1(+) subphenotype preferentially generated in response to lymphopenia. |
| 6342 | 20310083 | Control rats (n=18)underwent only buffer injection.Out of the 55 diabetic rats, 19 were chronically treated with insulin and 13 with the ACEI (ACE inhibitor) ramipril (3 mg x kg(-1 )of body weight x day(-1)). |
| 6343 | 20310083 | Left ventricular interstitial and perivascular fibrosis, and TGF-beta1 (transforming growth factor-beta1) protein levels were increased in diabetic rats, but not in insulin-treated diabetic rats and ramipril-treated diabetic rats, compared with control rats. |
| 6344 | 20310083 | This was accompanied by a significant reduction in active TGF-beta1 and phospho-Smad2/3 protein levels in myocardial tissue of diabetic rats. |
| 6345 | 20310083 | In conclusion, Ac-SDKP administration in diabetic rats reduces left ventricular interstitial and perivascular fibrosis, active TGF-beta1 and phospho-Smad2/3levels, and improves diastolic function. |
| 6346 | 20310083 | Control rats (n=18)underwent only buffer injection.Out of the 55 diabetic rats, 19 were chronically treated with insulin and 13 with the ACEI (ACE inhibitor) ramipril (3 mg x kg(-1 )of body weight x day(-1)). |
| 6347 | 20310083 | Left ventricular interstitial and perivascular fibrosis, and TGF-beta1 (transforming growth factor-beta1) protein levels were increased in diabetic rats, but not in insulin-treated diabetic rats and ramipril-treated diabetic rats, compared with control rats. |
| 6348 | 20310083 | This was accompanied by a significant reduction in active TGF-beta1 and phospho-Smad2/3 protein levels in myocardial tissue of diabetic rats. |
| 6349 | 20310083 | In conclusion, Ac-SDKP administration in diabetic rats reduces left ventricular interstitial and perivascular fibrosis, active TGF-beta1 and phospho-Smad2/3levels, and improves diastolic function. |
| 6350 | 20310083 | Control rats (n=18)underwent only buffer injection.Out of the 55 diabetic rats, 19 were chronically treated with insulin and 13 with the ACEI (ACE inhibitor) ramipril (3 mg x kg(-1 )of body weight x day(-1)). |
| 6351 | 20310083 | Left ventricular interstitial and perivascular fibrosis, and TGF-beta1 (transforming growth factor-beta1) protein levels were increased in diabetic rats, but not in insulin-treated diabetic rats and ramipril-treated diabetic rats, compared with control rats. |
| 6352 | 20310083 | This was accompanied by a significant reduction in active TGF-beta1 and phospho-Smad2/3 protein levels in myocardial tissue of diabetic rats. |
| 6353 | 20310083 | In conclusion, Ac-SDKP administration in diabetic rats reduces left ventricular interstitial and perivascular fibrosis, active TGF-beta1 and phospho-Smad2/3levels, and improves diastolic function. |
| 6354 | 20335317 | The pcDNA3.1-RSOR/MIOX transfectants had an increased NADH/NAD(+) ratio, PKC and TGF-beta activity, Raf1:Ras association, and p-ERK phosphorylation. |
| 6355 | 20335317 | These changes were significantly reduced by the inhibitors of PKC, aldose reductase, Ras farnesylation, and MEK1. |
| 6356 | 20335317 | Expression of E-cadherin and vimentin paralleled in cells overexpressing RSOR/MIOX or subjected to high-glucose ambience. |
| 6357 | 20375117 | Activation of glomerular PKC, along with increased transforming growth factor-beta1, VEGFR1, VEGFR2, and VEGF were all detected in glomeruli of GT1S mice, likely contributing to GS. |
| 6358 | 20382513 | Roasted licorice extracts dampen high glucose-induced mesangial hyperplasia and matrix deposition through blocking Akt activation and TGF-beta signaling. |
| 6359 | 20382513 | Exposure of cells to HG caused significant increases in collagen IV secretion and connective tissue growth factor (CTGF) expression, which was appeased by RLW and RLE at transcriptional levels. |
| 6360 | 20382513 | In addition, RLW and RLE but not LW modulated membrane type matrix metalloproteinase-1 (MT-1 MMP) expression, MMP-2 activity and tissue inhibitor of MMP-2 (TIMP-2), which facilitated the degradation of mesangial matrix. |
| 6361 | 20382513 | Furthermore, the augmented expression of CTGF and TIMP-2 in HG-exposed cells was mediated by Akt activation and TGF-beta/Smad signaling through PKCbeta2-responsive signaling pathways. |
| 6362 | 20382513 | However, HG-down-regulated MT-1 MMP expression was independent of activation of ERK1/2 and Akt when using their inhibitors of DB98059 (ERK1/2) and LY294002 (Akt) alone or in combination. |
| 6363 | 20382513 | Roasted licorice extracts dampen high glucose-induced mesangial hyperplasia and matrix deposition through blocking Akt activation and TGF-beta signaling. |
| 6364 | 20382513 | Exposure of cells to HG caused significant increases in collagen IV secretion and connective tissue growth factor (CTGF) expression, which was appeased by RLW and RLE at transcriptional levels. |
| 6365 | 20382513 | In addition, RLW and RLE but not LW modulated membrane type matrix metalloproteinase-1 (MT-1 MMP) expression, MMP-2 activity and tissue inhibitor of MMP-2 (TIMP-2), which facilitated the degradation of mesangial matrix. |
| 6366 | 20382513 | Furthermore, the augmented expression of CTGF and TIMP-2 in HG-exposed cells was mediated by Akt activation and TGF-beta/Smad signaling through PKCbeta2-responsive signaling pathways. |
| 6367 | 20382513 | However, HG-down-regulated MT-1 MMP expression was independent of activation of ERK1/2 and Akt when using their inhibitors of DB98059 (ERK1/2) and LY294002 (Akt) alone or in combination. |
| 6368 | 20384863 | We did not observe any difference in Treg percentages between study and control group but there was lower expression of some molecules including transforming growth factor-beta and interleukin-12 family members in Treg cells separated from children with MS compared to the healthy subjects. |
| 6369 | 20385725 | In this review, we will attempt to clarify the functions of these agents in in vitro differentiation strategies by focusing on the intracellular signaling pathways through which they operate - phosphatidylinositol 3-kinase, transforming growth factor beta, Wnt/beta-catenin, Hedgehog, and Notch. |
| 6370 | 20393144 | E-cadherin expression is regulated by miR-192/215 by a mechanism that is independent of the profibrotic effects of transforming growth factor-beta. |
| 6371 | 20393450 | Regulation of transforming growth factor-beta1 by insulin in prediabetic African Americans. |
| 6372 | 20393450 | The urinary TGF-beta1 level increased by 56% followed by a 23% decrease in the normal glucose tolerance group, changes that were significant and corresponded to the changes in the plasma glucose and insulin concentrations. |
| 6373 | 20393450 | At baseline, there was a significant correlation between the urinary TGF-beta1 level and urinary albumin excretion. |
| 6374 | 20393450 | Thus our results suggest that insulin contributes to increased TGF-beta1 production and possible early renal injury in prediabetic young African Americans. |
| 6375 | 20393450 | Regulation of transforming growth factor-beta1 by insulin in prediabetic African Americans. |
| 6376 | 20393450 | The urinary TGF-beta1 level increased by 56% followed by a 23% decrease in the normal glucose tolerance group, changes that were significant and corresponded to the changes in the plasma glucose and insulin concentrations. |
| 6377 | 20393450 | At baseline, there was a significant correlation between the urinary TGF-beta1 level and urinary albumin excretion. |
| 6378 | 20393450 | Thus our results suggest that insulin contributes to increased TGF-beta1 production and possible early renal injury in prediabetic young African Americans. |
| 6379 | 20393450 | Regulation of transforming growth factor-beta1 by insulin in prediabetic African Americans. |
| 6380 | 20393450 | The urinary TGF-beta1 level increased by 56% followed by a 23% decrease in the normal glucose tolerance group, changes that were significant and corresponded to the changes in the plasma glucose and insulin concentrations. |
| 6381 | 20393450 | At baseline, there was a significant correlation between the urinary TGF-beta1 level and urinary albumin excretion. |
| 6382 | 20393450 | Thus our results suggest that insulin contributes to increased TGF-beta1 production and possible early renal injury in prediabetic young African Americans. |
| 6383 | 20393450 | Regulation of transforming growth factor-beta1 by insulin in prediabetic African Americans. |
| 6384 | 20393450 | The urinary TGF-beta1 level increased by 56% followed by a 23% decrease in the normal glucose tolerance group, changes that were significant and corresponded to the changes in the plasma glucose and insulin concentrations. |
| 6385 | 20393450 | At baseline, there was a significant correlation between the urinary TGF-beta1 level and urinary albumin excretion. |
| 6386 | 20393450 | Thus our results suggest that insulin contributes to increased TGF-beta1 production and possible early renal injury in prediabetic young African Americans. |
| 6387 | 20399741 | Glycated albumin activates NADPH oxidase in rat mesangial cells through up-regulation of p47phox. |
| 6388 | 20399741 | Glycated albumin, an early-glycation Amadori-modified protein, stimulates transforming growth factor-beta (TGF-beta) expression and increases the production of the extracellular matrix proteins in mesangial cells, contributing to the pathogenesis of diabetic nephropathy. |
| 6389 | 20399741 | Glycated albumin has been shown to increase NADPH oxidase-dependent superoxide formation in mesangial cells. |
| 6390 | 20399741 | Therefore, in the present studies, we determined the mechanisms by which glycated albumin activates NADPH oxidase in primary rat mesangial cells and its contribution to glycated albumin-induced TGF-beta expression and extracellular matrix protein production. |
| 6391 | 20399741 | Our data showed that glycated albumin treatment stimulated NADPH oxidase activity and increased the formation of superoxide formation in rat mesangial cells. |
| 6392 | 20399741 | Moreover, glycated albumin treatment stimulated the expression and phosphorylation of p47phox, one of the cytosolic regulatory subunits of the NADPH oxidase. |
| 6393 | 20399741 | However, the levels of other NADPH oxidase subunits including Nox1, Nox2, Nox4, p22phox, and p67phox were not altered by glycated albumin. |
| 6394 | 20399741 | Moreover, siRNA-mediated knockdown of p47phox inhibited glycated albumin-induced NADPH oxidase activity and superoxide formation. |
| 6395 | 20399741 | Glycated albumin-induced TGF-beta expression and extracellular matrix production (fibronectin) was also inhibited by p47phox knock down. |
| 6396 | 20399741 | Taken together, these data suggest that up-regulation of p47phox is involved in glycated albumin-mediated activation of NADPH oxidase, leading to glycated albumin-induced expression of TGF-beta and extracellular matrix proteins in mesangial cells and contributing to the development of diabetic nephropathy. |
| 6397 | 20399741 | Glycated albumin activates NADPH oxidase in rat mesangial cells through up-regulation of p47phox. |
| 6398 | 20399741 | Glycated albumin, an early-glycation Amadori-modified protein, stimulates transforming growth factor-beta (TGF-beta) expression and increases the production of the extracellular matrix proteins in mesangial cells, contributing to the pathogenesis of diabetic nephropathy. |
| 6399 | 20399741 | Glycated albumin has been shown to increase NADPH oxidase-dependent superoxide formation in mesangial cells. |
| 6400 | 20399741 | Therefore, in the present studies, we determined the mechanisms by which glycated albumin activates NADPH oxidase in primary rat mesangial cells and its contribution to glycated albumin-induced TGF-beta expression and extracellular matrix protein production. |
| 6401 | 20399741 | Our data showed that glycated albumin treatment stimulated NADPH oxidase activity and increased the formation of superoxide formation in rat mesangial cells. |
| 6402 | 20399741 | Moreover, glycated albumin treatment stimulated the expression and phosphorylation of p47phox, one of the cytosolic regulatory subunits of the NADPH oxidase. |
| 6403 | 20399741 | However, the levels of other NADPH oxidase subunits including Nox1, Nox2, Nox4, p22phox, and p67phox were not altered by glycated albumin. |
| 6404 | 20399741 | Moreover, siRNA-mediated knockdown of p47phox inhibited glycated albumin-induced NADPH oxidase activity and superoxide formation. |
| 6405 | 20399741 | Glycated albumin-induced TGF-beta expression and extracellular matrix production (fibronectin) was also inhibited by p47phox knock down. |
| 6406 | 20399741 | Taken together, these data suggest that up-regulation of p47phox is involved in glycated albumin-mediated activation of NADPH oxidase, leading to glycated albumin-induced expression of TGF-beta and extracellular matrix proteins in mesangial cells and contributing to the development of diabetic nephropathy. |
| 6407 | 20399741 | Glycated albumin activates NADPH oxidase in rat mesangial cells through up-regulation of p47phox. |
| 6408 | 20399741 | Glycated albumin, an early-glycation Amadori-modified protein, stimulates transforming growth factor-beta (TGF-beta) expression and increases the production of the extracellular matrix proteins in mesangial cells, contributing to the pathogenesis of diabetic nephropathy. |
| 6409 | 20399741 | Glycated albumin has been shown to increase NADPH oxidase-dependent superoxide formation in mesangial cells. |
| 6410 | 20399741 | Therefore, in the present studies, we determined the mechanisms by which glycated albumin activates NADPH oxidase in primary rat mesangial cells and its contribution to glycated albumin-induced TGF-beta expression and extracellular matrix protein production. |
| 6411 | 20399741 | Our data showed that glycated albumin treatment stimulated NADPH oxidase activity and increased the formation of superoxide formation in rat mesangial cells. |
| 6412 | 20399741 | Moreover, glycated albumin treatment stimulated the expression and phosphorylation of p47phox, one of the cytosolic regulatory subunits of the NADPH oxidase. |
| 6413 | 20399741 | However, the levels of other NADPH oxidase subunits including Nox1, Nox2, Nox4, p22phox, and p67phox were not altered by glycated albumin. |
| 6414 | 20399741 | Moreover, siRNA-mediated knockdown of p47phox inhibited glycated albumin-induced NADPH oxidase activity and superoxide formation. |
| 6415 | 20399741 | Glycated albumin-induced TGF-beta expression and extracellular matrix production (fibronectin) was also inhibited by p47phox knock down. |
| 6416 | 20399741 | Taken together, these data suggest that up-regulation of p47phox is involved in glycated albumin-mediated activation of NADPH oxidase, leading to glycated albumin-induced expression of TGF-beta and extracellular matrix proteins in mesangial cells and contributing to the development of diabetic nephropathy. |
| 6417 | 20399741 | Glycated albumin activates NADPH oxidase in rat mesangial cells through up-regulation of p47phox. |
| 6418 | 20399741 | Glycated albumin, an early-glycation Amadori-modified protein, stimulates transforming growth factor-beta (TGF-beta) expression and increases the production of the extracellular matrix proteins in mesangial cells, contributing to the pathogenesis of diabetic nephropathy. |
| 6419 | 20399741 | Glycated albumin has been shown to increase NADPH oxidase-dependent superoxide formation in mesangial cells. |
| 6420 | 20399741 | Therefore, in the present studies, we determined the mechanisms by which glycated albumin activates NADPH oxidase in primary rat mesangial cells and its contribution to glycated albumin-induced TGF-beta expression and extracellular matrix protein production. |
| 6421 | 20399741 | Our data showed that glycated albumin treatment stimulated NADPH oxidase activity and increased the formation of superoxide formation in rat mesangial cells. |
| 6422 | 20399741 | Moreover, glycated albumin treatment stimulated the expression and phosphorylation of p47phox, one of the cytosolic regulatory subunits of the NADPH oxidase. |
| 6423 | 20399741 | However, the levels of other NADPH oxidase subunits including Nox1, Nox2, Nox4, p22phox, and p67phox were not altered by glycated albumin. |
| 6424 | 20399741 | Moreover, siRNA-mediated knockdown of p47phox inhibited glycated albumin-induced NADPH oxidase activity and superoxide formation. |
| 6425 | 20399741 | Glycated albumin-induced TGF-beta expression and extracellular matrix production (fibronectin) was also inhibited by p47phox knock down. |
| 6426 | 20399741 | Taken together, these data suggest that up-regulation of p47phox is involved in glycated albumin-mediated activation of NADPH oxidase, leading to glycated albumin-induced expression of TGF-beta and extracellular matrix proteins in mesangial cells and contributing to the development of diabetic nephropathy. |
| 6427 | 20404057 | Fenofibrate attenuates tubulointerstitial fibrosis and inflammation through suppression of nuclear factor-κB and transforming growth factor-β1/Smad3 in diabetic nephropathy. |
| 6428 | 20404057 | The diabetic condition of ZD rats was associated with an increase in collagen and alpha-smooth muscle actin accumulation in the kidney, which was significantly reduced by fenofibrate. |
| 6429 | 20404057 | Chronic treatment of ZD rats with fenofibrate attenuated renal inflammation and tubular injury as evidenced by a decrease in mRNA and protein expression of secreted phosphoprotein-1, monocyte chemotactic protein-1 and kidney injury molecule-1 in the kidneys. |
| 6430 | 20404057 | Moreover, renal nuclear factor (NF)-kappaB DNA-binding activity, transforming growth factor (TGF)-beta1 and phospho-Smad3 proteins were significantly higher in ZD animals compared with ZL ones. |
| 6431 | 20404057 | This increase in NF-kappaB activity, TGF-beta1 expression and Smad3 phosphorylation was greatly attenuated by fenofibrate in the diabetic kidneys. |
| 6432 | 20404057 | Taken together, fenofibrate suppressed NF-kappaB and TGF-beta1/Smad3 signaling pathways and reduced renal inflammation and tubulointerstitial fibrosis in diabetic ZD animals. |
| 6433 | 20404057 | Fenofibrate attenuates tubulointerstitial fibrosis and inflammation through suppression of nuclear factor-κB and transforming growth factor-β1/Smad3 in diabetic nephropathy. |
| 6434 | 20404057 | The diabetic condition of ZD rats was associated with an increase in collagen and alpha-smooth muscle actin accumulation in the kidney, which was significantly reduced by fenofibrate. |
| 6435 | 20404057 | Chronic treatment of ZD rats with fenofibrate attenuated renal inflammation and tubular injury as evidenced by a decrease in mRNA and protein expression of secreted phosphoprotein-1, monocyte chemotactic protein-1 and kidney injury molecule-1 in the kidneys. |
| 6436 | 20404057 | Moreover, renal nuclear factor (NF)-kappaB DNA-binding activity, transforming growth factor (TGF)-beta1 and phospho-Smad3 proteins were significantly higher in ZD animals compared with ZL ones. |
| 6437 | 20404057 | This increase in NF-kappaB activity, TGF-beta1 expression and Smad3 phosphorylation was greatly attenuated by fenofibrate in the diabetic kidneys. |
| 6438 | 20404057 | Taken together, fenofibrate suppressed NF-kappaB and TGF-beta1/Smad3 signaling pathways and reduced renal inflammation and tubulointerstitial fibrosis in diabetic ZD animals. |
| 6439 | 20422227 | Increased accumulation of extracellular matrix proteins in the glomeruli and marked upregulation of angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, transforming growth factor beta-1 (TGF-beta1), and plasminogen activator inhibitor-1 (PAI-1) gene expression were evident in the renal cortex of hypertensive offspring of diabetic mothers. |
| 6440 | 20422227 | By contrast, angiotensin-converting enzyme-2 (ACE2) gene expression was lower in the hypertensive offspring of diabetic mothers than in that of non-diabetic mothers. |
| 6441 | 20422227 | These data indicate that maternal diabetes induces perinatal programming of hypertension, renal injury, and glucose intolerance in the offspring and suggest a central role for the activation of the intrarenal renin-angiotensin system and TGF-beta1 gene expression in this process. |
| 6442 | 20422227 | Increased accumulation of extracellular matrix proteins in the glomeruli and marked upregulation of angiotensinogen, angiotensin II type 1 receptor, angiotensin-converting enzyme, transforming growth factor beta-1 (TGF-beta1), and plasminogen activator inhibitor-1 (PAI-1) gene expression were evident in the renal cortex of hypertensive offspring of diabetic mothers. |
| 6443 | 20422227 | By contrast, angiotensin-converting enzyme-2 (ACE2) gene expression was lower in the hypertensive offspring of diabetic mothers than in that of non-diabetic mothers. |
| 6444 | 20422227 | These data indicate that maternal diabetes induces perinatal programming of hypertension, renal injury, and glucose intolerance in the offspring and suggest a central role for the activation of the intrarenal renin-angiotensin system and TGF-beta1 gene expression in this process. |
| 6445 | 20437788 | These secretory proteins include cytokines and growth factors such as transforming growth factor-beta, vascular endothelia growth factor, platelet derived growth factor, and so on. |
| 6446 | 20444936 | Inhibition of dipeptidyl peptidase IV (DPP-IV) activity by NVP-DPP728, a DPP-IV inhibitor, improves the therapeutic efficacy of glucagon-like peptide-1 (GLP-1). |
| 6447 | 20444936 | Regulatory T cells in thymus and secondary lymph nodes, TGF-beta1 and GLP-1 in plasma, and the insulin content in the pancreas were measured. |
| 6448 | 20444936 | Insulitis was reduced and the percentage of CD4(+)CD25(+)FoxP3(+) regulatory T cells was increased in treated NOD mice with remission. |
| 6449 | 20444936 | Plasma TGF-beta1 and GLP-1, the insulin content, and both insulin(+) and BrdU(+) beta-cells in pancreas were also significantly increased. |
| 6450 | 20444936 | In conclusion, NVP-DPP728 treatment can reverse new-onset diabetes in NOD mice by reducing insulitis, increasing CD4(+)CD25(+)FoxP3(+) regulatory T cells, and stimulating beta-cell replication. beta-Cell replication is not associated with the degree of inflammation in NVP-DPP728-treated NOD mice. |
| 6451 | 20444936 | Inhibition of dipeptidyl peptidase IV (DPP-IV) activity by NVP-DPP728, a DPP-IV inhibitor, improves the therapeutic efficacy of glucagon-like peptide-1 (GLP-1). |
| 6452 | 20444936 | Regulatory T cells in thymus and secondary lymph nodes, TGF-beta1 and GLP-1 in plasma, and the insulin content in the pancreas were measured. |
| 6453 | 20444936 | Insulitis was reduced and the percentage of CD4(+)CD25(+)FoxP3(+) regulatory T cells was increased in treated NOD mice with remission. |
| 6454 | 20444936 | Plasma TGF-beta1 and GLP-1, the insulin content, and both insulin(+) and BrdU(+) beta-cells in pancreas were also significantly increased. |
| 6455 | 20444936 | In conclusion, NVP-DPP728 treatment can reverse new-onset diabetes in NOD mice by reducing insulitis, increasing CD4(+)CD25(+)FoxP3(+) regulatory T cells, and stimulating beta-cell replication. beta-Cell replication is not associated with the degree of inflammation in NVP-DPP728-treated NOD mice. |
| 6456 | 20445103 | Leptin-deficient ob/ob mice are overweight, develop insulin resistance, and serve as a model for type 2 diabetes (T2D). |
| 6457 | 20445103 | We induced TGF-beta-dependent CD4(+) latency-associated peptide (LAP)-positive Tregs by oral administration of anti-CD3 antibody plus beta-glucosylceramide. |
| 6458 | 20445103 | Adoptive transfer of orally induced CD4(+)LAP(+) Tregs ameliorated metabolic and cytokine abnormalities. |
| 6459 | 20447389 | The purpose of the present study was to investigate the effects of berberine on the nuclear factor-kappa B (NF-kappaB) activation, intercellular adhesion molecule-1, transforming growth factor-beta1 and fibronectin protein expression in renal tissue from alloxan-induced diabetic mice with renal damage. |
| 6460 | 20447389 | The distribution of NF-kappaB p65 in glomerulus and the degradation of I kappaB-alpha in renal cortex were examined by immunohistochemistry and Western blot, respectively. |
| 6461 | 20447389 | The protein expression of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin in renal cortex were also detected by Western blot. |
| 6462 | 20447389 | Our results revealed that in alloxan-induced diabetic mice, the nuclear staining of NF-kappaB p65 was increased in glomerulus, whereas renal I kappaB-alpha protein was significantly reduced. |
| 6463 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were upregulated in kidney from diabetic mice. |
| 6464 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were all downregulated by berberine compared with diabetic model group. |
| 6465 | 20447389 | The purpose of the present study was to investigate the effects of berberine on the nuclear factor-kappa B (NF-kappaB) activation, intercellular adhesion molecule-1, transforming growth factor-beta1 and fibronectin protein expression in renal tissue from alloxan-induced diabetic mice with renal damage. |
| 6466 | 20447389 | The distribution of NF-kappaB p65 in glomerulus and the degradation of I kappaB-alpha in renal cortex were examined by immunohistochemistry and Western blot, respectively. |
| 6467 | 20447389 | The protein expression of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin in renal cortex were also detected by Western blot. |
| 6468 | 20447389 | Our results revealed that in alloxan-induced diabetic mice, the nuclear staining of NF-kappaB p65 was increased in glomerulus, whereas renal I kappaB-alpha protein was significantly reduced. |
| 6469 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were upregulated in kidney from diabetic mice. |
| 6470 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were all downregulated by berberine compared with diabetic model group. |
| 6471 | 20447389 | The purpose of the present study was to investigate the effects of berberine on the nuclear factor-kappa B (NF-kappaB) activation, intercellular adhesion molecule-1, transforming growth factor-beta1 and fibronectin protein expression in renal tissue from alloxan-induced diabetic mice with renal damage. |
| 6472 | 20447389 | The distribution of NF-kappaB p65 in glomerulus and the degradation of I kappaB-alpha in renal cortex were examined by immunohistochemistry and Western blot, respectively. |
| 6473 | 20447389 | The protein expression of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin in renal cortex were also detected by Western blot. |
| 6474 | 20447389 | Our results revealed that in alloxan-induced diabetic mice, the nuclear staining of NF-kappaB p65 was increased in glomerulus, whereas renal I kappaB-alpha protein was significantly reduced. |
| 6475 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were upregulated in kidney from diabetic mice. |
| 6476 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were all downregulated by berberine compared with diabetic model group. |
| 6477 | 20447389 | The purpose of the present study was to investigate the effects of berberine on the nuclear factor-kappa B (NF-kappaB) activation, intercellular adhesion molecule-1, transforming growth factor-beta1 and fibronectin protein expression in renal tissue from alloxan-induced diabetic mice with renal damage. |
| 6478 | 20447389 | The distribution of NF-kappaB p65 in glomerulus and the degradation of I kappaB-alpha in renal cortex were examined by immunohistochemistry and Western blot, respectively. |
| 6479 | 20447389 | The protein expression of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin in renal cortex were also detected by Western blot. |
| 6480 | 20447389 | Our results revealed that in alloxan-induced diabetic mice, the nuclear staining of NF-kappaB p65 was increased in glomerulus, whereas renal I kappaB-alpha protein was significantly reduced. |
| 6481 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were upregulated in kidney from diabetic mice. |
| 6482 | 20447389 | The protein levels of intercellular adhesion molecule-1, transforming growth factor-beta 1 and fibronectin were all downregulated by berberine compared with diabetic model group. |
| 6483 | 20479236 | An insertion polymorphism of the angiotensin-I converting enzyme gene (ACE) is common in humans and the higher expressing allele is associated with an increased risk of diabetic complications. |
| 6484 | 20479236 | The ACE polymorphism does not significantly affect blood pressure or angiotensin II levels, suggesting that the kallikrein-kinin system partly mediates the effects of the polymorphism. |
| 6485 | 20479236 | We have therefore explored the influence of lack of both bradykinin receptors (B1R and B2R) on diabetic nephropathy, neuropathy, and osteopathy in male mice heterozygous for the Akita diabetogenic mutation in the insulin 2 gene (Ins2). |
| 6486 | 20479236 | We find that all of the detrimental phenotypes observed in Akita diabetes are enhanced by lack of both B1R and B2R, including urinary albumin excretion, glomerulosclerosis, glomerular basement membrane thickening, mitochondrial DNA deletions, reduction of nerve conduction velocities and of heat sensation, and bone mineral loss. |
| 6487 | 20479236 | Absence of the bradykinin receptors also enhances the diabetes-associated increases in plasma thiobarbituric acid-reactive substances, mitochondrial DNA deletions, and renal expression of fibrogenic genes, including transforming growth factor beta1, connective tissue growth factor, and endothelin-1. |
| 6488 | 20479236 | Thus, lack of B1R and B2R exacerbates diabetic complications. |
| 6489 | 20479236 | The enhanced renal injury in diabetic mice caused by lack of B1R and B2R may be mediated by a combination of increases in oxidative stress, mitochondrial DNA damage and over expression of fibrogenic genes. |
| 6490 | 20481316 | Serum creatine (Scr) and 24 hours urine protein, cross reaction protein (CRP) and tumor necrosis factor-alpha (TNF-alpha) were measured at the end of the study. |
| 6491 | 20481316 | The mRNA of transforming growth factor-beta1 (TGF-beta1) was measured by real-time PCR (RT-PCR), and the protein expression of TGF-beta1 was surveyed by Enzyme-Linked Immunosorbent Assay (ELISA). |
| 6492 | 20481316 | The renal pathological changes in DN rats given ginsenoside Rg1 treatment were ameliorated, and the expression levels of 24 h urine protein, serum creatinine, CRP, TNF-alpha, ED-1 and TGF-beta1 were significantly lower than those in the diabetic nephropathy group (P < 0.05). |
| 6493 | 20481316 | Serum creatine (Scr) and 24 hours urine protein, cross reaction protein (CRP) and tumor necrosis factor-alpha (TNF-alpha) were measured at the end of the study. |
| 6494 | 20481316 | The mRNA of transforming growth factor-beta1 (TGF-beta1) was measured by real-time PCR (RT-PCR), and the protein expression of TGF-beta1 was surveyed by Enzyme-Linked Immunosorbent Assay (ELISA). |
| 6495 | 20481316 | The renal pathological changes in DN rats given ginsenoside Rg1 treatment were ameliorated, and the expression levels of 24 h urine protein, serum creatinine, CRP, TNF-alpha, ED-1 and TGF-beta1 were significantly lower than those in the diabetic nephropathy group (P < 0.05). |
| 6496 | 20483351 | To examine the pharmacological effects of a butanol-soluble extract of CS under conditions of diabetic nephropathy, we evaluated the expression of transforming growth factor-beta1 (TGF-beta1) and fibronectin, key mediators of diabetic nephropathy, in mouse glomerular mesangial cells cultured in the presence of S100b (a specific ligand for receptor of advanced glycation end products). |
| 6497 | 20483351 | CS inhibited S100b-induced TGF-beta1 and fibronectin expression in mouse mesangial cells by suppressing activation of Smad2/3, extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK), and oxidative stress. |
| 6498 | 20483351 | Of these compounds, CS-A significantly decreased the expression of TGF-beta1 and fibronectin and NF-kappaB DNA binding activity. |
| 6499 | 20483351 | To examine the pharmacological effects of a butanol-soluble extract of CS under conditions of diabetic nephropathy, we evaluated the expression of transforming growth factor-beta1 (TGF-beta1) and fibronectin, key mediators of diabetic nephropathy, in mouse glomerular mesangial cells cultured in the presence of S100b (a specific ligand for receptor of advanced glycation end products). |
| 6500 | 20483351 | CS inhibited S100b-induced TGF-beta1 and fibronectin expression in mouse mesangial cells by suppressing activation of Smad2/3, extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK), and oxidative stress. |
| 6501 | 20483351 | Of these compounds, CS-A significantly decreased the expression of TGF-beta1 and fibronectin and NF-kappaB DNA binding activity. |
| 6502 | 20483351 | To examine the pharmacological effects of a butanol-soluble extract of CS under conditions of diabetic nephropathy, we evaluated the expression of transforming growth factor-beta1 (TGF-beta1) and fibronectin, key mediators of diabetic nephropathy, in mouse glomerular mesangial cells cultured in the presence of S100b (a specific ligand for receptor of advanced glycation end products). |
| 6503 | 20483351 | CS inhibited S100b-induced TGF-beta1 and fibronectin expression in mouse mesangial cells by suppressing activation of Smad2/3, extracellular signal-regulated kinase (ERK)/mitogen-activated protein kinase (MAPK), and oxidative stress. |
| 6504 | 20483351 | Of these compounds, CS-A significantly decreased the expression of TGF-beta1 and fibronectin and NF-kappaB DNA binding activity. |
| 6505 | 20483724 | The T cells from prediabetic NOD mice treated with an agonistic anti-CTLA-4 Ab-coated DC (anti-CTLA-4-Ab DC) showed significantly less proliferative response and enhanced IL-10 and TGF-beta1 production upon exposure to beta cell Ags. |
| 6506 | 20483724 | Furthermore, these mice showed increased frequency of Foxp3+ and IL-10+ T cells, less severe insulitis, and a significant delay in the onset of hyperglycemia compared with mice treated with control Ab-coated DCs. |
| 6507 | 20483724 | Further analyses showed that diabetogenic T cell function was modulated primarily through the induction of Foxp3 and IL-10 expression upon Ag presentation by anti-CTLA-4-Ab DCs. |
| 6508 | 20483724 | The induction of Foxp3 and IL-10 expression appeared to be a consequence of increased TGF-beta1 production by T cells activated using anti-CTLA-4-Ab DCs, and this effect could be enhanced by the addition of exogenous IL-2 or TGF-beta1. |
| 6509 | 20483724 | The T cells from prediabetic NOD mice treated with an agonistic anti-CTLA-4 Ab-coated DC (anti-CTLA-4-Ab DC) showed significantly less proliferative response and enhanced IL-10 and TGF-beta1 production upon exposure to beta cell Ags. |
| 6510 | 20483724 | Furthermore, these mice showed increased frequency of Foxp3+ and IL-10+ T cells, less severe insulitis, and a significant delay in the onset of hyperglycemia compared with mice treated with control Ab-coated DCs. |
| 6511 | 20483724 | Further analyses showed that diabetogenic T cell function was modulated primarily through the induction of Foxp3 and IL-10 expression upon Ag presentation by anti-CTLA-4-Ab DCs. |
| 6512 | 20483724 | The induction of Foxp3 and IL-10 expression appeared to be a consequence of increased TGF-beta1 production by T cells activated using anti-CTLA-4-Ab DCs, and this effect could be enhanced by the addition of exogenous IL-2 or TGF-beta1. |
| 6513 | 20498357 | Here we report that IL-9 is secreted by human naive CD4 T cells in response to differentiation by Th9 (TGF-beta and IL-4) or Th17 polarizing conditions. |
| 6514 | 20498357 | Yet, these differentiated naive cells did not coexpress IL-17 and IL-9, unless they were repeatedly stimulated under Th17 differentiation-inducing conditions. |
| 6515 | 20498357 | In contrast to the naive cells, memory CD4 T cells were induced to secrete IL-9 by simply providing TGF-beta during stimulation, as neither IL-4 nor proinflammatory cytokines were required. |
| 6516 | 20498357 | Furthermore, the addition of TGF-beta to the Th17-inducing cytokines (IL-1beta, IL-6, IL-21, IL-23) that induce memory cells to secrete IL-17, resulted in the marked coexpression of IL-9 in IL-17 producing memory cells. |
| 6517 | 20498357 | The proinflammatory cytokine mediating TGF-beta-dependent coexpression of IL-9 and IL-17 was identified to be IL-1beta. |
| 6518 | 20498357 | Moreover, circulating monocytes were potent costimulators of IL-9 production by Th17 cells via their capacity to secrete IL-1beta. |
| 6519 | 20498357 | Finally, to determine whether IL-9/IL-17 coproducing CD4 cells were altered in an inflammatory condition, we examined patients with autoimmune diabetes and demonstrated that these subjects exhibit a higher frequency of memory CD4 cells with the capacity to transition into IL-9(+)IL-17(+) cells. |
| 6520 | 20498357 | These data demonstrate the presence of IL-17(+)IL-9(+) CD4 cells induced by IL-1beta that may play a role in human autoimmune disease. |
| 6521 | 20498357 | Here we report that IL-9 is secreted by human naive CD4 T cells in response to differentiation by Th9 (TGF-beta and IL-4) or Th17 polarizing conditions. |
| 6522 | 20498357 | Yet, these differentiated naive cells did not coexpress IL-17 and IL-9, unless they were repeatedly stimulated under Th17 differentiation-inducing conditions. |
| 6523 | 20498357 | In contrast to the naive cells, memory CD4 T cells were induced to secrete IL-9 by simply providing TGF-beta during stimulation, as neither IL-4 nor proinflammatory cytokines were required. |
| 6524 | 20498357 | Furthermore, the addition of TGF-beta to the Th17-inducing cytokines (IL-1beta, IL-6, IL-21, IL-23) that induce memory cells to secrete IL-17, resulted in the marked coexpression of IL-9 in IL-17 producing memory cells. |
| 6525 | 20498357 | The proinflammatory cytokine mediating TGF-beta-dependent coexpression of IL-9 and IL-17 was identified to be IL-1beta. |
| 6526 | 20498357 | Moreover, circulating monocytes were potent costimulators of IL-9 production by Th17 cells via their capacity to secrete IL-1beta. |
| 6527 | 20498357 | Finally, to determine whether IL-9/IL-17 coproducing CD4 cells were altered in an inflammatory condition, we examined patients with autoimmune diabetes and demonstrated that these subjects exhibit a higher frequency of memory CD4 cells with the capacity to transition into IL-9(+)IL-17(+) cells. |
| 6528 | 20498357 | These data demonstrate the presence of IL-17(+)IL-9(+) CD4 cells induced by IL-1beta that may play a role in human autoimmune disease. |
| 6529 | 20529823 | The aim of our study was to test the hypothesis that T regulatory cells express pro- and anti-inflammatory cytokines, elements of cytotoxicity and OX40/4-1BB molecules. |
| 6530 | 20529823 | Concurrently with the flow cytometric assessment of Tregs we separated CD4+CD25+CD127dim/- cells for further mRNA analysis. mRNA levels for transcription factor FoxP3, pro- and anti-inflammatory cytokines (interferon gamma, interleukin-2, interleukin-4, interleukin-10, transforming growth factor beta1 and tumor necrosis factor alpha), activatory molecules (OX40, 4-1BB) and elements of cytotoxicity (granzyme B, perforin 1) were determined by real-time PCR technique. |
| 6531 | 20529823 | Lower OX40 and higher 4-1BB mRNA but not protein levels in Treg cells in diabetic patients compared to the healthy children were noted. |
| 6532 | 20529823 | Our observations confirm the presence of mRNA for pro- and anti-inflammatory cytokines in CD4+CD25+CD127dim/- cells in the peripheral blood of children with T1DM. |
| 6533 | 20544263 | IL-10/TGF-beta-treated dendritic cells, pulsed with insulin, specifically reduce the response to insulin of CD4+ effector/memory T cells from type 1 diabetic individuals. |
| 6534 | 20554001 | IL-17A, IL-17F, IL-21, IL-22, IL-23, IL-6, TGF-beta) production in splenocytes was decreased dramatically on day 18 following CFA immunization. |
| 6535 | 20554001 | IL-23 stimulation did not alter the distribution of IL-17 in myeloid cells. |
| 6536 | 20571025 | Thrombin stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by protease-activated receptor-1 transactivation of the transforming growth factor beta type I receptor. |
| 6537 | 20571025 | One component of classical G-protein-coupled receptor (GPCR) signaling invokes transactivation of protein tyrosine kinase receptors such as the epidermal growth factor receptor. |
| 6538 | 20571025 | We have used the model of proteoglycan synthesis to demonstrate that the signaling paradigm of GPCR signaling can be extended to include the transactivation of serine/threonine receptor, specifically the TGF-beta type I receptor (TbetaRI) also known as activin-like kinase (ALK) V. |
| 6539 | 20571025 | Thrombin stimulated elongation of GAG chains and increased proteoglycan core protein expression and these responses were blocked by the TbetaRI antagonist, SB431542 and TbetaRI siRNA knockdown, as well as several protease-activated receptor (PAR)-1 antagonists. |
| 6540 | 20571025 | The canonical downstream response to TGF-beta is increased C-terminal phosphorylation of the transcription factor Smad2 generating phospho-Smad2C (phosphorylation of Smad2 C-terminal region). |
| 6541 | 20571025 | The proteolytically inactive thrombin mimetic thrombin-receptor activating peptide also stimulated an increase in cytosolic phospho-Smad2C. |
| 6542 | 20571025 | Thrombin stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by protease-activated receptor-1 transactivation of the transforming growth factor beta type I receptor. |
| 6543 | 20571025 | One component of classical G-protein-coupled receptor (GPCR) signaling invokes transactivation of protein tyrosine kinase receptors such as the epidermal growth factor receptor. |
| 6544 | 20571025 | We have used the model of proteoglycan synthesis to demonstrate that the signaling paradigm of GPCR signaling can be extended to include the transactivation of serine/threonine receptor, specifically the TGF-beta type I receptor (TbetaRI) also known as activin-like kinase (ALK) V. |
| 6545 | 20571025 | Thrombin stimulated elongation of GAG chains and increased proteoglycan core protein expression and these responses were blocked by the TbetaRI antagonist, SB431542 and TbetaRI siRNA knockdown, as well as several protease-activated receptor (PAR)-1 antagonists. |
| 6546 | 20571025 | The canonical downstream response to TGF-beta is increased C-terminal phosphorylation of the transcription factor Smad2 generating phospho-Smad2C (phosphorylation of Smad2 C-terminal region). |
| 6547 | 20571025 | The proteolytically inactive thrombin mimetic thrombin-receptor activating peptide also stimulated an increase in cytosolic phospho-Smad2C. |
| 6548 | 20571025 | Thrombin stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by protease-activated receptor-1 transactivation of the transforming growth factor beta type I receptor. |
| 6549 | 20571025 | One component of classical G-protein-coupled receptor (GPCR) signaling invokes transactivation of protein tyrosine kinase receptors such as the epidermal growth factor receptor. |
| 6550 | 20571025 | We have used the model of proteoglycan synthesis to demonstrate that the signaling paradigm of GPCR signaling can be extended to include the transactivation of serine/threonine receptor, specifically the TGF-beta type I receptor (TbetaRI) also known as activin-like kinase (ALK) V. |
| 6551 | 20571025 | Thrombin stimulated elongation of GAG chains and increased proteoglycan core protein expression and these responses were blocked by the TbetaRI antagonist, SB431542 and TbetaRI siRNA knockdown, as well as several protease-activated receptor (PAR)-1 antagonists. |
| 6552 | 20571025 | The canonical downstream response to TGF-beta is increased C-terminal phosphorylation of the transcription factor Smad2 generating phospho-Smad2C (phosphorylation of Smad2 C-terminal region). |
| 6553 | 20571025 | The proteolytically inactive thrombin mimetic thrombin-receptor activating peptide also stimulated an increase in cytosolic phospho-Smad2C. |
| 6554 | 20578705 | The levels of low-grade inflammation biomarkers interleukin-6 and interleukin-8 (IL-6 and IL-8), angiogenic factors, and vascular endothelial growth factor (VEGF) were determined by the enzyme-linked immunosorbent assay (ELISA). |
| 6555 | 20578705 | The expression levels of protein kinase Cbeta (PKCbeta), connexin 43 (Cx43), transforming growth factor-beta1 (TGF-beta1), and cyclooxygenase-2 (COX-2) were determined by Western blot. |
| 6556 | 20578705 | Incubation of ARPE-19 cells with 33 mM glucose for 9 days significantly induced the accumulation of VEGF, IL-6, IL-8, TGF-beta, and COX-2, activation of PKCbeta, and reduction of Cx43 and GJIC. |
| 6557 | 20578705 | Incubation of ARPE-19 cells with 33 mM glucose in the presence of 0-10 microM trans-resveratrol dose-dependently inhibited VEGF, TGF-beta1, COX-2, IL-6, and IL-8 accumulation, PKCbeta activation, and Cx43 degradation and enhanced GJIC. |
| 6558 | 20578705 | The levels of low-grade inflammation biomarkers interleukin-6 and interleukin-8 (IL-6 and IL-8), angiogenic factors, and vascular endothelial growth factor (VEGF) were determined by the enzyme-linked immunosorbent assay (ELISA). |
| 6559 | 20578705 | The expression levels of protein kinase Cbeta (PKCbeta), connexin 43 (Cx43), transforming growth factor-beta1 (TGF-beta1), and cyclooxygenase-2 (COX-2) were determined by Western blot. |
| 6560 | 20578705 | Incubation of ARPE-19 cells with 33 mM glucose for 9 days significantly induced the accumulation of VEGF, IL-6, IL-8, TGF-beta, and COX-2, activation of PKCbeta, and reduction of Cx43 and GJIC. |
| 6561 | 20578705 | Incubation of ARPE-19 cells with 33 mM glucose in the presence of 0-10 microM trans-resveratrol dose-dependently inhibited VEGF, TGF-beta1, COX-2, IL-6, and IL-8 accumulation, PKCbeta activation, and Cx43 degradation and enhanced GJIC. |
| 6562 | 20578705 | The levels of low-grade inflammation biomarkers interleukin-6 and interleukin-8 (IL-6 and IL-8), angiogenic factors, and vascular endothelial growth factor (VEGF) were determined by the enzyme-linked immunosorbent assay (ELISA). |
| 6563 | 20578705 | The expression levels of protein kinase Cbeta (PKCbeta), connexin 43 (Cx43), transforming growth factor-beta1 (TGF-beta1), and cyclooxygenase-2 (COX-2) were determined by Western blot. |
| 6564 | 20578705 | Incubation of ARPE-19 cells with 33 mM glucose for 9 days significantly induced the accumulation of VEGF, IL-6, IL-8, TGF-beta, and COX-2, activation of PKCbeta, and reduction of Cx43 and GJIC. |
| 6565 | 20578705 | Incubation of ARPE-19 cells with 33 mM glucose in the presence of 0-10 microM trans-resveratrol dose-dependently inhibited VEGF, TGF-beta1, COX-2, IL-6, and IL-8 accumulation, PKCbeta activation, and Cx43 degradation and enhanced GJIC. |
| 6566 | 20599286 | In the diabetic state the kidney is involved by progressive sclerosis/fibrosis and proteinuria, due most likely to overactivity of the transforming growth factor-beta system and, to some extent, the vascular endothelial growth factor system, respectively. |
| 6567 | 20599709 | Further, nifedipine inhibited the AGE-induced reactive oxygen species generation, NF-kappaB activation and increases in intercellular adhesion molecule-1 and transforming growth factor-beta gene expression in tubular cells, all of which were blocked by GW9662. |
| 6568 | 20622454 | Additionally, diabetes-caused increased glomerular size, TGF-beta, and NF-kappaB decreased under treatment with cilostazol in diabetic rats. |
| 6569 | 20625315 | Endothelin-1 stimulation of proteoglycan synthesis in vascular smooth muscle is mediated by endothelin receptor transactivation of the transforming growth factor-[beta] type I receptor. |
| 6570 | 20625315 | The effect of endothelin-1 to stimulate an increase in glycosaminoglycan size on biglycan was also blocked in a concentration-dependent manner by SB431542. |
| 6571 | 20661431 | The high expression and strong co-localization with transforming growth factor-beta1 in diabetic kidneys suggests a role for Gremlin in the pathogenesis of diabetic nephropathy. |
| 6572 | 20661431 | Inhibition of Gremlin alleviated proteinuria and renal collagen IV accumulation 12 weeks after the STZ injection and inhibited renal cell proliferation and apoptosis. |
| 6573 | 20661431 | In vitro experiments, using mouse mesangial cells, revealed that the transfect ion of gremlin siRNA plasmid reversed high glucose induced abnormalities, such as increased cell proliferation and apoptosis and increased collagen IV production. |
| 6574 | 20661431 | Additionally, we observed recovery of bone morphogenetic protein-7 signaling activity, evidenced by increases in phosphorylated Smad 5 protein levels. |
| 6575 | 20686866 | Polymorphisms in the genes encoding TGF-beta1, TNF-alpha, and IL-6 show association with type 1 diabetes mellitus in the Slovak population. |
| 6576 | 20686866 | Furthermore, tumor necrosis factor (TNF)-alpha -308 A allele carriers were also significantly overrepresented among the diabetics (P (c) = 0.0031, OR = 2.62); however, the association of the -308 A allele with T1D might be due to its strong linkage disequilibrium with the susceptibility allele HLA-DRB1*0301. |
| 6577 | 20686866 | Moreover, a possible role of TNF-alpha and IL-6 SNPs cannot be ruled out, although their association with T1D was due to strong LD with the HLA class II susceptibility allele or did not withstand statistical correction, respectively. |
| 6578 | 20875828 | Immunocytochemistry was applied to examine TGF-beta1, ICAM-1 and RAGE protein expressions by SABC or SABC-AP method; mRNA expression of TGF-beta1, ICAM-1 and RAGE was determined by real-time RT-PCR. |
| 6579 | 20875828 | Blockade of PKC-beta strikingly decreased HUVEC TGF-beta1 and ICAM-1 expression in both protein and mRNA levels, RAGE protein level was also down-regulated. |
| 6580 | 20875828 | Immunocytochemistry was applied to examine TGF-beta1, ICAM-1 and RAGE protein expressions by SABC or SABC-AP method; mRNA expression of TGF-beta1, ICAM-1 and RAGE was determined by real-time RT-PCR. |
| 6581 | 20875828 | Blockade of PKC-beta strikingly decreased HUVEC TGF-beta1 and ICAM-1 expression in both protein and mRNA levels, RAGE protein level was also down-regulated. |
| 6582 | 21088486 | Transforming Growth Factor-b (TGFb) is a major driving force of the Epithelial-to-Mesenchymal (EMT) genetic program, which becomes overactive in the pathophysiology of many age-related human diseases. |
| 6583 | 21088486 | TGFb-driven EMT is sufficient to generate migrating cancer stem cells by directly linking the acquisition of cellular motility with the maintenance of tumor-initiating (stemness) capacity. |
| 6584 | 21088486 | Chronic diseases exhibiting excessive fibrosis can be caused by repeated and sustained infliction of TGFb-driven EMT, which increases collagen and extracellular matrix synthesis. |
| 6585 | 21088486 | Pharmacological prevention and/or reversal of TGFb-induced EMT may therefore have important clinical applications in the management of cancer metastasis as well as in the prevention and/or treatment of end-state organ failures. |
| 6586 | 21088486 | ZEB1, TWIST1, SNAIL2 [Slug], TGFbs), we recently hypothesized that prevention of TGFb-induced EMT might represent a common molecular mechanism underlying the anti-cancer stem cells and anti-fibrotic actions of metformin. |
| 6587 | 21088486 | Remarkably, metformin exposure not only impedes TGFb-promoted loss of the epithelial marker E-cadherin in MCF-7 breast cancer cells but it prevents further TGF-induced cell scattering and accumulation of the mesenchymal marker vimentin in Madin-Darby canine kidney (MDCK) cells. |
| 6588 | 21088486 | Transforming Growth Factor-b (TGFb) is a major driving force of the Epithelial-to-Mesenchymal (EMT) genetic program, which becomes overactive in the pathophysiology of many age-related human diseases. |
| 6589 | 21088486 | TGFb-driven EMT is sufficient to generate migrating cancer stem cells by directly linking the acquisition of cellular motility with the maintenance of tumor-initiating (stemness) capacity. |
| 6590 | 21088486 | Chronic diseases exhibiting excessive fibrosis can be caused by repeated and sustained infliction of TGFb-driven EMT, which increases collagen and extracellular matrix synthesis. |
| 6591 | 21088486 | Pharmacological prevention and/or reversal of TGFb-induced EMT may therefore have important clinical applications in the management of cancer metastasis as well as in the prevention and/or treatment of end-state organ failures. |
| 6592 | 21088486 | ZEB1, TWIST1, SNAIL2 [Slug], TGFbs), we recently hypothesized that prevention of TGFb-induced EMT might represent a common molecular mechanism underlying the anti-cancer stem cells and anti-fibrotic actions of metformin. |
| 6593 | 21088486 | Remarkably, metformin exposure not only impedes TGFb-promoted loss of the epithelial marker E-cadherin in MCF-7 breast cancer cells but it prevents further TGF-induced cell scattering and accumulation of the mesenchymal marker vimentin in Madin-Darby canine kidney (MDCK) cells. |
| 6594 | 21088486 | Transforming Growth Factor-b (TGFb) is a major driving force of the Epithelial-to-Mesenchymal (EMT) genetic program, which becomes overactive in the pathophysiology of many age-related human diseases. |
| 6595 | 21088486 | TGFb-driven EMT is sufficient to generate migrating cancer stem cells by directly linking the acquisition of cellular motility with the maintenance of tumor-initiating (stemness) capacity. |
| 6596 | 21088486 | Chronic diseases exhibiting excessive fibrosis can be caused by repeated and sustained infliction of TGFb-driven EMT, which increases collagen and extracellular matrix synthesis. |
| 6597 | 21088486 | Pharmacological prevention and/or reversal of TGFb-induced EMT may therefore have important clinical applications in the management of cancer metastasis as well as in the prevention and/or treatment of end-state organ failures. |
| 6598 | 21088486 | ZEB1, TWIST1, SNAIL2 [Slug], TGFbs), we recently hypothesized that prevention of TGFb-induced EMT might represent a common molecular mechanism underlying the anti-cancer stem cells and anti-fibrotic actions of metformin. |
| 6599 | 21088486 | Remarkably, metformin exposure not only impedes TGFb-promoted loss of the epithelial marker E-cadherin in MCF-7 breast cancer cells but it prevents further TGF-induced cell scattering and accumulation of the mesenchymal marker vimentin in Madin-Darby canine kidney (MDCK) cells. |
| 6600 | 21088486 | Transforming Growth Factor-b (TGFb) is a major driving force of the Epithelial-to-Mesenchymal (EMT) genetic program, which becomes overactive in the pathophysiology of many age-related human diseases. |
| 6601 | 21088486 | TGFb-driven EMT is sufficient to generate migrating cancer stem cells by directly linking the acquisition of cellular motility with the maintenance of tumor-initiating (stemness) capacity. |
| 6602 | 21088486 | Chronic diseases exhibiting excessive fibrosis can be caused by repeated and sustained infliction of TGFb-driven EMT, which increases collagen and extracellular matrix synthesis. |
| 6603 | 21088486 | Pharmacological prevention and/or reversal of TGFb-induced EMT may therefore have important clinical applications in the management of cancer metastasis as well as in the prevention and/or treatment of end-state organ failures. |
| 6604 | 21088486 | ZEB1, TWIST1, SNAIL2 [Slug], TGFbs), we recently hypothesized that prevention of TGFb-induced EMT might represent a common molecular mechanism underlying the anti-cancer stem cells and anti-fibrotic actions of metformin. |
| 6605 | 21088486 | Remarkably, metformin exposure not only impedes TGFb-promoted loss of the epithelial marker E-cadherin in MCF-7 breast cancer cells but it prevents further TGF-induced cell scattering and accumulation of the mesenchymal marker vimentin in Madin-Darby canine kidney (MDCK) cells. |
| 6606 | 21088486 | Transforming Growth Factor-b (TGFb) is a major driving force of the Epithelial-to-Mesenchymal (EMT) genetic program, which becomes overactive in the pathophysiology of many age-related human diseases. |
| 6607 | 21088486 | TGFb-driven EMT is sufficient to generate migrating cancer stem cells by directly linking the acquisition of cellular motility with the maintenance of tumor-initiating (stemness) capacity. |
| 6608 | 21088486 | Chronic diseases exhibiting excessive fibrosis can be caused by repeated and sustained infliction of TGFb-driven EMT, which increases collagen and extracellular matrix synthesis. |
| 6609 | 21088486 | Pharmacological prevention and/or reversal of TGFb-induced EMT may therefore have important clinical applications in the management of cancer metastasis as well as in the prevention and/or treatment of end-state organ failures. |
| 6610 | 21088486 | ZEB1, TWIST1, SNAIL2 [Slug], TGFbs), we recently hypothesized that prevention of TGFb-induced EMT might represent a common molecular mechanism underlying the anti-cancer stem cells and anti-fibrotic actions of metformin. |
| 6611 | 21088486 | Remarkably, metformin exposure not only impedes TGFb-promoted loss of the epithelial marker E-cadherin in MCF-7 breast cancer cells but it prevents further TGF-induced cell scattering and accumulation of the mesenchymal marker vimentin in Madin-Darby canine kidney (MDCK) cells. |
| 6612 | 21088486 | Transforming Growth Factor-b (TGFb) is a major driving force of the Epithelial-to-Mesenchymal (EMT) genetic program, which becomes overactive in the pathophysiology of many age-related human diseases. |
| 6613 | 21088486 | TGFb-driven EMT is sufficient to generate migrating cancer stem cells by directly linking the acquisition of cellular motility with the maintenance of tumor-initiating (stemness) capacity. |
| 6614 | 21088486 | Chronic diseases exhibiting excessive fibrosis can be caused by repeated and sustained infliction of TGFb-driven EMT, which increases collagen and extracellular matrix synthesis. |
| 6615 | 21088486 | Pharmacological prevention and/or reversal of TGFb-induced EMT may therefore have important clinical applications in the management of cancer metastasis as well as in the prevention and/or treatment of end-state organ failures. |
| 6616 | 21088486 | ZEB1, TWIST1, SNAIL2 [Slug], TGFbs), we recently hypothesized that prevention of TGFb-induced EMT might represent a common molecular mechanism underlying the anti-cancer stem cells and anti-fibrotic actions of metformin. |
| 6617 | 21088486 | Remarkably, metformin exposure not only impedes TGFb-promoted loss of the epithelial marker E-cadherin in MCF-7 breast cancer cells but it prevents further TGF-induced cell scattering and accumulation of the mesenchymal marker vimentin in Madin-Darby canine kidney (MDCK) cells. |
| 6618 | 21158157 | [The effect of angiotensin-(1-7) on the mRNA expression of PDGF and TGF-beta1 in the kidney of diabetic rats]. |
| 6619 | 21177088 | SR-ONO significantly suppressed albuminuria, glomerular hypertrophy, mesangial matrix accumulation, glomerular accumulation of monocyte/macrophage, increase in glomerular levels of pro-fibrotic factor transforming growth factor (TGF)-beta1 and the number of glomerular alpha-smooth muscle actin (SMA)(+) cells in diabetic animals. |
| 6620 | 21177088 | Taken together, these results suggest the potential therapeutic efficacy of intermittent administration of SR-ONO in treating diabetic nephropathy potentially via inducing HGF, thus counteracting the pro-fibrotic effects of TGF-beta1. |
| 6621 | 21324893 | TGF-beta regulates miR-206 and miR-29 to control myogenic differentiation through regulation of HDAC4. |
| 6622 | 21324893 | Here, we demonstrate in the myogenic C2C12 cell line, and in primary muscle cells, that miR-206 and miR-29-two miRs that act on transcriptional events implicated in muscle differentiation are down-regulated by TGF-β. |
| 6623 | 21324893 | We further demonstrate that TGF-β treatment of myogenic cells is associated with increased expression of histone deacetylase 4 (HDAC4), a key inhibitor of muscle differentiation that has been identified as a target for regulation by miR-206 and miR-29. |
| 6624 | 21324893 | We confirmed that increased expression of miR-206 and miR-29 resulted in the translational repression of HDAC4 in the presence or absence of TGF-β via interaction with the HDAC4 3'-untranslated region. |
| 6625 | 21324893 | Furthermore, we present evidence that the mechanism by which miR-206 and miR-29 can inhibit the TGF-β-mediated up-regulation of HDAC4 is via the inhibition of Smad3 expression, a transducer of TGF-β signaling. |
| 6626 | 21324893 | These findings identify a novel mechanism of interaction between TGF-β and miR-206 and -29 in the regulation of myogenic differentiation through HDAC4. |
| 6627 | 21417026 | As Tregs, the Bregs are capable of performing both pathogenic and regulatory functions by production of suppressive cytokines, such as IL-10 or TGF-beta1, or by interaction with pathogen T cells or other immune cells. |
| 6628 | 21478477 | Cation-independent mannose 6-phosphate receptor inhibitor (PXS25) inhibits fibrosis in human proximal tubular cells by inhibiting conversion of latent to active TGF-beta1. |
| 6629 | 21478477 | Cellular fibronectin, collagen IV, and matrix metalloproteinase-2 (MMP-2) and MMP-9 were assessed. |
| 6630 | 21478477 | Hyperglycemia induced fibronectin and collagen IV production (P < 0.05), as did hypoxia, but only hyperglycemia-induced increases in matrix proteins were suppressed by concurrent PXS25 exposure. |
| 6631 | 21478477 | High glucose induced MMP-2 and -9 in normoxic and hypoxic conditions, which was not modified in the presence of PXS25. |
| 6632 | 21560355 | [Effects of sericine on TGF-beta1/Smad3 signal pathway of diabetic mephropathy rats kidney]. |
| 6633 | 21753123 | The aim of this study was to determine the effects of EPA and the LXR agonist T0901317 on saturated fatty acid (palmitic acid)-induced apoptosis in the insulinoma β-cell line INS-1, a model for insulin-secreting β-cells. |
| 6634 | 21753123 | Consistent with these results, caspase-3 activity and BAX and sterol regulatory element binding protein-1c (SREBP-1c) mRNA levels were markedly increased in INS-1 cells co-administered palmitic acid and T0901317. |
| 6635 | 21753123 | Finally, T0901317 up-regulated the palmitic acid-induced expression of p27(KIP1), transforming growth factor beta 1, and SMAD3 proteins in INS-1 cells. |
| 6636 | 21866671 | [Effects of zhenqing recipe and earthworm on the expressions of transforming growth factor-beta1 and plasminogen activator inhibitor 1 in renal tissues of type 2 diabetic rats]. |
| 6637 | 21890375 | Adiponectin stimulates release of CCL2, -3, -4 and -5 while the surface abundance of CCR2 and -5 is simultaneously reduced in primary human monocytes. |
| 6638 | 21890375 | The adipokine adiponectin is well known to affect the function of immune cells and upregulation of CCL2 by adiponectin in monocytes/macrophages has already been reported. |
| 6639 | 21890375 | In the current study the effect of adiponectin on CCL2, -3, -4, and -5 and their corresponding receptors CCR1, CCR2, and CCR5 has been analyzed. |
| 6640 | 21890375 | Simultaneously the surface abundance of CCR2 and CCR5 is reduced while CCR1 is not affected. |
| 6641 | 21890375 | Downregulation of CCR2 by adiponectin is blocked by a CCR2 antagonist although expression of the CCL2 regulated genes CCR2 and TGF-beta 1 is not altered in the adiponectin-incubated monocytes. |
| 6642 | 21890375 | The degree of adiponectin-mediated induction of the chemokines CCL3, -4, and -5 negatively correlates with their basal levels and upregulation of CCL3 and CCL5 is significantly impaired in OW and T2D cells. |
| 6643 | 21890375 | In conclusion these data demonstrate that adiponectin stimulates release of CCL2 to CCL5 in primary human monocytes, and induction in cells of overweight probands is partly impaired. |
| 6644 | 21890375 | Adiponectin also lowers surface abundance of CCR2 and CCR5 and downregulation of CCR2 seems to depend on autocrine/paracrine effects of CCL2. |
| 6645 | 21908416 | STZ-SHRs had elevated kidney weight/body weight ratio, glomerular size, glomerular macrophages (ED-1-positive cells), tissue transforming growth factor beta 1 (TGFβ1) concentrations and glomerular collagen IV staining (all P < 0.05 versus control animals). |
| 6646 | 21908416 | EPL reduced glomerular volume, TGFβ1 expression and glomerular collagen IV without changing glomerular macrophage infiltration. |
| 6647 | 21984919 | Compared with the healthy control mice, diabetic mice had significantly fewer c-kit+ stem cells, and these cells had a lower potency of endothelial differentiation; however, the production of the angiogenic growth factor VEGF did not differ between groups. |
| 6648 | 21984919 | A pathway-focused array showed that the c-kit+ stem cells from diabetic mice had up-regulated expression levels of many inflammatory factors, including Tlr4, Cxcl9, Il9, Tgfb1, Il4, and Tnfsf5, but no obvious change in the expression levels of cell cycle molecules. |
| 6649 | 21984919 | Interestingly, diabetes-related alterations of the extracellular matrix and adhesion molecules were varied; Pecam, Mmp10, Lamc1, Itgb7, Mmp9, and Timp4 were up-regulated, but Col11a1, Fn1, Admts2, and Itgav were down-regulated. |
| 6650 | 22075749 | We studied normal and streptozotocin-induced diabetic (DM) Sprague-Dawley rats treated for 6 weeks with vehicle, ALISK, HCTZ, or AMLO individually and combined and evaluated the effects of treatments on BP, urine albumin to creatinine ratio, renal interstitial fluid levels of angiotensin II, tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) and renal expression of TNF-α, IL-6, transforming growth factor beta 1, and nuclear factor kappa B. |
| 6651 | 22075749 | Renal interstitial fluid TNF-α and IL-6, and the renal expression of TNF-α, IL-6, transforming growth factor beta 1, and nuclear factor kappa B were increased in DM rats. |
| 6652 | 22075749 | We studied normal and streptozotocin-induced diabetic (DM) Sprague-Dawley rats treated for 6 weeks with vehicle, ALISK, HCTZ, or AMLO individually and combined and evaluated the effects of treatments on BP, urine albumin to creatinine ratio, renal interstitial fluid levels of angiotensin II, tumor necrosis factor alpha (TNF-α), and interleukin 6 (IL-6) and renal expression of TNF-α, IL-6, transforming growth factor beta 1, and nuclear factor kappa B. |
| 6653 | 22075749 | Renal interstitial fluid TNF-α and IL-6, and the renal expression of TNF-α, IL-6, transforming growth factor beta 1, and nuclear factor kappa B were increased in DM rats. |
| 6654 | 22179526 | Interferon-γ (IFN-γ), TNF-α, interleukin-1 β (IL-1β), fibroblast growth factor-2 (FGF-2), transforming growth factor beta-1 (TGFβ-1), bone morphogenetic protein-2 (BMP-2), and BMP-6 were measured by real-time RT-PCR, and histological sections were examined for leukocyte infiltration and several parameters related to bone resorption and formation. |
| 6655 | 22179526 | TNF inhibition in diabetic animals also reduced apoptosis, increased proliferation of bone-lining cells, and increased mRNA levels of FGF-2, TGFβ-1, BMP-2, and BMP-6. |
| 6656 | 22266139 | ARK5, encoding an AMP-related kinase, and TGFBI - encoding transforming growth factor, beta-induced protein were induced by TGF-β1 and also upregulated in human DN. |
| 6657 | 22266139 | Suppression of ARK5 attenuated fibrotic responses of renal epithelia to TGF-β1 exposure; and silencing of TGFBI induced expression of the epithelial cell marker - E-cadherin. |
| 6658 | 22266139 | We identified low abundance transcripts in sequence data and validated expression levels of several transcripts (ANKRD56, ENTPD8) in tubular enriched kidney biopsies of DN patients versus living donors. |
| 6659 | 22293942 | Association of glutathione S-transferase Ω 1-1 polymorphisms (A140D and E208K) with the expression of interleukin-8 (IL-8), transforming growth factor beta (TGF-β), and apoptotic protease-activating factor 1 (Apaf-1) in humans chronically exposed to arsenic in drinking water. |
| 6660 | 22293942 | Glutathione S-transferase omega 1-1 (GSTO1-1), which had been associated with iAs metabolism, is also known to participate in inflammatory and apoptotic cellular responses. |
| 6661 | 22293942 | A140D polymorphism was associated with higher expression of genes codifying for IL-8 and Apaf-1 mainly in heterozygous individuals, while E208K was associated with higher expression of IL-8 and TGF- gene, in both cases, the association was independently of iAs exposure level; however, the exposure to iAs increased slightly but significantly the influence of A140D and E208K polymorphisms on such genes expression. |
| 6662 | 22623064 | Is the expression of Transforming Growth Factor-Beta1 after fracture of long bones solely influenced by the healing process? |
| 6663 | 22773754 | We generated a murine model, the POKO mouse, obtained by crossing the peroxisome proliferator-activated receptor gamma 2 (PPARγ2) knockout (KO) mouse into a genetically obese ob/ob background. |
| 6664 | 22773754 | Similar to ob/ob mice, at 4 weeks of age these animals exhibited an increased urinary albumin:creatinine ratio and significantly increased blood pressure, but in contrast showed a significant increase in the renal hypertrophy index and an associated increase in p27(Kip1) expression compared with their obese littermates. |
| 6665 | 22773754 | Moreover, at 4 weeks of age POKO mice showed insulin resistance, an alteration of lipid metabolism and glomeruli damage associated with increased transforming growth factor beta (TGFβ) and parathyroid hormone-related protein (PTHrP) expression. |
| 6666 | 22903132 | Q-RT-PCR verified that Atp5b (F1-ATPase beta subunit), Col1a1 (collagen type 1 alpha 1), Cox6c (cytochrome c oxidase subunit VIc), Ndufs3 (NADH dehydrogenase [ubiquinone] Fe-S protein 3) and Tgfb1 (transforming growth factor β1) were significantly up-regulated in the DN group. |
| 6667 | 23028342 | After additional genotyping of 41 top ranked SNPs representing 24 independent signals in 5,873 individuals, combined meta-analysis revealed association of two SNPs with ESRD: rs7583877 in the AFF3 gene (P = 1.2 × 10(-8)) and an intergenic SNP on chromosome 15q26 between the genes RGMA and MCTP2, rs12437854 (P = 2.0 × 10(-9)). |
| 6668 | 23028342 | Functional data suggest that AFF3 influences renal tubule fibrosis via the transforming growth factor-beta (TGF-β1) pathway. |
| 6669 | 23071669 | These included five that were common to both ages (TNF, HNF4A, IL15, Progesterone, and YWHAZ), and others that were unique to 2 weeks (e.g. |
| 6670 | 23071669 | MYC/MYCN, TGFB1, and IL2) and to 4 weeks (e.g. |
| 6671 | 23071669 | IFNG, beta-estradiol, p53, NFKB, AKT, PRKCA, IL12, and HLA-C). |
| 6672 | 23071669 | Based on the literature, genes that may play a role in regulating metabolic pathways at 2 weeks include Myc and HNF4A, and at 4 weeks, beta-estradiol, p53, Akt, HNF4A and AR. |
| 6673 | 23196710 | Type IV collagen and transforming growth factor-beta1 (TGF-β1) were detected by immunohistochemistry and ultrastructure of glomeruli was observed. |
| 6674 | 23196710 | Furthermore, BBR down-regulated total protein expression of GRK2, GRK3 and up-regulated expression of GRK6 of renal cortex in DN rats, but had a slight effects on GRK4 and GRK5. |
| 6675 | 23213275 | Association of vascular endothelial growth factor, transforming growth factor beta, and interferon gamma gene polymorphisms with proliferative diabetic retinopathy in patients with type 2 diabetes. |
| 6676 | 23243433 | Renal morphology was analysed, and plasma transforming growth factor-beta1 (TGF-β1) was measured. |
| 6677 | 23293752 | Recently, several novel therapeutic strategies have been explored in treating DN patients including Islet cell transplant, Aldose reductase inhibitors, Sulodexide (GAC), Protein Kinase C (PKC) inhibitors, Connective tissue growth factor (CTGF) inhibitors, Transforming growth factor-beta (TGF-β) inhibitors and bardoxolone. |
| 6678 | 23469611 | [Effects of qiwei granule on the protein and mRNA expressions of renal tissue transforming growth factor-beta1 in KK-Ay mice with spontaneous type 2 diabetes mellitus]. |
| 6679 | 23477149 | [Regulatory effect of berberine on unbalanced expressions of renal tissue TGF-beta1/SnoN and smad signaling pathway in rats with early diabetic nephropathy]. |
| 6680 | 23515495 | Transforming growth factor beta 1 and monocyte chemoattractant protein-1 as prognostic markers of diabetic nephropathy. |
| 6681 | 23515495 | We aimed to find the relationship between serum transforming growth factor beta 1(TGF-β(1)) and urinary monocyte chemoattractant protein-1 (MCP-1) throughout the course of diabetic nephropathy (DN) and to assess the relationship between both levels and other parameters of renal injury such as albumin/creatinine ratio and estimated glomerular filtration rate (eGFR). |
| 6682 | 23515495 | Serum TGF-β(1), urinary MCP-1, eGFR, and glycosylated hemoglobin (HbA1c) were measured in 60 patients with type II diabetes mellitus with different degrees of nephropathy (20 patients with normoalbuminuria, 20 patients with microalbuminuria, and 20 patients with macroalbuminuria) and compared with 20 matched healthy control subjects. |
| 6683 | 23515495 | Also, serum TGF-β(1) and urinary MCP-1 correlated positively with HbA1c (r = 0.49 and 0.55, respectively, p < 0.05 for both) and inversely with eGFR (r = -0.69 and -0.60, respectively, p < 0.001 for both). |
| 6684 | 23515495 | Transforming growth factor beta 1 and monocyte chemoattractant protein-1 as prognostic markers of diabetic nephropathy. |
| 6685 | 23515495 | We aimed to find the relationship between serum transforming growth factor beta 1(TGF-β(1)) and urinary monocyte chemoattractant protein-1 (MCP-1) throughout the course of diabetic nephropathy (DN) and to assess the relationship between both levels and other parameters of renal injury such as albumin/creatinine ratio and estimated glomerular filtration rate (eGFR). |
| 6686 | 23515495 | Serum TGF-β(1), urinary MCP-1, eGFR, and glycosylated hemoglobin (HbA1c) were measured in 60 patients with type II diabetes mellitus with different degrees of nephropathy (20 patients with normoalbuminuria, 20 patients with microalbuminuria, and 20 patients with macroalbuminuria) and compared with 20 matched healthy control subjects. |
| 6687 | 23515495 | Also, serum TGF-β(1) and urinary MCP-1 correlated positively with HbA1c (r = 0.49 and 0.55, respectively, p < 0.05 for both) and inversely with eGFR (r = -0.69 and -0.60, respectively, p < 0.001 for both). |
| 6688 | 23603139 | Specific tissues with impaired angiogenesis exhibit microenvironment features, such as increased PAI-1/uPA ratio and decreased blood flow, whereas TGFbeta increases extracellular matrix deposition, preventing the vascularization process. |
| 6689 | 23691527 | The canonical Notch ligand , Jagged1, is upregulated in a transforming growth factor-beta- (TGF- β -) dependent manner during chronic kidney disease. |
| 6690 | 23737649 | In addition, genistein treatment decreased inflammatory markers such as nuclear factor kappa B (p65), phosphorylated inhibitory kappa B alpha, C-reactive protein, monocyte chemotactic protein-1, cyclooxygenase-2, and tumor necrosis factor-alpha and improved oxidative stress markers (nuclear-related factor E2, heme oxygenase-1, glutathione peroxidase, and superoxide dismutase isoforms) in treatment groups, regardless of the genistein treatment dose. |
| 6691 | 23737649 | Furthermore, genistein supplementation inhibited the fibrosis-related markers (protein kinase C, protein kinase C-beta II, and transforming growth factor-beta I) in the DN state. |
| 6692 | 23754846 | It has been previously shown that elastin degradation products work synergistically with transforming growth factor-beta 1 (TGF-β1) to induce osteogenesis in vascular smooth muscle cells. |
| 6693 | 23754846 | Thus, the goal of this study was to analyse the effects of high concentration of glucose, elastin peptides and TGF-β1 on bone-specific markers like alkaline phosphatase (ALP), osteocalcin (OCN) and runt-related transcription factor 2 (RUNX2). |
| 6694 | 23754846 | We demonstrated using relative gene expression and specific protein assays that elastin degradation products in the presence of high glucose cause the increase in expression of the specific elastin-laminin receptor-1 (ELR-1) and activin receptor-like kinase-5 (ALK-5) present on the surface of the vascular cells, in turn leading to overexpression of typical osteogenic markers like ALP, OCN and RUNX2. |
| 6695 | 23754846 | In conclusion, our results indicate that glucose plays an important role in amplifying the osteogenesis induced by elastin peptides and TGF-β1, possibly by activating the ELR-1 and ALK-5 signalling pathways. |
| 6696 | 16973718 | Here, we treated diabetic rats with TETA and evaluated its ability to ameliorate Cu(2+)-mediated LV and arterial damage by modifying the expression of molecular targets that included transforming growth factor (TGF)-beta1, Smad4, extracellular matrix (ECM) proteins, extracellular superoxide dismutase (EC-SOD), and heparan sulfate (HS). |
| 6697 | 16973718 | LV and aortic mRNAs corresponding to TGF-beta1, Smad4, collagen types I, III, and IV, and fibronectin-1, and plasminogen activator inhibitor-1, were elevated in untreated diabetic animals and normalized after TETA treatment. |
| 6698 | 16973718 | Candidate molecular mechanisms by which TETA could ameliorate diabetic cardiac and arteriovascular disease include the suppression of an activated TGF-beta/Smad signaling pathway that mediates increased ECM gene expression and restoration of normal EC-SOD and HS regulation. |
| 6699 | 16973718 | Here, we treated diabetic rats with TETA and evaluated its ability to ameliorate Cu(2+)-mediated LV and arterial damage by modifying the expression of molecular targets that included transforming growth factor (TGF)-beta1, Smad4, extracellular matrix (ECM) proteins, extracellular superoxide dismutase (EC-SOD), and heparan sulfate (HS). |
| 6700 | 16973718 | LV and aortic mRNAs corresponding to TGF-beta1, Smad4, collagen types I, III, and IV, and fibronectin-1, and plasminogen activator inhibitor-1, were elevated in untreated diabetic animals and normalized after TETA treatment. |
| 6701 | 16973718 | Candidate molecular mechanisms by which TETA could ameliorate diabetic cardiac and arteriovascular disease include the suppression of an activated TGF-beta/Smad signaling pathway that mediates increased ECM gene expression and restoration of normal EC-SOD and HS regulation. |