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Gene Information
Gene symbol: PDGFB
Gene name: platelet-derived growth factor beta polypeptide
HGNC ID: 8800
Synonyms: SSV
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 1312960 | Platelet-derived growth factor is a potent inhibitor of angiotensin II-induced aldosterone synthesis. |
| 2 | 1312960 | Platelet-derived growth factor (PDGF) is a potent mitogen for several cell types. |
| 3 | 1312960 | In addition, PDGF has vasoconstrictive action and shares some signal transduction mechanisms with angiotensin II (AII). |
| 4 | 1312960 | Platelet-derived growth factor is a potent inhibitor of angiotensin II-induced aldosterone synthesis. |
| 5 | 1312960 | Platelet-derived growth factor (PDGF) is a potent mitogen for several cell types. |
| 6 | 1312960 | In addition, PDGF has vasoconstrictive action and shares some signal transduction mechanisms with angiotensin II (AII). |
| 7 | 1352286 | Substitution of the insulin receptor transmembrane domain with the c-neu/erbB2 transmembrane domain constitutively activates the insulin receptor kinase in vitro. |
| 8 | 1352286 | To examine the role of the transmembrane domain (TM) of the insulin receptor in insulin-induced receptor kinase activation, we prepared four mutated insulin receptors: 1) a Val938----Asp substitution (IR/TMv----D), 2) insertion of a 3-amino acid repeat (Val938-Phe939-Leu940) (IR/TM+3), or the entire TM was replaced by the corresponding domain of either the 3) platelet-derived growth factor (PDGF) receptor (IR/TMPDGFR) or 4) c-neu/erbB2 proto-oncogene product (IR/TMc-neu). |
| 9 | 1373394 | Thymidine uptake was stimulated by the following factors: 11 mmol/l glucose (50% increase); 10% amino acids (126% increase); 10% fetal calf serum (39% increase); 100 ng/ml insulin (45% increase); 250 ng/ml growth hormone (65% increase); 1.5 nmol/l aldosterone (29% increase); 2 U/ml platelet derived growth factor (116% increase). |
| 10 | 1559774 | Bovine collagen type I or human placental copolymerized collagen type I/III was used to create the lattices. |
| 11 | 1559774 | Growth factors included epidermal growth factor (EGF), basic fibroblastic growth factor (FGF), insulin-like growth factor (IGF-I), and platelet-derived growth factor homodimer beta beta (PDGF). |
| 12 | 1559774 | Dose-response experiments (0.01-100 ng/ml) demonstrated that PDGF at 10 ng/ml (P less than 0.005) and EGF at 1 and 10 ng/ml (P less than 0.0001) were the most effective in promoting gel contraction, compared to IGF-I and FGF. |
| 13 | 1559774 | Cells from insulin-dependent diabetics and cells from a donor with macular dystrophy contracted lattices more rapidly than cells from normal neonates (P less than 0.0001). |
| 14 | 1559774 | Lattices of copolymerized human collagen type III/I demonstrated significantly reduced contraction rates (P less than 0.0001) and increased optical transmittance, compared to bovine collagen type I lattices. |
| 15 | 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. |
| 16 | 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. |
| 17 | 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). |
| 18 | 1572403 | When PDGF, EGF, and IGF-I were added at submaximally effective concentrations, their effects were additive. |
| 19 | 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. |
| 20 | 1572403 | The concentration of TGF-beta needed to inhibit 50% of the combined effect of EGF, IGF-1, and PDGF was 5 ng/ml. |
| 21 | 1613332 | Platelet-derived growth factor and growth-promoting activity in the serum samples and platelets of patients with non-insulin-dependent diabetes mellitus. |
| 22 | 1613332 | Although platelet-derived growth factor (PDGF) is thought to be a major mediator of atherosclerotic disease, the pathophysiology of diabetic vasculopathy, including atherosclerosis, is unclear. |
| 23 | 1613332 | By means of an enzyme immunoassay that used a monoclonal antibody against human PDGF-B chain, PDGF-like immunoreactivity was determined in serum, platelet-poor plasma, and platelet lysate of 28 patients with non-insulin-dependent diabetes mellitus and 11 control subjects. |
| 24 | 1613332 | Platelet-derived growth factor and growth-promoting activity in the serum samples and platelets of patients with non-insulin-dependent diabetes mellitus. |
| 25 | 1613332 | Although platelet-derived growth factor (PDGF) is thought to be a major mediator of atherosclerotic disease, the pathophysiology of diabetic vasculopathy, including atherosclerosis, is unclear. |
| 26 | 1613332 | By means of an enzyme immunoassay that used a monoclonal antibody against human PDGF-B chain, PDGF-like immunoreactivity was determined in serum, platelet-poor plasma, and platelet lysate of 28 patients with non-insulin-dependent diabetes mellitus and 11 control subjects. |
| 27 | 1613332 | Platelet-derived growth factor and growth-promoting activity in the serum samples and platelets of patients with non-insulin-dependent diabetes mellitus. |
| 28 | 1613332 | Although platelet-derived growth factor (PDGF) is thought to be a major mediator of atherosclerotic disease, the pathophysiology of diabetic vasculopathy, including atherosclerosis, is unclear. |
| 29 | 1613332 | By means of an enzyme immunoassay that used a monoclonal antibody against human PDGF-B chain, PDGF-like immunoreactivity was determined in serum, platelet-poor plasma, and platelet lysate of 28 patients with non-insulin-dependent diabetes mellitus and 11 control subjects. |
| 30 | 1671798 | The effect of insulin and insulin-like growth factors were examined in closer detail because of the clinical association between insulin and hyperandrogenism. |
| 31 | 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. |
| 32 | 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. |
| 33 | 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. |
| 34 | 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). |
| 35 | 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. |
| 36 | 1698682 | Fibroblast growth factors, platelet-derived growth factor, and calcium acted as mitogens for parathyroid endothelial cells, whereas transforming growth factor beta inhibited proliferation. |
| 37 | 1733809 | Because Au10-Ins is essentially gold-bovine serum albumin (Au-BSA) with a few insulin molecules attached, the effect of insulin and other growth factors on the nuclear accumulation of BSA coupled to 10-, 15-, and 24-nm-diam colloidal gold particles (Au10-BSA, Au15-BSA, and Au24-BSA) was determined. |
| 38 | 1733809 | Glucagon, epidermal growth factor, platelet-derived growth factor, insulinlike growth factor I, and insulin A or B chains did not stimulate the accumulation of Au10-BSA. |
| 39 | 1849136 | This review focuses on the receptors for insulin, epidermal growth factor, and platelet-derived growth factor. |
| 40 | 1922015 | Agents such as epidermal growth factor, insulin and platelet derived growth factor which stimulate their respective receptor-PTK activities were without effect on PTK activities of mammary carcinoma. |
| 41 | 2239081 | Epidermal growth factor and platelet-derived growth factor in blood in diabetes mellitus. |
| 42 | 2239081 | Type of diabetes, its duration, mode of therapy, control, presence of retinopathy or albuminuria (in case of epidermal growth factor), as well as C-peptide age and sex did not correlate with epidermal or platelet-derived growth factor levels. |
| 43 | 2239081 | It is concluded that diabetes itself and not its complications cause increased levels of epidermal growth factor in plasma and serum and of platelet-derived growth factor in serum. |
| 44 | 2239081 | Epidermal growth factor and platelet-derived growth factor in blood in diabetes mellitus. |
| 45 | 2239081 | Type of diabetes, its duration, mode of therapy, control, presence of retinopathy or albuminuria (in case of epidermal growth factor), as well as C-peptide age and sex did not correlate with epidermal or platelet-derived growth factor levels. |
| 46 | 2239081 | It is concluded that diabetes itself and not its complications cause increased levels of epidermal growth factor in plasma and serum and of platelet-derived growth factor in serum. |
| 47 | 2239081 | Epidermal growth factor and platelet-derived growth factor in blood in diabetes mellitus. |
| 48 | 2239081 | Type of diabetes, its duration, mode of therapy, control, presence of retinopathy or albuminuria (in case of epidermal growth factor), as well as C-peptide age and sex did not correlate with epidermal or platelet-derived growth factor levels. |
| 49 | 2239081 | It is concluded that diabetes itself and not its complications cause increased levels of epidermal growth factor in plasma and serum and of platelet-derived growth factor in serum. |
| 50 | 2356856 | Recombinant human platelet-derived growth factor (rPDGF-BB, 1 or 10 micrograms), recombinant human basic fibroblast growth factor (rbFGF, 1 micrograms), or combinations of both were applied topically to the wounds for 5 to 14 days after wounding. |
| 51 | 2413420 | Insulin promotes the growth of these cells by binding, with low affinity, to the type I insulin-like growth factor (IGF) receptor, not through the high affinity insulin receptor. |
| 52 | 2413420 | Insulin acts synergistically with other factors, such as platelet-derived growth factor and epidermal growth factor, to stimulate the progression of cells through the cycle of proliferation. |
| 53 | 2464943 | Fifty percent inhibition of IGF-1 specific binding to the receptor required 1 X 10(-9) M IGF-1, greater than 1 X 10(-6) M insulin and 1 X 10(-7) M multiplication stimulating activity (MSA). |
| 54 | 2464943 | Examination of the effect of IGF-1 on the cell cycle revealed that exposure of cells to both IGF-1 and platelet-derived growth factor (PDGF) led to a significant increase in 3H-thymidine incorporation into cell layers. |
| 55 | 2464943 | Similarly, the labeling index of cells pretreated with PDGF, washed, and then exposed to IGF-1 was increased, whereas if the order of ligand exposure was reversed, there was no such additive effect. |
| 56 | 2464943 | Finally, PDGF increased RNA and protein synthesis, and this response was not enhanced by IGF-1. |
| 57 | 2497284 | Mean population doubling times, population doublings until senescence, saturation density at confluence (cells/cm2), tritiated thymidine incorporation, and response to platelet-derived growth factor (PDGF) were inhibited with the increasing glucose concentrations (11.0, 22, 44, or 55 mM glucose) (P less than 0.05). |
| 58 | 2497284 | Aldose reductase activity was present in the cultured fibroblasts (3.9 +/- 0.5 nmol/min per mg protein), and inhibitors of aldose reductase, including sorbinil (10(-4) M--10(-6) M) and tolrestat (10(-6) M--10(-8) M), completely prevented glucose-mediated inhibition of fibroblast proliferation, restored the response to PDGF, and allowed a normal replicative life span. |
| 59 | 2525095 | Platelet-derived growth factor (PDGF) in type 1 diabetes mellitus. |
| 60 | 2525095 | In 10 patients with type 1 diabetes mellitus, platelet-derived growth factor (PDGF) was assessed using an in vitro assay based on the stimulation of DNA synthesis in the 3T3 mouse fibroblast cell line. beta-Thromboglobulin (beta-TG) was used as an index for platelet alpha-granules content. |
| 61 | 2525095 | Platelet beta-TG content and PDGF were markedly decreased in diabetic patients while plasma beta-TG was increased as compared with control subjects. |
| 62 | 2525095 | In diabetic patients, a significant negative correlation was found between plasma beta-TG level and beta-TG total platelet content, associated with a significant positive correlation between platelet beta-TG content and PDGF. |
| 63 | 2525095 | Platelet-derived growth factor (PDGF) in type 1 diabetes mellitus. |
| 64 | 2525095 | In 10 patients with type 1 diabetes mellitus, platelet-derived growth factor (PDGF) was assessed using an in vitro assay based on the stimulation of DNA synthesis in the 3T3 mouse fibroblast cell line. beta-Thromboglobulin (beta-TG) was used as an index for platelet alpha-granules content. |
| 65 | 2525095 | Platelet beta-TG content and PDGF were markedly decreased in diabetic patients while plasma beta-TG was increased as compared with control subjects. |
| 66 | 2525095 | In diabetic patients, a significant negative correlation was found between plasma beta-TG level and beta-TG total platelet content, associated with a significant positive correlation between platelet beta-TG content and PDGF. |
| 67 | 2536936 | The cells showed mitogenic responses to endothelial cell growth factor, basic fibroblast growth factor, insulin-like growth factor types I and II, platelet-derived growth factor, ascorbic acid, and progesterone. |
| 68 | 2674692 | Insulin, insulin-like growth factor I and platelet-derived growth factor interact additively in the induction of the protooncogene c-myc and cellular proliferation in cultured bovine aortic smooth muscle cells. |
| 69 | 2674692 | We demonstrate that platelet-derived growth factor (PDGF) stimulates DNA synthesis of cultured bovine aortic SMCs by 2.5- to 3.5-fold. |
| 70 | 2674692 | PDGF also exhibits additivity with insulin and insulin-like growth factor I (IGF-I) for DNA synthesis and cellular proliferation. |
| 71 | 2674692 | Insulin (2 x 10(-6) M), IGF-I (1 x 10(-8) M), and PDGF (1 x 10(-9) M) cause a 60-80% increase in cell numbers over basal, but PDGF with insulin or IGF causes a 40-150% increase over basal. |
| 72 | 2674692 | No additivity between insulin and IGF-I is evident. |
| 73 | 2674692 | PDGF also induces commitment to DNA synthesis earlier than insulin or IGF-I. |
| 74 | 2674692 | Insulin and IGF-I exposure for 4 h, on the other hand, achieves 3H-thymidine incorporation that is only a 20-30% of maximum (with insulin or IGF-I alone). |
| 75 | 2674692 | Insulin, IGF-I, and PDGF increase mRNA levels of the protooncogene c-myc. |
| 76 | 2674692 | Additivity is also observed between PDGF with insulin or IGF-I, but not between insulin or IGF-I, in c-myc induction. |
| 77 | 2674692 | C-myc mRNA levels remain elevated as long as the hormones are present, although there's a tendency for the mRNA levels to fall off with insulin and IGF-I. |
| 78 | 2674692 | Insulin, insulin-like growth factor I and platelet-derived growth factor interact additively in the induction of the protooncogene c-myc and cellular proliferation in cultured bovine aortic smooth muscle cells. |
| 79 | 2674692 | We demonstrate that platelet-derived growth factor (PDGF) stimulates DNA synthesis of cultured bovine aortic SMCs by 2.5- to 3.5-fold. |
| 80 | 2674692 | PDGF also exhibits additivity with insulin and insulin-like growth factor I (IGF-I) for DNA synthesis and cellular proliferation. |
| 81 | 2674692 | Insulin (2 x 10(-6) M), IGF-I (1 x 10(-8) M), and PDGF (1 x 10(-9) M) cause a 60-80% increase in cell numbers over basal, but PDGF with insulin or IGF causes a 40-150% increase over basal. |
| 82 | 2674692 | No additivity between insulin and IGF-I is evident. |
| 83 | 2674692 | PDGF also induces commitment to DNA synthesis earlier than insulin or IGF-I. |
| 84 | 2674692 | Insulin and IGF-I exposure for 4 h, on the other hand, achieves 3H-thymidine incorporation that is only a 20-30% of maximum (with insulin or IGF-I alone). |
| 85 | 2674692 | Insulin, IGF-I, and PDGF increase mRNA levels of the protooncogene c-myc. |
| 86 | 2674692 | Additivity is also observed between PDGF with insulin or IGF-I, but not between insulin or IGF-I, in c-myc induction. |
| 87 | 2674692 | C-myc mRNA levels remain elevated as long as the hormones are present, although there's a tendency for the mRNA levels to fall off with insulin and IGF-I. |
| 88 | 2960669 | Insulin and insulin-like growth factor-I stimulate a common endogenous phosphoprotein substrate (pp185) in intact neuroblastoma cells. |
| 89 | 2960669 | Mouse neuroblastoma N18 cells contain specific high affinity insulin and insulin-like growth factor-I (IGF-I) receptors. |
| 90 | 2960669 | Insulin and IGF-I induce phosphorylation, in intact cells, of their respective receptor beta subunits. |
| 91 | 2960669 | In addition, both insulin and IGF-I induced phosphorylation of an endogenous protein of molecular mass 185 kDa (pp185). |
| 92 | 2960669 | The rapidity and dose dependency of the phosphorylation of pp185 suggested that it may represent a common endogenous substrate for the insulin and IGF-I receptors in these neural-derived cells. |
| 93 | 2960669 | Phosphorylation was primarily on phosphoserine and phosphotyrosine residues. pp185 did not absorb to wheat germ agglutinin-agarose and was not stimulated by either epidermal growth factor or platelet-derived growth factor. |
| 94 | 2960669 | The finding of pp185 in these neural-related cells as well as in non-neural tissues suggests that it may represent a ubiquitous endogenous substrate for both the insulin and IGF-I receptor kinases. |
| 95 | 3516381 | Porcine insulin, human insulin-like growth factors I and II, human growth hormone, platelet-derived growth factor, epidermal growth factor, and fibroblast growth factor have negligible influence on growth of melanoma B16. |
| 96 | 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. |
| 97 | 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. |
| 98 | 3906357 | The effect of insulin and IGFs was also additive with other growth factors tested, including platelet-derived growth factor. |
| 99 | 3906358 | Platelets from normal subjects contain platelet-derived growth factor (PDGF), epithelial growth factor (EGF), and transforming growth factor. |
| 100 | 3906358 | The cationic factor corresponds to PDGF, whereas the anionic factor appears to be identical to EGF. |
| 101 | 3908487 | Addition of platelet-derived growth factor (PDGF; 50 ng/chamber) to the collagen-filled chambers caused an earlier influx of connective tissue cells, a marked increase in DNA synthesis, and a greater collagen deposition in the chamber during the first 2 wk after implantation. |
| 102 | 3908487 | After 3 wk, however, the levels of collagen were similar in PDGF-supplemented and control chambers. |
| 103 | 3908487 | Combinations of PDGF and insulin caused an even more rapid increase in collagen deposition. |
| 104 | 6816718 | The cultured arterial endothelial cells released prostacyclin in response to challenge with thrombin and protamine sulfate but not in response to bradykinin or the platelet-derived growth factor. |
| 105 | 7505273 | The activity was inhibited by an anti-platelet-derived growth factor (PDGF) antibody, but not by an anti-bFGF antibody. |
| 106 | 7505273 | The response was induced by PDGF-BB and PDGF-AB dose dependently, but not by PDGF-AA, indicating that it was mediated by PDGF-beta receptor-dependent pathways, and that the PDGF-like factor was PDGF-BB or -AB. |
| 107 | 7505273 | The activity was inhibited by an anti-platelet-derived growth factor (PDGF) antibody, but not by an anti-bFGF antibody. |
| 108 | 7505273 | The response was induced by PDGF-BB and PDGF-AB dose dependently, but not by PDGF-AA, indicating that it was mediated by PDGF-beta receptor-dependent pathways, and that the PDGF-like factor was PDGF-BB or -AB. |
| 109 | 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. |
| 110 | 7508064 | Additive effects were observed for EGF and PDGF or EGF and insulin. |
| 111 | 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. |
| 112 | 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. |
| 113 | 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. |
| 114 | 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. |
| 115 | 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. |
| 116 | 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. |
| 117 | 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. |
| 118 | 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. |
| 119 | 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. |
| 120 | 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. |
| 121 | 7544540 | Transforming growth factor-beta 1 mRNA levels were elevated 1.8-fold, but platelet-derived growth factor-B mRNA levels remained normal. |
| 122 | 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. |
| 123 | 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. |
| 124 | 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. |
| 125 | 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. |
| 126 | 7658918 | Platelet-Derived Growth Factor (PDGF) levels were examined by radioimmunoassay in wound tissue of normal and diabetic rats (streptozotocin-induced diabetes). |
| 127 | 7732887 | Regulation of 12-lipoxygenase by platelet-derived growth factor in vascular smooth muscle cells. |
| 128 | 7737268 | Effects of epidermal growth factor (EGF), platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) on human adipocyte development and function. |
| 129 | 7737268 | We investigated the effects of epidermal growth factor (EGF), platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) on the differentiation of human adipocyte precursor cells and some metabolic aspects of newly formed fat cells kept in primary culture. |
| 130 | 7737268 | Exposure of stromal cells from human adipose tissue to EGF (0.01-100 ng mL-1) resulted in a dose- and time-dependent decrease in the number of developing fat cells and the activity of glycerol-3-phosphate dehydrogenase (GPDH), a marker of adipose differentiation. |
| 131 | 7737268 | Effects of epidermal growth factor (EGF), platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) on human adipocyte development and function. |
| 132 | 7737268 | We investigated the effects of epidermal growth factor (EGF), platelet-derived growth factor (PDGF) and fibroblast growth factor (FGF) on the differentiation of human adipocyte precursor cells and some metabolic aspects of newly formed fat cells kept in primary culture. |
| 133 | 7737268 | Exposure of stromal cells from human adipose tissue to EGF (0.01-100 ng mL-1) resulted in a dose- and time-dependent decrease in the number of developing fat cells and the activity of glycerol-3-phosphate dehydrogenase (GPDH), a marker of adipose differentiation. |
| 134 | 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. |
| 135 | 7752595 | PDGF B-chain mRNA was slightly increased at day one, and PDGF B-chain immunostaining was slightly increased at days one and six. |
| 136 | 7752595 | Insulin treatment prevented mesangial cell proliferation, actin expression, and macrophage infiltration, and normalized TGF-beta expression at 14 and 30 days. |
| 137 | 7752595 | These multiple cellular events preceded any detectable increases in glomerular gene expression or deposition of collagen I, IV or laminin. |
| 138 | 7852393 | Replacement of the TM domain with that of the platelet-derived growth factor receptor, insertion of 3 amino acids, and substitution of Asp for Val938 or of Ala for either Gly933 or Pro934 had no effect on internalization. |
| 139 | 7867886 | Platelet-derived growth factor (PDGF) is a powerful mitogen for many cell types, and is believed to play a major role in wound healing when released from platelets at sites of injury. |
| 140 | 7867886 | Neither plasma nor serum PDGF concentrations differed significantly between control subjects, insulin-dependent, and non-insulin-dependent diabetic patients. |
| 141 | 7867886 | However, limited joint mobility was not associated with elevated serum or plasma PDGF in insulin-dependent or non-insulin-dependent diabetes. |
| 142 | 7957489 | Cultured aortic smooth muscle cells (SMC) of diabetic rats and rabbits, which overexpress platelet-derived growth factor (PDGF) beta-receptor compared with controls, have a unique phenotype. |
| 143 | 7983060 | Demonstration that the p85 subunit binds directly to the COOH terminus of the insulin receptor in intact cells. |
| 144 | 7983060 | Phosphorylated IRS-1 binds to SH2 domains in the p85 regulatory subunit of phosphatidyl inositol (PI) 3-kinase, thereby stimulating the catalytic activity of PI 3-kinase. |
| 145 | 7983060 | For most growth factor receptor tyrosine kinases (including receptors for epidermal growth factor and platelet-derived growth factor), the p85 regulatory subunit of PI 3-kinase binds directly to phosphorylated YXXM motifs contained in the cytoplasmic domain of the receptor itself. |
| 146 | 7983060 | Previous studies in cell-free systems have shown that the phosphorylated YHTM sequence (amino acid residues 1322-1325) in the COOH terminus of the insulin receptor has the ability to bind to the p85 subunit of PI 3-kinase, thereby activating the enzyme. |
| 147 | 7983060 | Subsequent to insulin-stimulated phosphorylation of the insulin receptor, a complex is formed that contains the insulin receptor and PI 3-kinase. |
| 148 | 7983060 | This complex can be immunoprecipitated by antibodies directed against either the insulin receptor or the p85 subunit of PI 3-kinase. |
| 149 | 7983060 | The delta 43 mutant insulin receptor that lacks 43 amino acids at the COOH terminus does not bind p85. |
| 150 | 7983060 | Thus, by binding directly to p85, the phosphorylated YHTM motif in the COOH terminus of the insulin receptor contributes partially to mediating the effect of insulin to activate PI 3-kinase. |
| 151 | 8015312 | PDGF and TGF-alpha act synergistically to improve wound healing in the genetically diabetic mouse. |
| 152 | 8015312 | Previous studies have demonstrated that the fibroblast mitogens, BB homodimer of platelet-derived growth factor (PDGF-BB) or basic fibroblast growth factor, plus insulin-like growth factor, act synergistically to enhance wound closure in the genetically diabetic mouse. |
| 153 | 8015312 | The purpose of this study was to determine whether the keratinocyte mitogens, epidermal growth factor (EGF) or transforming growth factor-alpha (TGF-alpha), in combination with the fibroblast mitogen, PDGF-BB, would produce a similar synergistic enhancement in tissue repair. |
| 154 | 8015312 | Full-thickness skin wounds created on the backs of diabetic mice received topical applications of vehicle (5% polyethylene glycol), PDGF-BB (10 micrograms), EGF (1 microgram), TGF-alpha (1 microgram), or the combination of PDGF (10 micrograms) and EGF (1 microgram) or TGF-alpha (1 microgram) for 5 consecutive days starting at wounding. |
| 155 | 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. |
| 156 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 157 | 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. |
| 158 | 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. |
| 159 | 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. |
| 160 | 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. |
| 161 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 162 | 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. |
| 163 | 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. |
| 164 | 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. |
| 165 | 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. |
| 166 | 8094359 | The mRNA levels for PCNA, TNF-alpha, PDGF-B chain, TGF-beta, and bFGF increased with age in STZ-induced diabetic rats. |
| 167 | 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. |
| 168 | 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. |
| 169 | 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. |
| 170 | 8144631 | SH-PTP2/Syp SH2 domain binding specificity is defined by direct interactions with platelet-derived growth factor beta-receptor, epidermal growth factor receptor, and insulin receptor substrate-1-derived phosphopeptides. |
| 171 | 8144631 | The cytoplasmic phosphotyrosine phosphatase SH-PTP2 (Syp, PTP 1D, PTP-2C) contains two SH2 domains (N and C) which mediate its association with and activation by the platelet-derived growth factor (PDGF) and epidermal growth factor receptors and IRS-1. |
| 172 | 8144631 | The sequence surrounding Tyr1009 bound with greatest affinity (ID50 = 14 microM) of eight PDGF receptor-derived phosphopeptides tested. |
| 173 | 8144631 | These findings are consistent with recent mutational analyses of the PDGF receptor and predict site-specific interactions between SH-PTP2 and each of these phosphoproteins. |
| 174 | 8144631 | SH-PTP2/Syp SH2 domain binding specificity is defined by direct interactions with platelet-derived growth factor beta-receptor, epidermal growth factor receptor, and insulin receptor substrate-1-derived phosphopeptides. |
| 175 | 8144631 | The cytoplasmic phosphotyrosine phosphatase SH-PTP2 (Syp, PTP 1D, PTP-2C) contains two SH2 domains (N and C) which mediate its association with and activation by the platelet-derived growth factor (PDGF) and epidermal growth factor receptors and IRS-1. |
| 176 | 8144631 | The sequence surrounding Tyr1009 bound with greatest affinity (ID50 = 14 microM) of eight PDGF receptor-derived phosphopeptides tested. |
| 177 | 8144631 | These findings are consistent with recent mutational analyses of the PDGF receptor and predict site-specific interactions between SH-PTP2 and each of these phosphoproteins. |
| 178 | 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. |
| 179 | 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. |
| 180 | 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. |
| 181 | 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. |
| 182 | 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. |
| 183 | 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. |
| 184 | 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. |
| 185 | 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. |
| 186 | 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. |
| 187 | 8265565 | This structural motif, without the 77-77 disulfide bond, defines also the common fold for a general family of growth factors, including the nerve growth factor and platelet-derived growth factor families. |
| 188 | 8340422 | Mitogen regulation of c-Raf-1 protein kinase activity toward mitogen-activated protein kinase-kinase. |
| 189 | 8340422 | The c-raf-1 protooncogene encodes a Ser/Thr protein kinase. |
| 190 | 8340422 | A mitogen-activated protein kinase-kinase (MAPKK) purified from bovine brain is phosphorylated and activated 4-9-fold in vitro by c-Raf-1 from mitogen-treated cells. c-Raf-1 protein kinase activity, measured by the phosphorylation of brain MAPKK substrate, is detectably activated within 1 min after addition of platelet-derived growth factor (PDGF) to 3T3 cells, increasing more rapidly than the endogenous NIH 3T3 cell MAPKK activity. c-Raf-1 activation is also induced by insulin, phorbol ester, thrombin, and endothelin. |
| 191 | 8340422 | PDGF-, epidermal groth factor-, and insulin-stimulated 32P-c-Raf-1 yield very similar, complex tryptic 32P-peptide maps, wherein only 2 of 10 32P-peptides appear entirely de novo after growth factor addition. |
| 192 | 8340422 | Mitogen-activated protein kinase/extracellular signal-regulated kinase-2 can phosphorylate c-Raf-1 in vitro on 4-6 tryptic 32P-peptides, all of which comigrate with tryptic 32P-peptides derived from c-Raf-1 labeled in situ. |
| 193 | 8340422 | Mitogen-activated protein kinase phosphorylation of c-Raf-1 in vitro, however, does not 1) generate 32P-peptides that comigrate with those that appear de novo after PDGF or insulin treatment in situ; 2) does not convert c-Raf-1 polypeptides to a slower mobility on SDS-polyacrylamide gel electrophoresis as is seen after PDGF or insulin; 3) does not alter c-Raf-1 kinase activity toward MAPKK. |
| 194 | 8340422 | Thus, based on overlapping site specificity, Erk-2 is a viable candidate to be among the PDGF-stimulated c-Raf-1 kinases. |
| 195 | 8340422 | Although PDGF/insulin-stimulated c-Raf-1 Ser/Thr phosphorylation may be necessary to sustain the active state, a role for mitogen-activated protein kinase/extracellular signal-regulated kinase-2 phosphorylation in the initiation of c-Raf-1 activation is unlikely. |
| 196 | 8440708 | MTA had no effect on either epidermal growth factor- or platelet-derived growth factor-stimulated protein tyrosine phosphorylation in fibroblasts. |
| 197 | 8462625 | This difference of the growth responses was observed specifically with platelet-derived growth factor (PDGF). |
| 198 | 8476260 | Angiotensin converting enzyme transforms angiotensin I into angiotensin II and breaks down bradykinin into inactive products. |
| 199 | 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. |
| 200 | 8530404 | Insulin-induced phosphorylation of insulin receptors and insulin receptor substrate-1 displaces phosphorylated platelet-derived growth factor receptors from binding sites on PI 3-kinase. |
| 201 | 8530404 | The p85 regulatory subunit of PI 3-kinase binds to phosphotyrosine residues of various phosphoproteins including the platelet-derived growth factor (PDGF) receptor, the insulin receptor, and insulin receptor substrate-1 (IRS-1). |
| 202 | 8530404 | Using NIH-3T3 cells overexpressing the human insulin receptor, we demonstrate that the p85 regulatory subunit of PI 3-kinase binds to phosphorylated PDGF receptor in cells incubated in the absence of insulin. |
| 203 | 8530404 | When insulin is added, p85 is released from phosphorylated PDGF receptors and binds to phosphorylated insulin receptors and insulin receptor substrate-1. |
| 204 | 8530404 | Moreover, insulin-induced dissociation of PDGF receptors from binding sites on PI 3-kinase requires a functional insulin receptor and is not prevented by vanadate treatment. |
| 205 | 8530404 | In contrast, insulin activation does not displace PDGF receptors from binding sites on Ras GTPase-activating protein. |
| 206 | 8530404 | This competition for binding to PI 3-kinase provides a mechanism for cross-talk among signaling pathways initiated by distinct peptide hormones and growth factors such as insulin and PDGF. |
| 207 | 8530404 | Insulin-induced phosphorylation of insulin receptors and insulin receptor substrate-1 displaces phosphorylated platelet-derived growth factor receptors from binding sites on PI 3-kinase. |
| 208 | 8530404 | The p85 regulatory subunit of PI 3-kinase binds to phosphotyrosine residues of various phosphoproteins including the platelet-derived growth factor (PDGF) receptor, the insulin receptor, and insulin receptor substrate-1 (IRS-1). |
| 209 | 8530404 | Using NIH-3T3 cells overexpressing the human insulin receptor, we demonstrate that the p85 regulatory subunit of PI 3-kinase binds to phosphorylated PDGF receptor in cells incubated in the absence of insulin. |
| 210 | 8530404 | When insulin is added, p85 is released from phosphorylated PDGF receptors and binds to phosphorylated insulin receptors and insulin receptor substrate-1. |
| 211 | 8530404 | Moreover, insulin-induced dissociation of PDGF receptors from binding sites on PI 3-kinase requires a functional insulin receptor and is not prevented by vanadate treatment. |
| 212 | 8530404 | In contrast, insulin activation does not displace PDGF receptors from binding sites on Ras GTPase-activating protein. |
| 213 | 8530404 | This competition for binding to PI 3-kinase provides a mechanism for cross-talk among signaling pathways initiated by distinct peptide hormones and growth factors such as insulin and PDGF. |
| 214 | 8603774 | These results indicated that PDGF-beta receptor expression was enhanced by high glucose through the activation of protein kinase C. |
| 215 | 8603774 | Furthermore, we observed similar effects of high glucose on both PDGF-beta receptor expression and protein kinase C activation in rat mesangial cells and human capillary endothelial cells. |
| 216 | 8603774 | These results indicated that PDGF-beta receptor expression was enhanced by high glucose through the activation of protein kinase C. |
| 217 | 8603774 | Furthermore, we observed similar effects of high glucose on both PDGF-beta receptor expression and protein kinase C activation in rat mesangial cells and human capillary endothelial cells. |
| 218 | 8674900 | At least three mitogens for SMCs, platelet-derived growth factor (PDGF), fibroblast growth factor, and heparin-binding epidermal growth factor-like growth factor (HB-EGF), are known to be produced by SMCs themselves and are considered to be the most potent growth factors in the progression of macroangiopathy as seen in diabetes. |
| 219 | 8674900 | HB-EGF, but not PDGF, is regulated at the transcriptional level by 3-deoxyglucosone (3-DG), a major and highly reactive intermediate in the glycation reaction. |
| 220 | 8676507 | We have identified sequences related to the Rep recognition sequence in the AAV P5 promoter in or near the c-sis proto-oncogene and the genes coding for a hepatocyte glucose transporter, alpha-A-crystallin, and carcinoma marker GA733-1. |
| 221 | 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. |
| 222 | 8764141 | TNF-alpha and IL-1 alpha induce mannose receptors and apoptosis in glomerular mesangial but not endothelial cells. |
| 223 | 8764141 | Mannose receptor mRNA was induced in a dose- and time-dependent manner in mesangial cells by interleukin-1 alpha (IL-1 alpha) or tumor necrosis factor-alpha (TNF-alpha) but not by platelet-derived growth factor-B or IL-6. |
| 224 | 8764141 | TNF-alpha and IL-1 alpha also induced apoptosis in mesangial cells. |
| 225 | 8817104 | The proliferation of human smooth muscle cells in the presence of 10% fetal calf serum or platelet derived growth factor-BB (10 ng/ml) was inhibited by type 1 collagen coated on the dishes. |
| 226 | 8890924 | The aim of this investigation was to assess the effects of angiotensin II and high glucose on the production of platelet-derived growth factor (PDGF) in human endothelial cells. |
| 227 | 8890924 | Angiotensin II significantly increased PDGF in human endothelial cells and the effect was accompanied by a transient increase in cytosolic calcium. |
| 228 | 8890924 | The angiotensin II-induced intracellular Ca2+ increases, PDGF production were completely abolished by saralasin and neomycin, respectively. |
| 229 | 8890924 | We postulate that the increased production of PDGF by the vascular endothelium in response to high glucose and angiotensin II may participate in the development of the diabetic angiopathy. |
| 230 | 8908207 | Platelet-derived growth factor BB mediated regulation of 12-lipoxygenase in porcine aortic smooth muscle cells. |
| 231 | 8908207 | Platelet-derived growth factor BB (PDGF) is a potent mitogen and chemoattractant for vascular smooth muscle cells (VSMC). |
| 232 | 8908207 | In the present study, we have examined the effect of PDGF on the 12-lipoxygenase (12-LO) pathway of arachidonate metabolism in porcine aortic VSMC (PVSMC). |
| 233 | 8908207 | Platelet-derived growth factor BB mediated regulation of 12-lipoxygenase in porcine aortic smooth muscle cells. |
| 234 | 8908207 | Platelet-derived growth factor BB (PDGF) is a potent mitogen and chemoattractant for vascular smooth muscle cells (VSMC). |
| 235 | 8908207 | In the present study, we have examined the effect of PDGF on the 12-lipoxygenase (12-LO) pathway of arachidonate metabolism in porcine aortic VSMC (PVSMC). |
| 236 | 8910437 | We have reported previously that substitution of the transmembrane domain of the insulin receptor with that of the erbB-2 oncogene (IRerbV-->E) results in constitutive activation of the insulin receptor kinase. |
| 237 | 8910437 | Compared to NIH3T3 cells overexpressing wild-type insulin receptors (IRwt), cells overexpressing IRerbV-->E displayed a decrease in IRS-1 protein content by 55%, but basal tyrosine phosphorylation of IRS-1 was increased. |
| 238 | 8910437 | This resulted in an increased association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase, increased phosphatidylinositol 3-kinase activity in anti-IRS-1 immunoprecipitates, constitutive activation of p70 S6 protein kinase, and an increased association of Grb2 with Shc in the absence of ligand. |
| 239 | 8910437 | However, Grb2 association with IRS-1 could not be detected in the basal or insulin-stimulated states, and mitogen-activated protein kinase (MAPK) activity could not be stimulated by insulin, epidermal growth factor, or platelet-derived growth factor. |
| 240 | 8910437 | With decreased IRS-1 content, tyrosine phosphorylation of IRS-1 was decreased by over 75%, leading to decreased IRS-1-associated PI 3-kinase and Grb2. |
| 241 | 8910437 | In addition, Grb2 association with Shc and activation of MAPK and the p70 S6 kinase were insensitive to insulin stimulation. |
| 242 | 8910437 | By contrast, association of Grb2 with Shc and activation of MAPK, but not the p70 S6 kinase, could be stimulated by epidermal growth factor or platelet-derived growth factor. |
| 243 | 8910437 | We have reported previously that substitution of the transmembrane domain of the insulin receptor with that of the erbB-2 oncogene (IRerbV-->E) results in constitutive activation of the insulin receptor kinase. |
| 244 | 8910437 | Compared to NIH3T3 cells overexpressing wild-type insulin receptors (IRwt), cells overexpressing IRerbV-->E displayed a decrease in IRS-1 protein content by 55%, but basal tyrosine phosphorylation of IRS-1 was increased. |
| 245 | 8910437 | This resulted in an increased association of IRS-1 with the p85 subunit of phosphatidylinositol 3-kinase, increased phosphatidylinositol 3-kinase activity in anti-IRS-1 immunoprecipitates, constitutive activation of p70 S6 protein kinase, and an increased association of Grb2 with Shc in the absence of ligand. |
| 246 | 8910437 | However, Grb2 association with IRS-1 could not be detected in the basal or insulin-stimulated states, and mitogen-activated protein kinase (MAPK) activity could not be stimulated by insulin, epidermal growth factor, or platelet-derived growth factor. |
| 247 | 8910437 | With decreased IRS-1 content, tyrosine phosphorylation of IRS-1 was decreased by over 75%, leading to decreased IRS-1-associated PI 3-kinase and Grb2. |
| 248 | 8910437 | In addition, Grb2 association with Shc and activation of MAPK and the p70 S6 kinase were insensitive to insulin stimulation. |
| 249 | 8910437 | By contrast, association of Grb2 with Shc and activation of MAPK, but not the p70 S6 kinase, could be stimulated by epidermal growth factor or platelet-derived growth factor. |
| 250 | 8952619 | Furthermore, the over-expression of the fibronectin receptor resulted in a suppressed chemotactic response of these cells to platelet-derived growth factor. |
| 251 | 8956981 | A polyclonal anti-platelet-derived growth factor (PDGF)-BB (0.21-3.3 micrograms/ml) inhibited (by 66.5 +/- 6.6%) the tube-forming activity of conditioned medium (CM) from M phi in diabetic GK rats, but not that in age-matched normal Wistar rats. |
| 252 | 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. |
| 253 | 9006901 | Splice variants of an insulin and growth factor receptor-binding protein with PH and SH2 domains. |
| 254 | 9006901 | cDNA clones encoding human (h) Grb7 and a previously unknown protein with high homology to hGrb-IR and mGrb10 (where m indicates mouse) were found by screening expressed sequence tag data bases. hGrb7 mRNA expression is greatest in pancreas and restricted to a few other tissues. |
| 255 | 9006901 | In cells, Grb-IRbeta/Grb10 protein translocates from cytosol to membrane upon insulin stimulation, most likely due to direct interactions with the insulin receptor. |
| 256 | 9006901 | Studies with mutated receptors and synthetic phosphopeptides show that the hGrb-IRbeta/Grb10 SH2 domain binds at least two sites in the insulin receptor: the kinase activation loop > the juxtamembrane site. hGrb-IRbeta/Grb10 also binds a 135-kDa phosphoprotein in unstimulated 3T3-L1 adipocytes; binding is reduced upon insulin stimulation. |
| 257 | 9006901 | In addition, the c-Abl SH3 domain binds Grb-IR/Grb10, whereas Fyn, phosphatidylinositol 3-kinase p85, and Grb2 SH3 domains do not. |
| 258 | 9006901 | The site of c-Abl SH3 domain interaction is highly conserved within the Grb-IR/Grb10/Grb7/Grb14 family. hGrb-IRbeta/Grb10 also binds platelet-derived growth factor and epidermal growth factor receptors, suggesting a broader role in the signaling pathways of numerous receptors. |
| 259 | 9006901 | We conclude that hGrb-IRbeta/Grb10 is a widely expressed, PH and SH2 domain-containing, SH3 domain-binding protein that functions downstream from activated insulin and growth factor receptors. |
| 260 | 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. |
| 261 | 9067916 | The interleukin-1 receptor antagonist gene (IL1RN) was also genotyped due to its reported association with diabetic nephropathy. |
| 262 | 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. |
| 263 | 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). |
| 264 | 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. |
| 265 | 9111509 | At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. |
| 266 | 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. |
| 267 | 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. |
| 268 | 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). |
| 269 | 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. |
| 270 | 9111509 | At 12 to 18 months, the alpha 1(IV) collagen, TGF-beta 1, and tenascin levels increased by nearly another 50%. |
| 271 | 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. |
| 272 | 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. |
| 273 | 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. |
| 274 | 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. |
| 275 | 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). |
| 276 | 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. |
| 277 | 9137900 | Elevated intravitreal levels of IGF-1 and VEGF correlating with neovascular activity have been found in some patients. |
| 278 | 9137900 | Inhibition of IGF-1 by somatostatin analogs has produced unsatisfactory results. |
| 279 | 9148380 | The latter include angiotensin II, thromboxane, platelet-derived growth factor, endothelins, insulin-like growth factor-1, and transforming growth factor-beta. |
| 280 | 9288548 | In the present study the modulatory action of captopril on the angiotensin II (AngII), arginine vasopressin (AVP), and platelet derived growth factor (PDGF)-induced increase of cytosolic free calcium concentration ([Ca2+]i) was investigated in cultured vascular smooth muscle cells (VSMC) and cultured glomerular mesangial cells (MC) from rats using the fluorescent dye technique. |
| 281 | 9336387 | Increasing evidence suggests that cytokines such as interleukin-1beta (IL-1), IL-4, and IL-8 may play an important role in the chronic inflammation and cellular growth observed in cardiovascular diseases. |
| 282 | 9336387 | Furthermore, earlier studies have shown that vascular smooth muscle cell (VSMC) growth factors such as angiotensin II and platelet-derived growth factor can increase LO activity and expression in VSMCs. |
| 283 | 9336387 | In the present study, we have examined whether vasoactive and inflammatory cytokines such as IL-1, IL-4, and IL-8 can modulate 12-LO activity and expression in porcine VSMCs and also whether they have growth-promoting effects in these cells. |
| 284 | 9407457 | Urinary excretion of TGF-beta 1, PDGF-BB and fibronectin in insulin-dependent diabetes mellitus patients. |
| 285 | 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. |
| 286 | 9407457 | IDDM patients had higher urinary excretion of TGF-beta 1, PDGF and FN compared to controls. |
| 287 | 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. |
| 288 | 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. |
| 289 | 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. |
| 290 | 9422724 | To test this, binding studies were conducted with tandem domains from the five signaling enzymes: phosphatidylinositol 3-kinase p85, ZAP-70, Syk, SHP-2, and phospholipase C-gamma1. |
| 291 | 9422724 | Bisphosphorylated TAMs (tyrosine-based activation motifs) were derived from biologically relevant sites in platelet-derived growth factor, T cell, B cell, and high affinity IgE receptors and the receptor substrates IRS-1 (insulin receptor substrate-1) and SHPS-1/SIRP. |
| 292 | 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. |
| 293 | 9526909 | Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. |
| 294 | 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). |
| 295 | 9526909 | Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. |
| 296 | 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. |
| 297 | 9526909 | Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. |
| 298 | 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). |
| 299 | 9526909 | Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. |
| 300 | 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. |
| 301 | 9526909 | Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. |
| 302 | 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). |
| 303 | 9526909 | Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. |
| 304 | 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. |
| 305 | 9526909 | Diabetes prevents periodontitis-induced increases in gingival platelet derived growth factor-B and interleukin 1-beta in a rat model. |
| 306 | 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). |
| 307 | 9526909 | Periodontitis alone demonstrated a significant increase (P < 0.05) in levels of PDGF-B and IL-1beta. |
| 308 | 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. |
| 309 | 9593635 | Some of these effects occur in part through induction of cytokines such as platelet-derived growth factor (PDGF), which is expressed by the retinal pigment epithelium (RPE). |
| 310 | 9593725 | Association of the insulin receptor with phospholipase C-gamma (PLCgamma) in 3T3-L1 adipocytes suggests a role for PLCgamma in metabolic signaling by insulin. |
| 311 | 9593725 | Phospholipase C-gamma (PLCgamma) is the isozyme of PLC phosphorylated by multiple tyrosine kinases including epidermal growth factor, platelet-derived growth factor, nerve growth factor receptors, and nonreceptor tyrosine kinases. |
| 312 | 9593725 | To determine the functional significance of the interaction of PLCgamma and the IR, we used a specific inhibitor of PLC, U73122, or microinjection of SH2 domain glutathione S-transferase fusion proteins derived from PLCgamma to block insulin-stimulated GLUT4 translocation. |
| 313 | 9593725 | U73122 selectively inhibits mitogen-activated protein kinase, leaving the Akt and p70 S6 kinase pathways unperturbed. |
| 314 | 9625357 | Growth factors such as epidermal growth factor, nerve growth factor, platelet-derived growth factor (PDGF) and insulin-like growth factor-I act as survival factors and inhibit apoptosis in a number of cell types such as haematopoietic cells, preovulatory follicles, the mammary gland, phaeochromocytoma cells and neurones. |
| 315 | 9655183 | Here, we report that in baboon aortic smooth muscle cells (SMCs), vanadate induced p42/p44 mitogen-activated protein kinase (MAPK) activity. |
| 316 | 9655183 | Although activation of p42/p44MAPK/MAPKK is generally thought to be necessary for proliferation, in SMCs, vanadate did not promote DNA synthesis and inhibited thymidine incorporation stimulated by platelet-derived growth factor (PDGF)-BB in a dose dependent fashion (IC50: 30 microM). |
| 317 | 9655183 | The addition of PDGF-BB further activated p42/p44MAPK/MAPKK in the presence of vanadate and substantially increased vanadate toxicity. |
| 318 | 9655183 | We conclude from these observations that activation of the p42/p44MAPK/MAPKK signalling module contributes to the cytotoxic effects induced by vanadate. |
| 319 | 9784857 | Receptor tyrosine kinases (RTKs), such as the epidermal growth factor receptor (EGFR) and the platelet-derived growth factor receptor (PDGFR), are critically involved in the transduction of mitogenic signals across the plasma membrane and therefore in the regulation of cell growth and proliferation. |
| 320 | 9784857 | EGFR and PDGFR are selectively inhibited by analogues of the marine natural product aeroplysinin. |
| 321 | 9812917 | Atrial natriuretic factor 1-28 (ANF) and C-type natriuretic factor-22 (CNP) reduced angiotensin II (Ang II)- and platelet-derived growth factor-stimulated PAI-1 mRNA expression in rat aortic smooth muscle cells by 50% to 70%, with corresponding reductions in PAI-1 protein release. |
| 322 | 9812917 | Treatment of human aortic smooth muscle cells with CNP similarly inhibited both platelet-derived growth factor-induced PAI-1 mRNA expression and PAI-1 protein release by 50%. |
| 323 | 9812917 | Dose-response studies revealed that the inhibitory effects of CNP and ANF on PAI-1 expression were concentration dependent, with IC50s of approximately 1 nmol/L for both natriuretic peptides. |
| 324 | 9812917 | Ang II-stimulated PAI-1 expression was also inhibited by the nitric oxide donor S-nitroso-N-acetylpenicillamine. |
| 325 | 9812917 | The membrane-permeant cGMP analogue 8-Br-cGMP reduced Ang II-stimulated PAI-1 expression by 60%, and an inhibitor of soluble guanylyl cyclase (1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one) significantly impaired the inhibitory effects of S-nitroso-N-acetylpenicillamine on Ang II-stimulated PAI-1 expression. |
| 326 | 9812917 | Atrial natriuretic factor 1-28 (ANF) and C-type natriuretic factor-22 (CNP) reduced angiotensin II (Ang II)- and platelet-derived growth factor-stimulated PAI-1 mRNA expression in rat aortic smooth muscle cells by 50% to 70%, with corresponding reductions in PAI-1 protein release. |
| 327 | 9812917 | Treatment of human aortic smooth muscle cells with CNP similarly inhibited both platelet-derived growth factor-induced PAI-1 mRNA expression and PAI-1 protein release by 50%. |
| 328 | 9812917 | Dose-response studies revealed that the inhibitory effects of CNP and ANF on PAI-1 expression were concentration dependent, with IC50s of approximately 1 nmol/L for both natriuretic peptides. |
| 329 | 9812917 | Ang II-stimulated PAI-1 expression was also inhibited by the nitric oxide donor S-nitroso-N-acetylpenicillamine. |
| 330 | 9812917 | The membrane-permeant cGMP analogue 8-Br-cGMP reduced Ang II-stimulated PAI-1 expression by 60%, and an inhibitor of soluble guanylyl cyclase (1H-[1,2,4]oxadiazolo[4, 3-a]quinoxalin-1-one) significantly impaired the inhibitory effects of S-nitroso-N-acetylpenicillamine on Ang II-stimulated PAI-1 expression. |
| 331 | 9819414 | Sorting nexin 1 (SNX1) is a protein that binds to the epidermal growth factor (EGF) receptor and is proposed to play a role in directing EGF receptors to lysosomes for degradation (R. |
| 332 | 9819414 | We have obtained full-length cDNAs and deduced the amino acid sequences of three novel homologous proteins, which were denoted human sorting nexins (SNX2, SNX3, and SNX4). |
| 333 | 9819414 | Human SNX1 (522 amino acids), SNX1A (457 amino acids), SNX2 (519 amino acids), SNX3 (162 amino acids), and SNX4 (450 amino acids) are part of a larger family of hydrophilic molecules including proteins identified in Caenorhabditis elegans and Saccharomyces cerevisiae. |
| 334 | 9819414 | When expressed in COS7 cells, epitope-tagged sorting nexins SNX1, SNX1A, SNX2, and SNX4 coimmunoprecipitated with receptor tyrosine kinases for EGF, platelet-derived growth factor, and insulin. |
| 335 | 9819414 | Interestingly, endogenous COS7 transferrin receptors associated exclusively with SNX1 and SNX1A, while SNX3 was not found to associate with any of the receptors studied. |
| 336 | 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). |
| 337 | 9916172 | Expression of mRNA for vascular endothelial growth factor (VEGF), platelet-derived growth factor A chain, and insulin-like growth factor-1 was reduced >83% in subtherapeutic compared with therapeutic Dermagraft. |
| 338 | 9916172 | Granulocyte colony-stimulating factor and VEGF protein secretion, determined by enzyme-linked immunosorbent assay (ELISA), and angiogenic activity also depended on therapeutic range. |
| 339 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 340 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 341 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 342 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 343 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 344 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 345 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 346 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 347 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 348 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 349 | 9931102 | TNF-alpha-induced migration of vascular smooth muscle cells is MAPK dependent. |
| 350 | 9931102 | Because activation of the extracellular signal-regulated kinase 1/2 mitogen-activated protein kinase (MAPK) is known to be required in platelet-derived growth factor-directed and angiotensin II-directed migration of these cells, we used the MAPK-inhibitor PD98059 to determine if chemotactic signaling by TNF-alpha involves the MAPK pathway as well. |
| 351 | 9931102 | TNF-alpha (100 U/mL) transiently activated MAPK with a maximal induction 10 minutes after stimulation that returned to baseline levels by 2 hours after treatment. |
| 352 | 9931102 | PD98059 also blocked TNF-alpha-stimulated MAPK activation in a concentration-dependent manner, which is consistent with its inhibition of TNF-alpha-directed migration. |
| 353 | 9931102 | To identify which TNF-alpha receptor is involved in TNF-alpha-induced MAPK activation, antibodies against the p55 TNF-alpha receptor-1 (TNF-R1) and the p75 TNF-alpha receptor-2 (TNF-R2) were used. |
| 354 | 9931102 | VSMC express both receptors, but TNF-alpha-induced MAPK activation was inhibited only by the TNF-R1 antibody. |
| 355 | 9931102 | Thiazolidinediones are known to inhibit TNF-alpha signaling in adipose tissue and attenuate platelet-derived growth factor-directed and angiotensin II-directed migration in VSMC. |
| 356 | 9931102 | Both TRO and RSG inhibited migration, but neither attenuated TNF-alpha-induced MAPK activation, indicating that their antimigration activity was exerted downstream of MAPK. |
| 357 | 9931102 | These experiments provide the first evidence that early activation of MAPK is a crucial event in TNF-alpha-mediated signal transduction leading to VSMC migration. |
| 358 | 9931102 | Moreover, inhibition of TNF-alpha-directed migration by the insulin sensitizers TRO and RSG underscores their potential as vasculoprotective agents. |
| 359 | 10102683 | Activation of protein kinase B and induction of adipogenesis by insulin in 3T3-L1 preadipocytes: contribution of phosphoinositide-3,4,5-trisphosphate versus phosphoinositide-3,4-bisphosphate. |
| 360 | 10102683 | PKB was also activated by insulin, in a dose- and time-dependent manner. |
| 361 | 10102683 | Wortmannin and LY294002, inhibitors of PI 3-kinase, reduced insulin-dependent activation of PKB, whereas rapamycin, an inhibitor of p70 S6 kinase, had no effect. |
| 362 | 10102683 | Platelet-derived growth factor (PDGF), which is not adipogenic, stimulated the production of both 3-phosphorylated phosphoinositide species, and this was associated with a greater activation of PKB than that observed with insulin. |
| 363 | 10102683 | A low dose of PDGF (1 ng/ml), which increased the production of only PI(3,4,5)P3 and mirrored the insulin effect, was unable to induce adipocyte differentiation. |
| 364 | 10102683 | In summary, insulin and PDGF differ with respect to the accumulation of 3-phosphorylated phosphoinositides and to PKB activation in 3T3-L1 preadipocytes, but these responses do not themselves explain why insulin, but not PDGF, is adipogenic. |
| 365 | 10102704 | Treatment of the cells with cytokines, such as tumor necrosis factor (TNF)-alpha and interleukin-1beta, or with growth factors, such as platelet-derived growth factor, insulin-like growth factor-I, and epidermal growth factor, all led to NF-kappaB activation in cells cultured in both NG and HG. |
| 366 | 10102704 | The augmented TNF-alpha-induced NF-kappaB activation in HG was associated with increased TNF-alpha-mediated transcriptional activation of the vascular cell adhesion molecule-1 promoter. |
| 367 | 10102704 | HG-induced NF-kappaB activation was inhibited by a protein kinase C inhibitor, calphostin C. |
| 368 | 10318852 | Membrane-targeted phosphatidylinositol 3-kinase mimics insulin actions and induces a state of cellular insulin resistance. |
| 369 | 10318852 | Even at this submaximal PI 3-kinase activity, p110(CAAX) fully stimulated p70 S6 kinase, Akt, 2-deoxyglucose uptake, and Ras, whereas, p110(WT) had little or no effect on these downstream effects. |
| 370 | 10318852 | Interestingly p110(CAAX) did not activate MAP kinase, despite its stimulation of p21(ras). |
| 371 | 10318852 | Surprisingly, p110(CAAX) did not increase basal glycogen synthase activity, and inhibited insulin stimulated activity, indicative of cellular resistance to this action of insulin. p110(CAAX) also inhibited insulin stimulated, but not platelet-derived growth factor-stimulated mitogen-activated protein kinase phosphorylation, demonstrating that the p110(CAAX) induced inhibition of mitogen-activated protein kinase and insulin signaling is specific, and not due to some toxic or nonspecific effect on the cells. |
| 372 | 10318852 | Moreover, p110(CAAX) stimulated IRS-1 Ser/Thr phosphorylation, and inhibited IRS-1 associated PI 3-kinase activity, without affecting insulin receptor tyrosine phosphorylation, suggesting that it may play an important role as a negative regulator for insulin signaling. |
| 373 | 10320053 | It has been known for some time that down-regulation and reduced kinase activity of the insulin receptor play a role in insulin resistance; however, it has recently emerged that defects in the intracellular responses to insulin are also very important. |
| 374 | 10320053 | We found that the insulin-stimulated activation of MAP kinase was defective in obese, insulin-resistant mice. |
| 375 | 10320053 | Similarly, we investigated insulin-stimulated PI3-kinase activation in the isolated soleus muscle of lean and obese mice, and found a marked reduction in the PI3-kinase activation of obese animals. |
| 376 | 10320053 | The magnitude of the effect was greater than the reduction in insulin receptor activation, suggesting that impairment of PI3-kinase activation is a very important element in the development of insulin resistance in obese mice. |
| 377 | 10320053 | In keeping with this, we found that the defect in PI3-kinase activation developed in young obese mice before the emergence of overt insulin resistance. |
| 378 | 10320053 | In adipocytes from young obese mice in which insulin resistance had not yet developed, we found that there were already marked defects in IRS-1 tyrosine phosphorylation. |
| 379 | 10320053 | Such a process could contribute to the defective IRS-1 tyrosine phosphorylation in insulin-resistant animals. |
| 380 | 10320053 | We found that brief exposure of 3T3-L1 adipocytes to platelet-derived growth factor led to IRS-1 serine/threonine phosphorylation through a PI3-kinase-dependent pathway, and that this prevented phosphorylation of the tyrosine residues of IRS-1. |
| 381 | 10320053 | Such a mechanism, induced by growth factors, TNF-alpha or some other agent, may play an important role in the development of insulin resistance in obese mice. |
| 382 | 10328554 | Tetrandrine and KS-1-4, but not KS-1-1, inhibited vascular endothelial growth factor- and platelet-derived growth factor-BB-stimulated angiogenesis in normal choroids. |
| 383 | 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. |
| 384 | 10384364 | This article reports the author's experience with treatment of chronic lower extremity ulcers of mixed etiologies with recombinant human platelet-derived growth factor--BB [rhPDGF-BB, REGRANEX (becaplermin) Gel 0.01%] in a patient with multiple risk factors including long-standing insulin-dependent type 2 diabetes. |
| 385 | 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. |
| 386 | 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. |
| 387 | 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. |
| 388 | 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. |
| 389 | 10432377 | High-glucose-induced activation of protein kinase C and stimulated TGF-beta expression appear to be essential for stimulated expression of p27Kip1. |
| 390 | 10482316 | Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes. |
| 391 | 10482316 | Specifically, we examined whether the administration of either platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in sub-nephritogenic doses might lead to an aggravation of kidney structural changes associated with hyperglycemia, resulting in progressive kidney damage in the Goto Kakizaki (GK) rat, which is a genetic model of non-obese non-insulin-dependent diabetes mellitus (NIDDM), in which progressive kidney disease does not develop spontaneously. |
| 392 | 10482316 | The results demonstrate that the administration of PDGF to hyperglycemic GK rats led to acute mesangial cell proliferation and activation as assessed by 5-bromo-2'-deoxyuridine-positive nuclei and immunostaining for alpha-smooth muscle actin. |
| 393 | 10482316 | Augmentation of kidney injury by basic fibroblast growth factor or platelet-derived growth factor does not induce progressive diabetic nephropathy in the Goto Kakizaki model of non-insulin-dependent diabetes. |
| 394 | 10482316 | Specifically, we examined whether the administration of either platelet-derived growth factor (PDGF) or basic fibroblast growth factor (bFGF) in sub-nephritogenic doses might lead to an aggravation of kidney structural changes associated with hyperglycemia, resulting in progressive kidney damage in the Goto Kakizaki (GK) rat, which is a genetic model of non-obese non-insulin-dependent diabetes mellitus (NIDDM), in which progressive kidney disease does not develop spontaneously. |
| 395 | 10482316 | The results demonstrate that the administration of PDGF to hyperglycemic GK rats led to acute mesangial cell proliferation and activation as assessed by 5-bromo-2'-deoxyuridine-positive nuclei and immunostaining for alpha-smooth muscle actin. |
| 396 | 10657238 | Sequence analysis of the proximal promoter region revealed several potential regulatory elements; these include the recognition elements of Sp1, Nkx, CP2, E2A, SIF (SIS-inducible factor), TFII-I and cAMP-responsive element (CRE), but no TATA sequences. |
| 397 | 10657238 | Furthermore, electrophoretic mobility-shift assays demonstrated that Sp3 but not other Sp (specificity protein) family members binds to three of the Sp1 sites. |
| 398 | 10657238 | Our present study suggests that Sp3 is involved in the basal transcriptional activation of the mStaf gene. |
| 399 | 10712383 | We have previously reported that high glucose stimulates osteopontin (OPN) expression through protein kinase C-dependent pathways as well as hexosamine pathways in cultured rat aortic smooth muscle cells. |
| 400 | 10712383 | We also found that OPN stimulated the migration and enhanced platelet-derived growth factor (PDGF)-mediated DNA synthesis of cultured rat aortic smooth muscle cells. |
| 401 | 10712383 | OPN and PDGF synergistically activated focal adhesion kinase as well as extracellular signal-regulated kinase; this finding seems to explain the OPN-induced enhancement of PDGF-mediated DNA synthesis. |
| 402 | 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. |
| 403 | 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. |
| 404 | 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. |
| 405 | 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. |
| 406 | 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. |
| 407 | 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. |
| 408 | 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. |
| 409 | 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. |
| 410 | 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. |
| 411 | 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. |
| 412 | 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. |
| 413 | 10801895 | Peroxisome proliferator-activated receptor gamma (PPARgamma) is a member of the nuclear receptor superfamily that is activated by binding certain fatty acids, eicosanoids, and insulin-sensitizing thiazolidinediones (TZD). |
| 414 | 10801895 | Flow cytometry demonstrated that both TRO and another TZD, rosiglitazone, prevented G(1) --> S progression induced by platelet-derived growth factor and insulin. |
| 415 | 10801895 | TRO and rosiglitazone attenuated both the mitogen-induced degradation of p27(kip1) and the mitogenic induction of p21(cip1). 15d-PGJ(2) and PD98059 inhibited both the degradation of p27(kip1) and the induction of cyclin D1 in response to mitogens. |
| 416 | 10802145 | To examine the role of PDGF in the development of diabetic nephropathy, we conducted immunohistochemical analysis for PDGF B-chain (PDGF-B) and PDGF beta-receptor (PDGFR-beta) in the glomeruli of streptozotocin-induced diabetic rats. |
| 417 | 10802145 | The immunostaining of mirror sections revealed the existence of PDGF-B or PDGFR-beta not only in mesangial cells but also in visceral epithelial cells. |
| 418 | 10802145 | To examine the role of PDGF in the development of diabetic nephropathy, we conducted immunohistochemical analysis for PDGF B-chain (PDGF-B) and PDGF beta-receptor (PDGFR-beta) in the glomeruli of streptozotocin-induced diabetic rats. |
| 419 | 10802145 | The immunostaining of mirror sections revealed the existence of PDGF-B or PDGFR-beta not only in mesangial cells but also in visceral epithelial cells. |
| 420 | 10802150 | IDL isolated from diabetics also increased not only platelet-derived growth factor B-chain, but also intercellular adhesion molecule-1 mRNA contents. |
| 421 | 10807736 | Flow cytometry demonstrated that Dox prevents mitogen-induced G(1)-->S progression of human coronary artery smooth muscle cells (CASMCs) in a dose-dependent manner, with a maximal reduction of S-phase transition by 88+/-10.5% in 20 ng/mL platelet-derived growth factor and 1 micromol/L insulin (P+I)-stimulated cells (P<0.01 for 10 micromol/L Dox versus P+I alone) and 52+/-18.7% for 10% FBS-induced mitogenesis (P<0.05 for 10 micromol/L Dox versus 10% FBS alone). |
| 422 | 10853682 | Vascular endothelial growth factor- and platelet-derived growth factor-angiogenesis depressed but fetal bovine serum-angiogenesis enhanced choroidal tissue cultures of streptozotocin-diabetic Wistar and GK rats. |
| 423 | 10887940 | By flow cytometric cell cycle analysis, VEGF showed quite different transition patterns from those of platelet-derived growth factor (PDGF) in 5-day (at the progression phase) cultured normal rat EC even though VEGF belongs to the PDGF family. |
| 424 | 10887940 | VEGF promoted cell cycle transition from the G0 to the G1 phase at 3 ng/ml, but at 30 ng/ml, VEGF weakly inhibited it compared with the effect of PDGF. |
| 425 | 10967116 | We recently described the identification of a non-peptidyl fungal metabolite (l-783,281, compound 1), which induced activation of human insulin receptor (IR) tyrosine kinase and mediated insulin-like effects in cells, as well as decreased blood glucose levels in murine models of Type 2 diabetes (Zhang, B., Salituro, G., Szalkowski, D., Li, Z., Zhang, Y., Royo, I., Vilella, D., Diez, M. |
| 426 | 10967116 | Here we report the characterization of an active analog (compound 2) with enhanced IR kinase activation potency and selectivity over related receptors (insulin-like growth factor I receptor, epidermal growth factor receptor, and platelet-derived growth factor receptor). |
| 427 | 10997698 | Regulation of inositol 1,4,5-trisphosphate receptors by transforming growth factor-beta: implications for vascular dysfunction in diabetes. |
| 428 | 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). |
| 429 | 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). |
| 430 | 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. |
| 431 | 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. |
| 432 | 10997698 | We conclude that the vascular dysfunction of diabetes leading to glomerular hypertrophy is mediated, in part, by TGF-beta-induced regulation of IP3Rs. |
| 433 | 11081306 | [Cytokines in the vitreous fluid of patients with proliferative diabetic retinopathy--vascular endothelial growth factor and platelet-derived growth factor are elevated in proliferative diabetic retinopathy]. |
| 434 | 11085978 | We have identified a novel 342-amino acid residue sorting nexin, SNX15, and a 252-amino acid splice variant, SNX15A. |
| 435 | 11085978 | The phox homology domain of SNX15 is required for its membrane association and for association with the platelet-derived growth factor receptor. |
| 436 | 11085978 | We did not detect association of SNX15 with receptors for epidermal growth factor or insulin. |
| 437 | 11085978 | However, overexpression of SNX15 led to a decrease in the processing of insulin and hepatocyte growth factor receptors to their mature subunits. |
| 438 | 11085978 | Immunofluorescence studies showed that SNX15 overexpression resulted in mislocalization of furin, the endoprotease responsible for cleavage of insulin and hepatocyte growth factor receptors. |
| 439 | 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). |
| 440 | 11180921 | Alkaline phosphatase (ALP) activity was standardized by the DNA content of the cells. |
| 441 | 11195866 | Transfer of platelet-derived growth factor-BB gene by gene gun increases contraction of collagen lattice by fibroblasts in diabetic and non-diabetic human skin. |
| 442 | 11195866 | We have used an in vitro model of wound contraction, the fibroblast-populated collagen lattice, to examine the effect of platelet-derived growth factor BB (PDGF-BB) and PDGF-BB gene transfer by gene gun on the contraction of lattices composed of either diabetic or non-diabetic human fibroblasts. |
| 443 | 11195866 | Transfer of platelet-derived growth factor-BB gene by gene gun increases contraction of collagen lattice by fibroblasts in diabetic and non-diabetic human skin. |
| 444 | 11195866 | We have used an in vitro model of wound contraction, the fibroblast-populated collagen lattice, to examine the effect of platelet-derived growth factor BB (PDGF-BB) and PDGF-BB gene transfer by gene gun on the contraction of lattices composed of either diabetic or non-diabetic human fibroblasts. |
| 445 | 11230363 | P:eroxisome proliferator-activated receptor-gamma (PPARgamma) is a novel nuclear receptor, which enhances insulin-mediated glucose uptake. |
| 446 | 11230363 | PPARgamma ligands rosiglitazone (1 to 10 micromol/L) and troglitazone (1 to 10 micromol/L) inhibited platelet-derived growth factor-induced DNA synthesis, measured as bromodeoxyuridine incorporation (P<0.01). |
| 447 | 11230363 | These data suggest that PPARgamma activation may directly attenuate diabetic glomerular disease, possibly by inhibiting mesangial growth, which occurs early in the process of diabetic nephropathy, or by inhibiting PAI-1 expression. |
| 448 | 11279102 | Sorting nexin 6, a novel SNX, interacts with the transforming growth factor-beta family of receptor serine-threonine kinases. |
| 449 | 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. |
| 450 | 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. |
| 451 | 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. |
| 452 | 11279102 | Conversely, SNX6 behaved similarly to the other SNX proteins in its interactions with receptor tyrosine kinases. |
| 453 | 11289052 | Furthermore, the mitogenic actions of platelet-derived growth factor, IGF-I, or serum are not enhanced by high glucose. |
| 454 | 11297552 | Platelet-derived growth factor C (PDGF-C), a novel growth factor that binds to PDGF alpha and beta receptor. |
| 455 | 11297552 | We have characterized platelet-derived growth factor (PDGF) C, a novel growth factor belonging to the PDGF family. |
| 456 | 11297552 | PDGF-C is a multidomain protein with the N-terminal region homologous to the extracellular CUB domain of neuropilin-1, and the C-terminal region consists of a growth factor domain (GFD) with homology to vascular endothelial growth factor (25%) and PDGF A-chain (23%). |
| 457 | 11297552 | Competition binding and immunoprecipitation studies on cells bearing both PDGF alpha and beta receptors reveal a high affinity binding of recombinant GFD (PDGF-CC) to PDGF receptor-alpha homodimers and PDGF receptor-alpha/beta heterodimers. |
| 458 | 11297552 | Together, these studies describe a third member of the PDGF family (PDGF-C) as a potent mitogen for cells of mesenchymal origin in in vitro and in vivo systems with a binding pattern similar to PDGF-AB. |
| 459 | 11297552 | Platelet-derived growth factor C (PDGF-C), a novel growth factor that binds to PDGF alpha and beta receptor. |
| 460 | 11297552 | We have characterized platelet-derived growth factor (PDGF) C, a novel growth factor belonging to the PDGF family. |
| 461 | 11297552 | PDGF-C is a multidomain protein with the N-terminal region homologous to the extracellular CUB domain of neuropilin-1, and the C-terminal region consists of a growth factor domain (GFD) with homology to vascular endothelial growth factor (25%) and PDGF A-chain (23%). |
| 462 | 11297552 | Competition binding and immunoprecipitation studies on cells bearing both PDGF alpha and beta receptors reveal a high affinity binding of recombinant GFD (PDGF-CC) to PDGF receptor-alpha homodimers and PDGF receptor-alpha/beta heterodimers. |
| 463 | 11297552 | Together, these studies describe a third member of the PDGF family (PDGF-C) as a potent mitogen for cells of mesenchymal origin in in vitro and in vivo systems with a binding pattern similar to PDGF-AB. |
| 464 | 11348869 | The RAR ligands all-trans-retinoic acid (atRA) and ethyl-p-[(E)-2-(5,6,7,8-tetrahydro-5,5,8,8-tetramethyl-2-naphthyl)-l-propenyl]-benzoic acid (TTNPB); a pan-RXR/RAR agonist, 9-cis-retinoic acid (9cRA); and the RXR-selective ligand AGN4204 all inhibited DNA synthesis stimulated with platelet-derived growth factor and insulin (IC(50): TTNPB 63 nmol/L, atRA 120 nmol/L, AGN4204 460 nmol/L, 9cRA 1.5 micromol/L). |
| 465 | 11348869 | All retinoids attenuated mitogen-induced downregulation of CDKI p27(Kip1), a major negative regulator of Rb phosphorylation, partly through stabilizing p27(Kip1) turnover. |
| 466 | 11348869 | These data demonstrate that retinoids have antiproliferative activity by modulating G(1) --> S cell cycle regulators in human CASMCs through inhibition of Rb phosphorylation and elevation of p27(Kip1) levels. |
| 467 | 11375352 | Hyperglycemia potentiated both platelet aggregation and the subsequent release of platelet-derived growth factor AB induced by a nonaggregating subthreshold concentration of collagen, which were also completely inhibited by TTFA or CCCP. |
| 468 | 11375352 | Furthermore, hyperglycemia was found to inhibit protein tyrosine phosphatase (PTP) activity and increase phosphorylation of the tyrosine kinase Syk in platelets exposed to collagen. |
| 469 | 11375352 | Hyperglycemia-induced PTP inhibition and Syk phosphorylation were found to be completely prevented by TTFA, CCCP, or Mn(III)tetrakis (4-benzoic acid) porphyrin, a stable cell-permeable superoxide dismutase mimetic. |
| 470 | 11402048 | Insulin-stimulated activation of eNOS is independent of Ca2+ but requires phosphorylation by Akt at Ser(1179). |
| 471 | 11402048 | Vasodilator actions of insulin are mediated by activation of endothelial nitric-oxide synthase (eNOS) and subsequent production of NO. |
| 472 | 11402048 | Phosphatidylinositol 3-kinase and Akt play important roles in insulin-signaling pathways leading to production of NO in vascular endothelium. |
| 473 | 11402048 | Here we dissected mechanisms whereby insulin activates eNOS by using the fluorescent dye DAF-2 to directly measure NO production in single cells. |
| 474 | 11402048 | Insulin caused a rapid increase in intracellular NO in NIH-3T3(IR) cells transiently transfected with eNOS. |
| 475 | 11402048 | However, cells expressing the eNOS-S1179A mutant (disrupted Akt phosphorylation site) did not produce detectable NO in response to insulin, whereas the response to LPA was similar to that observed in cells expressing wild-type eNOS. |
| 476 | 11402048 | Moreover, production of NO in response to insulin was blocked by coexpression of an inhibitory mutant of Akt, whereas the response to LPA was unaffected. |
| 477 | 11402048 | Phosphorylation of eNOS at Ser(1179) was observed only in response to treatment with insulin, but not with LPA. |
| 478 | 11402048 | Interestingly, platelet-derived growth factor treatment of cells activated Akt but not eNOS. |
| 479 | 11402048 | We conclude that insulin regulates eNOS activity using a Ca(2+)-independent mechanism requiring phosphorylation of eNOS by Akt. |
| 480 | 11415460 | We have previously shown that unsaturated fatty acids amplify platelet-derived-growth-factor (PDGF)-induced protein kinase C (PKC) activation in vascular smooth-muscle cells (VSMCs). |
| 481 | 11415460 | Fractionation of VSMC extracts demonstrated that the DGK alpha isoform was the major DGK activity present. |
| 482 | 11415460 | PDGF markedly increased the DGK activity of cultured cells. |
| 483 | 11415460 | An inhibitor selective for the DGK alpha isoform, R59949 [3-[2-[4-(bis-(4-fluorophenyl)methylene]piperidin-1-yl)ethyl]-2,3-dihydro-2-thioxo-4(1H)-quinazolinone], abolished the growth-factor-induced increase in DGK activity, but had little effect on basal activity. |
| 484 | 11415460 | PDGF thus selectively activates DGKalpha. |
| 485 | 11415460 | Epidermal growth factor and alpha-thrombin stimulated total DGK activity similarly to PDGF. |
| 486 | 11415460 | Activation by epidermal growth factor was sensitive to R59949, again suggesting involvement of DGKalpha. |
| 487 | 11440895 | TZDs inhibit vascular smooth muscle cell growth independently of the cyclin kinase inhibitors p21 and p27. |
| 488 | 11440895 | Because of reports that the cyclin kinase inhibitors (CKIs) p21(Waf1/Cip1) and p27(Kip1) can exhibit both growth-inhibitory and growth-permissive effects in VSM cells, we asked whether alterations in these cell cycle regulatory proteins are the mechanism by which the TZDs inhibit VSM cell growth. |
| 489 | 11440895 | We show that platelet-derived growth factor-BB increases p21 and p27 and that this increase is attenuated by TZDs. |
| 490 | 11440895 | Surprisingly, when VSM cells were transfected with antisense oligodeoxynucleotides to p21 and p27, inhibition of DNA synthesis by TZDs occurred to the same degree as in control cells. |
| 491 | 11446768 | Total RNA was isolated from normal and diseased corneas. cDNA was synthesized from individual corneas and semiquantitative reverse transcription-polymerase chain reaction (RT-PCR) was performed with primers to IL-1alpha, 1IL-8, PDGF-B, BMP-2, BMP-4, IGF-I, TGF-beta2, FGF-2, and VEGF. |
| 492 | 11446768 | Antibodies to IGF-I, BMP-2, VEGF and TGF-beta2 were used for immunohistochemistry. |
| 493 | 11446768 | IGF-I and BMP-4 RNA levels were increased in PBK/ABK. |
| 494 | 11446768 | In contrast, PBK/ABK corneas had specific significant elevations of BMP-4 and IGF-I. |
| 495 | 11457715 | Regulation of ANP clearance receptors by EGF in mesangial cells from NOD mice. |
| 496 | 11457715 | Mesangial cells from nonobese diabetic (NOD) mice (D-NOD) that develop diabetes at 2-4 mo express an increased density of atrial natriuretic peptide (ANP) clearance receptors [natriuretic peptide C receptor (NPR-C)] and produce less GMP in response to ANP than their nondiabetic counterparts (ND-NOD). |
| 497 | 11457715 | Epidermal growth factor (EGF) and heparin-binding (HB)-EGF, but not platelet-derived growth factor or insulin-like growth factor I, inhibited (125)I-ANP binding to ND-NOD and D-NOD mesangial cells, particularly in the latter. |
| 498 | 11457715 | The EGF effect depended on activation of its receptor tyrosine kinase but not on that of protein kinase C, mitogen-activated protein kinases, or phosphoinositide-3 kinase. |
| 499 | 11457715 | The cGMP response to physiological concentrations of ANP was greater in EGF-treated D-NOD cells. |
| 500 | 11457715 | These studies suggest that EGF potentiates the ANP glomerular effects in diabetes by inhibition of its degradation by mesangial NPR-C via a mechanism involving AP-1. |
| 501 | 11472620 | While platelet-derived growth factor had no effect on keratinocyte proliferation, angiotensin II and angiotensin (1-7) significantly increased keratinocyte proliferation. |
| 502 | 11472733 | Glucosamine enhances platelet-derived growth factor-induced DNA synthesis via phosphatidylinositol 3-kinase pathway in rat aortic smooth muscle cells. |
| 503 | 11472733 | Culture of vascular smooth muscle A10 cells with high glucose for 4 weeks enhanced platelet-derived growth factor (PDGF)-induced BrdU incorporation. |
| 504 | 11472733 | Of the subsequent intracellular signaling pathways, PDGF-induced PDGF beta-receptor association with PLC gamma was not affected, whereas tyrosine phosphorylation of Shc, subsequent association of Shc with Grb2, and MAP kinase activation were relatively decreased. |
| 505 | 11472733 | In contrast, PDGF-induced PDGF beta-receptor association with the p85 regulatory subunit of PI3-kinase and PI3-kinase activation were increased by 20% (P<0.01) and 36% (P<0.01), respectively. |
| 506 | 11472733 | Pretreatment with PLC inhibitor (U73122) had negligible effects, and MEK1 inhibitor (PD98059) showed only a slight inhibitory effect on the PDGF-induced BrdU incorporation. |
| 507 | 11472733 | In contrast, pretreatment with PI3-kinase inhibitor (LY294002) significantly inhibited glucosamine enhancement of PDGF-induced BrdU incorporation. |
| 508 | 11472733 | These findings suggest that glucosamine is involved in the development of atherosclerosis by enhancing PDGF-induced mitogenesis specifically via the PI3-kinase pathway. |
| 509 | 11472733 | Glucosamine enhances platelet-derived growth factor-induced DNA synthesis via phosphatidylinositol 3-kinase pathway in rat aortic smooth muscle cells. |
| 510 | 11472733 | Culture of vascular smooth muscle A10 cells with high glucose for 4 weeks enhanced platelet-derived growth factor (PDGF)-induced BrdU incorporation. |
| 511 | 11472733 | Of the subsequent intracellular signaling pathways, PDGF-induced PDGF beta-receptor association with PLC gamma was not affected, whereas tyrosine phosphorylation of Shc, subsequent association of Shc with Grb2, and MAP kinase activation were relatively decreased. |
| 512 | 11472733 | In contrast, PDGF-induced PDGF beta-receptor association with the p85 regulatory subunit of PI3-kinase and PI3-kinase activation were increased by 20% (P<0.01) and 36% (P<0.01), respectively. |
| 513 | 11472733 | Pretreatment with PLC inhibitor (U73122) had negligible effects, and MEK1 inhibitor (PD98059) showed only a slight inhibitory effect on the PDGF-induced BrdU incorporation. |
| 514 | 11472733 | In contrast, pretreatment with PI3-kinase inhibitor (LY294002) significantly inhibited glucosamine enhancement of PDGF-induced BrdU incorporation. |
| 515 | 11472733 | These findings suggest that glucosamine is involved in the development of atherosclerosis by enhancing PDGF-induced mitogenesis specifically via the PI3-kinase pathway. |
| 516 | 11473053 | Growth hormone induces cellular insulin resistance by uncoupling phosphatidylinositol 3-kinase and its downstream signals in 3T3-L1 adipocytes. |
| 517 | 11473053 | In this study, we demonstrated that chronic GH treatment of differentiated 3T3-L1 adipocytes reduces insulin-stimulated 2-deoxyglucose (DOG) uptake and activation of Akt (also known as protein kinase B), both of which are downstream effects of phosphatidylinositol (PI) 3-kinase, despite enhanced tyrosine phosphorylation of insulin receptor substrate (IRS)-1, association of IRS-1 with the p85 subunit of PI 3-kinase, and IRS-1-associated PI 3-kinase activity. |
| 518 | 11473053 | In contrast, chronic GH treatment did not affect 2-DOG uptake and Akt activation induced by overexpression of a membrane-targeted form of the p110 subunit of PI 3-kinase (p110(CAAX)) or Akt activation stimulated by platelet-derived growth factor. |
| 519 | 11473053 | Fractionation studies indicated that chronic GH treatment reduces insulin-stimulated translocation of Akt from the cytosol to the plasma membrane. |
| 520 | 11473053 | Interestingly, chronic GH treatment increased insulin-stimulated association of IRS-1 with p85 and IRS-1-associated PI 3-kinase activity preferentially in the cytosol. |
| 521 | 11480453 | GLDL-LOX induced SMC proliferation and migration, and increased the number of platelet-derived growth factor receptor, beta subunits, (PDGF-R) positive SMC. |
| 522 | 11485910 | In parallel with accelerated wound closure at later times, blockade of RAGE suppressed levels of cytokines; tumor necrosis factor-alpha; interleukin-6; and matrix metalloproteinases-2, -3, and -9. |
| 523 | 11485910 | In addition, generation of thick, well-vascularized granulation tissue was enhanced, in parallel with increased levels of platelet-derived growth factor-B and vascular endothelial growth factor. |
| 524 | 11526109 | The localization of insulin receptor substrate (IRS) molecules may be responsible for the differential biological activities of insulin and other peptides such as platelet-derived growth factor. |
| 525 | 11526109 | In response to insulin, recombinant IRS-1 translocated to the plasma membrane. |
| 526 | 11526109 | Mutations of phosphoinositide-binding sites in both the pleckstrin homology and phosphotyrosine-binding domains significantly reduced the ability of Myc-tagged IRS-1 to translocate to the plasma membrane following insulin stimulation. |
| 527 | 11560924 | Exposure to proliferative stimuli such as hypoxia or platelet-derived growth factor decreased SMC CREB content. |
| 528 | 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. |
| 529 | 11562408 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and PDGF-B mRNA in renal tubules. |
| 530 | 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). |
| 531 | 11562408 | TGF-beta1 and PDGF mRNA within glomeruli were also similarly increased with diabetes and attenuated with aminoguanidine. |
| 532 | 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. |
| 533 | 11562408 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and PDGF-B mRNA in renal tubules. |
| 534 | 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). |
| 535 | 11562408 | TGF-beta1 and PDGF mRNA within glomeruli were also similarly increased with diabetes and attenuated with aminoguanidine. |
| 536 | 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. |
| 537 | 11562408 | In situ hybridization demonstrated a diffuse increase in both TGF-beta1 and PDGF-B mRNA in renal tubules. |
| 538 | 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). |
| 539 | 11562408 | TGF-beta1 and PDGF mRNA within glomeruli were also similarly increased with diabetes and attenuated with aminoguanidine. |
| 540 | 11598137 | Peroxisome proliferator-activated receptor gamma ligands inhibit mitogenic induction of p21(Cip1) by modulating the protein kinase Cdelta pathway in vascular smooth muscle cells. |
| 541 | 11598137 | PPARgamma ligands troglitazone (TRO, 10 microm) and rosiglitazone (RSG, 10 microm) attenuated the induction of p21(Cip1) protein by platelet-derived growth factor (PDGF) and insulin without affecting cognate mRNA levels in rat aortic smooth muscle cells (RASMC). |
| 542 | 11598137 | Kinetic studies using the protein synthesis inhibitor cycloheximide showed that TRO, RSG, and rottlerin shortened the half-life of p21(Cip1) protein. |
| 543 | 11598137 | TRO, RSG, and rottlerin inhibited PDGF-induced expression of p21(Cip1), but they did not affect insulin-induced expression of p21(Cip1). |
| 544 | 11598137 | Both ligands inhibited PKCdelta enzymatic activity in PDGF-stimulated RASMC but not in insulin-stimulated cells. |
| 545 | 11598137 | Adenovirus-mediated overexpression of PKCdelta rescued the down-regulation of p21(Cip1) expression both by TRO and RSG in PDGF-treated RASMC. |
| 546 | 11598137 | These data suggested that the PKCdelta pathway plays a critical role in PDGF-induced expression of p21(Cip1) in RASMC and may be the potential target for PPARgamma ligand effects. |
| 547 | 11598137 | Tyrosine phosphorylation and activation of c-Src in response to PDGF were unaffected by either PPARgamma ligand. |
| 548 | 11598137 | Both inhibitors also reversed PPARgamma ligand effects on p21(Cip1) expression in PDGF-treated RASMC. |
| 549 | 11598137 | PPARgamma ligands regulate p21(Cip1) at a post-translational level by blocking PKCdelta signaling and accelerating p21(Cip1) turnover. |
| 550 | 11785657 | Protein kinase C inhibits insulin-induced Akt activation in vascular smooth muscle cells. |
| 551 | 11785657 | We hypothesized that the negative regulation of Akt in the vasculature by PKC could contribute to insulin resistant states and, may therefore play a role in the pathogenesis of cardiovascular disease. |
| 552 | 11785657 | In this study, we specifically looked at the ability of PKC to inhibit Akt activation induced by insulin in cultured rat aortic vascular smooth muscle cells (VSMCs). |
| 553 | 11785657 | A PKC activator, phorbol 12-myristate 13-acetate (PMA), inhibited insulin-dependent Akt phosphorylation. |
| 554 | 11785657 | However, PMA did not inhibit platelet-derived growth factor (PDGF)-induced activation of Akt. |
| 555 | 11785657 | In addition, we demonstrated that PMA inhibited the insulin-induced tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1). |
| 556 | 11823933 | Topical platelet-derived growth factor (PDGF)-BB has proven effective in improving healing in impaired wounds but has the disadvantage of requiring large and repeated doses. |
| 557 | 11838000 | The ensuing inflammatory response is modulated by cytokines and growth factors, among them platelet-derived growth factor (PDGF), and monocyte chemoattractant protein-1 (MCP-1). |
| 558 | 11838000 | In two independent studies, we demonstrated that mRNA levels for PDGF-A and -B and for MCP-1 are reduced after ingestion of n-3 fatty acids by human volunteers. |
| 559 | 11838000 | Together, our investigations lend support to the importance of PDGF-A, PDGF-B, and MCP-1 in the pathogenesis of atherosclerosis, and the beneficial role of n-3 fatty acids therein. |
| 560 | 11838000 | The ensuing inflammatory response is modulated by cytokines and growth factors, among them platelet-derived growth factor (PDGF), and monocyte chemoattractant protein-1 (MCP-1). |
| 561 | 11838000 | In two independent studies, we demonstrated that mRNA levels for PDGF-A and -B and for MCP-1 are reduced after ingestion of n-3 fatty acids by human volunteers. |
| 562 | 11838000 | Together, our investigations lend support to the importance of PDGF-A, PDGF-B, and MCP-1 in the pathogenesis of atherosclerosis, and the beneficial role of n-3 fatty acids therein. |
| 563 | 11849120 | The healing of wounds is a complex procedure involving multiple growth factors, some of which have multiple effects on different cell types, in particular, platelet derived growth factor (PDGF) is a prominent agent, active in all stages of the healing process. |
| 564 | 11849120 | Becaplermin (0.01% Regranex gel) is a homodimeric protein produced by recombinant DNA technology through the insertion of the gene for the B chain PDGF into the yeast Saccharomyces cerevisiae. |
| 565 | 11849120 | The healing of wounds is a complex procedure involving multiple growth factors, some of which have multiple effects on different cell types, in particular, platelet derived growth factor (PDGF) is a prominent agent, active in all stages of the healing process. |
| 566 | 11849120 | Becaplermin (0.01% Regranex gel) is a homodimeric protein produced by recombinant DNA technology through the insertion of the gene for the B chain PDGF into the yeast Saccharomyces cerevisiae. |
| 567 | 11861803 | Close relationship between the platelet activation marker CD62 and the granular release of platelet-derived growth factor. |
| 568 | 11861803 | We characterized the relationship between CD62 expression and platelet-derived growth factor (PDGF)(AB) and PDGF(BB) secretion in response to thrombin-receptor activating peptide (TRAP). |
| 569 | 11861803 | The principal findings were 1) expression of CD62 as a constituent of platelet alpha-granule membrane and secretion of PDGF, an important ingredient of alpha-granules, can be stimulated by TRAP-induced activation in a dose-dependent fashion; 2) the activation marker and secretion product are closely correlated with each other; and 3) changes in the CD62 expression induced by a drug, namely clopidogrel, or by a disease, namely diabetes, are paralleled by changes in PDGF secretion. |
| 570 | 11861803 | Although CD62 is perceived as an activation marker of platelets indicating enhanced aggregability and secretion of alpha-granular content, the proof that the CD62 status and its modifications reflect directly the actual secretion of the most important platelet mitogen, PDGF, has so far not been given. |
| 571 | 11861803 | This ex vivo-in vitro study shows that at least for the activation pathway provided by the PAR-1 receptor for which TRAP is the selective agonist, CD62 expression on platelets could be a surrogate for their secretory activity. |
| 572 | 11861803 | Close relationship between the platelet activation marker CD62 and the granular release of platelet-derived growth factor. |
| 573 | 11861803 | We characterized the relationship between CD62 expression and platelet-derived growth factor (PDGF)(AB) and PDGF(BB) secretion in response to thrombin-receptor activating peptide (TRAP). |
| 574 | 11861803 | The principal findings were 1) expression of CD62 as a constituent of platelet alpha-granule membrane and secretion of PDGF, an important ingredient of alpha-granules, can be stimulated by TRAP-induced activation in a dose-dependent fashion; 2) the activation marker and secretion product are closely correlated with each other; and 3) changes in the CD62 expression induced by a drug, namely clopidogrel, or by a disease, namely diabetes, are paralleled by changes in PDGF secretion. |
| 575 | 11861803 | Although CD62 is perceived as an activation marker of platelets indicating enhanced aggregability and secretion of alpha-granular content, the proof that the CD62 status and its modifications reflect directly the actual secretion of the most important platelet mitogen, PDGF, has so far not been given. |
| 576 | 11861803 | This ex vivo-in vitro study shows that at least for the activation pathway provided by the PAR-1 receptor for which TRAP is the selective agonist, CD62 expression on platelets could be a surrogate for their secretory activity. |
| 577 | 11872370 | We have previously reported that high glucose stimulates osteopontin (OPN) expression through protein kinase C-dependent pathway, as well as the hexosamine pathway, in cultured rat aortic smooth muscle cells (SMC). |
| 578 | 11872370 | We also found that OPN stimulated migration and enhanced platelet-derived growth factor (PDGF)-mediated DNA synthesis of cultured rat aortic SMC. |
| 579 | 11872370 | OPN and PDGF synergistically activated focal adhesion kinase (FAK), as well as extracellular signal-regulated kinase (ERK), which seems to be a reason for OPN-induced enhancement of PDGF-mediated DNA synthesis. |
| 580 | 11936867 | Incubation of IRPTC with BSA-AGE-degradation products increased the expression of endothelin-1 (ET-1) mRNA to 210% after 1 hr; the expression of platelet-derived growth factor-B (PDGF-B) mRNA reached 184% after 2 hr. |
| 581 | 11991199 | Potentiation of mitogenic activity of platelet-derived growth factor by physiological concentrations of insulin via the MAP kinase cascade in rat A10 vascular smooth muscle cells. |
| 582 | 11991199 | In this study, we attempted to determine whether insulin affects mitogenic signaling induced by platelet-derived growth factor (PDGF) in a rat VSMC cell line (A10 cells). |
| 583 | 11991199 | Initiation of DNA synthesis was preceded by activation of Raf-1, MEK and MAP kinases (Erk 1 and Erk2). |
| 584 | 11991199 | Treatment of the cells with PD98059, an inhibitor of MAPK kinase (MEK) attenuated but did not abolish PDGF-stimulated DNA synthesis, suggesting that MAPK is required but not essential for DNA synthesis. |
| 585 | 11991199 | PDGF also stimulated phosphorylation of protein kinase B (Akt/PKB) and p70 S6Kinase (p70S6K) in a wortmannin-sensitive manner. |
| 586 | 11991199 | Low concentrations of insulin (1-10 nmol/l) alone showed little mitogenic activity and no significant effect on MAPK activity. |
| 587 | 11991199 | However, the presence of insulin enhanced both DNA synthesis and MAPK activation by PDGF. |
| 588 | 11991199 | Insulin was without effect on PDGF-stimulated activations of protein kinase B (Akt/PKB) and p70S6K. |
| 589 | 11991199 | We conclude that insulin, at pathophysiologically relevant concentrations, potentiates the PDGF-stimulated DNA synthesis, at least in part, by potentiating activation of the MAPK cascade. |
| 590 | 11991199 | Potentiation of mitogenic activity of platelet-derived growth factor by physiological concentrations of insulin via the MAP kinase cascade in rat A10 vascular smooth muscle cells. |
| 591 | 11991199 | In this study, we attempted to determine whether insulin affects mitogenic signaling induced by platelet-derived growth factor (PDGF) in a rat VSMC cell line (A10 cells). |
| 592 | 11991199 | Initiation of DNA synthesis was preceded by activation of Raf-1, MEK and MAP kinases (Erk 1 and Erk2). |
| 593 | 11991199 | Treatment of the cells with PD98059, an inhibitor of MAPK kinase (MEK) attenuated but did not abolish PDGF-stimulated DNA synthesis, suggesting that MAPK is required but not essential for DNA synthesis. |
| 594 | 11991199 | PDGF also stimulated phosphorylation of protein kinase B (Akt/PKB) and p70 S6Kinase (p70S6K) in a wortmannin-sensitive manner. |
| 595 | 11991199 | Low concentrations of insulin (1-10 nmol/l) alone showed little mitogenic activity and no significant effect on MAPK activity. |
| 596 | 11991199 | However, the presence of insulin enhanced both DNA synthesis and MAPK activation by PDGF. |
| 597 | 11991199 | Insulin was without effect on PDGF-stimulated activations of protein kinase B (Akt/PKB) and p70S6K. |
| 598 | 11991199 | We conclude that insulin, at pathophysiologically relevant concentrations, potentiates the PDGF-stimulated DNA synthesis, at least in part, by potentiating activation of the MAPK cascade. |
| 599 | 11998867 | Fibroblasts derived from chronic diabetic ulcers differ in their response to stimulation with EGF, IGF-I, bFGF and PDGF-AB compared to controls. |
| 600 | 11998867 | Healing can be accelerated by application of growth factors like platelet-derived growth factor (PDGF). |
| 601 | 11998867 | We investigated the mitogenic responses, measured by 3[H]thymidine incorporation, of fibroblasts cultured from diabetic ulcers, non-diabetic ulcers, and non-lesional diabetic and age-matched controls, to recombinant human PDGF-AB, epidermal growth factor (EGF), basic fibroblast growth factor (bFGF) and insulin-like growth factor (IGF-I). |
| 602 | 11998867 | Also the addition of bFGF, PDGF-AB and EGF prior to IGF-I induced a higher 3[H]thymidine uptake in all fibroblasts compared to the combination of each in reverse order. |
| 603 | 12028051 | Platelet-derived growth factor promotes ex vivo expansion of CD34+ cells from human cord blood and enhances long-term culture-initiating cells, non-obese diabetic/severe combined immunodeficient repopulating cells and formation of adherent cells. |
| 604 | 12028051 | Platelet-derived growth factor (PDGF) is a major mitogen for connective tissue cells. |
| 605 | 12028051 | In this study, we investigated the effects and mechanism of PDGF on the ex vivo expansion of cord blood CD34+ cells. |
| 606 | 12028051 | Our data demonstrated that among various cytokine combinations of thrombopoietin (TPO), interleukin 1 beta (IL-1beta), IL-3, IL-6 and Flt-3 ligand (Flt-3L), TPO + IL-6 + Flt-3L was most efficient in promoting the expansion of CD34+ cells, CD34+CD38- cells, mixed-lineage colony-forming units (CFU-GEMM) and long-term culture-initiating cells (LTC-IC) by 21.7 +/- 5.00-, 103 +/- 27.9-, 10.7 +/- 7.94- and 6.52 +/- 1.51-fold, respectively, after 12-14 d of culture. |
| 607 | 12028051 | More significantly, PDGF enhanced the engraftment of human CD45+ cells and their myeloid subsets (CD33+, CD14+ cells) in non-obese diabetic (NOD)/severe-combined immunodeficient (SCID) mice. |
| 608 | 12028051 | The expression of PDGF receptor (PDGFR)-beta was not detectable in fresh CD34+ cells but was upregulated after culture for 3 d. |
| 609 | 12028051 | PDGF also enhanced the development of adherent cells/clusters that expressed the endothelial markers VE-cadherin and CD31. |
| 610 | 12028051 | The mechanism could be mediated by PDGFR-beta on committed CD34+ progenitor cells and/or secondary to the stimulation of autologous, stromal feeder cells. |
| 611 | 12028051 | Platelet-derived growth factor promotes ex vivo expansion of CD34+ cells from human cord blood and enhances long-term culture-initiating cells, non-obese diabetic/severe combined immunodeficient repopulating cells and formation of adherent cells. |
| 612 | 12028051 | Platelet-derived growth factor (PDGF) is a major mitogen for connective tissue cells. |
| 613 | 12028051 | In this study, we investigated the effects and mechanism of PDGF on the ex vivo expansion of cord blood CD34+ cells. |
| 614 | 12028051 | Our data demonstrated that among various cytokine combinations of thrombopoietin (TPO), interleukin 1 beta (IL-1beta), IL-3, IL-6 and Flt-3 ligand (Flt-3L), TPO + IL-6 + Flt-3L was most efficient in promoting the expansion of CD34+ cells, CD34+CD38- cells, mixed-lineage colony-forming units (CFU-GEMM) and long-term culture-initiating cells (LTC-IC) by 21.7 +/- 5.00-, 103 +/- 27.9-, 10.7 +/- 7.94- and 6.52 +/- 1.51-fold, respectively, after 12-14 d of culture. |
| 615 | 12028051 | More significantly, PDGF enhanced the engraftment of human CD45+ cells and their myeloid subsets (CD33+, CD14+ cells) in non-obese diabetic (NOD)/severe-combined immunodeficient (SCID) mice. |
| 616 | 12028051 | The expression of PDGF receptor (PDGFR)-beta was not detectable in fresh CD34+ cells but was upregulated after culture for 3 d. |
| 617 | 12028051 | PDGF also enhanced the development of adherent cells/clusters that expressed the endothelial markers VE-cadherin and CD31. |
| 618 | 12028051 | The mechanism could be mediated by PDGFR-beta on committed CD34+ progenitor cells and/or secondary to the stimulation of autologous, stromal feeder cells. |
| 619 | 12037011 | Retina-specific expression of PDGF-B versus PDGF-A: vascular versus nonvascular proliferative retinopathy. |
| 620 | 12130557 | Content and activity of cAMP response element-binding protein regulate platelet-derived growth factor receptor-alpha content in vascular smooth muscles. |
| 621 | 12130557 | Experiments in vascular smooth muscle cells (SMCs) indicate that the transcription factor cAMP response element-binding protein (CREB), the cyclic nucleotide response element-binding protein, suppresses expression of the platelet-derived growth factor-alpha receptor gene (PDGFRalpha). |
| 622 | 12130557 | Adenovirus-mediated expression of constitutively active CREB mutants decreases PDGFRalpha mRNA, PDGFRalpha protein, and PDGFRalpha promoter-luciferase reporter activity in cultured SMCs. |
| 623 | 12130557 | Expression of dominant negative CREB protein, A-CREB, increases PDGFRalpha protein content and the PDGFRalpha-promoter activity in SMCs. |
| 624 | 12130557 | Active CREB prevents activation of PDGFRalpha promoter-luciferase reporter activity by CCAAT/enhancer-binding protein-delta (C/EBPdelta), shown to mediate IL-1beta stimulation of PDGFRalpha expression. |
| 625 | 12130557 | Exposure of cultured SMCs to high glucose or reactive oxidant stress, which decrease CREB protein content and activity, increases PDGFRalpha protein content and promoter activity. |
| 626 | 12130557 | Expression of active CREB blunts reactive oxidant stress-induced PDGFRalpha accumulation in SMCs. |
| 627 | 12130557 | Loss of CREB protein in aortic walls of rats with streptozotocin-induced diabetes is accompanied by an increase in PDGFRalpha content. |
| 628 | 12130557 | Ob/- controls), treatment with the peroxisomal proliferator-activated receptor gamma rosiglitazone increases CREB content and decreases PDGFRalpha content in the aortic wall. |
| 629 | 12130557 | Thus, both in vitro and in vivo loss of CREB content and activity and subsequent accumulation of PDGFRalpha may contribute to SMC activation during diabetes. |
| 630 | 12130557 | Content and activity of cAMP response element-binding protein regulate platelet-derived growth factor receptor-alpha content in vascular smooth muscles. |
| 631 | 12130557 | Experiments in vascular smooth muscle cells (SMCs) indicate that the transcription factor cAMP response element-binding protein (CREB), the cyclic nucleotide response element-binding protein, suppresses expression of the platelet-derived growth factor-alpha receptor gene (PDGFRalpha). |
| 632 | 12130557 | Adenovirus-mediated expression of constitutively active CREB mutants decreases PDGFRalpha mRNA, PDGFRalpha protein, and PDGFRalpha promoter-luciferase reporter activity in cultured SMCs. |
| 633 | 12130557 | Expression of dominant negative CREB protein, A-CREB, increases PDGFRalpha protein content and the PDGFRalpha-promoter activity in SMCs. |
| 634 | 12130557 | Active CREB prevents activation of PDGFRalpha promoter-luciferase reporter activity by CCAAT/enhancer-binding protein-delta (C/EBPdelta), shown to mediate IL-1beta stimulation of PDGFRalpha expression. |
| 635 | 12130557 | Exposure of cultured SMCs to high glucose or reactive oxidant stress, which decrease CREB protein content and activity, increases PDGFRalpha protein content and promoter activity. |
| 636 | 12130557 | Expression of active CREB blunts reactive oxidant stress-induced PDGFRalpha accumulation in SMCs. |
| 637 | 12130557 | Loss of CREB protein in aortic walls of rats with streptozotocin-induced diabetes is accompanied by an increase in PDGFRalpha content. |
| 638 | 12130557 | Ob/- controls), treatment with the peroxisomal proliferator-activated receptor gamma rosiglitazone increases CREB content and decreases PDGFRalpha content in the aortic wall. |
| 639 | 12130557 | Thus, both in vitro and in vivo loss of CREB content and activity and subsequent accumulation of PDGFRalpha may contribute to SMC activation during diabetes. |
| 640 | 12138086 | Epidermal growth factor and transforming growth factor alpha mimic the effects of insulin in human fat cells and augment downstream signaling in insulin resistance. |
| 641 | 12138086 | The ability of the growth factors epidermal growth factor (EGF), transforming growth factor alpha, and platelet-derived growth factor to exert insulin-like effects on glucose transport and lipolysis were examined in human and rat fat cells. |
| 642 | 12138086 | No effects were found in rat fat cells, whereas EGF (EC(50) for glucose transport approximately 0.02 nm) and transforming growth factor alpha (EC(50) approximately 0.2 nm), but not platelet-derived growth factor, mimicked the effects of insulin (EC(50) approximately 0.2 nm) on both pathways. |
| 643 | 12138086 | EGF increased the tyrosine phosphorylation of several proteins (the EGF receptor, insulin receptor substrate (IRS)-1, IRS-2, and Grb2-associated binder 1), whereas Shc and Gab2 were only weakly and inconsistently phosphorylated. p85, the regulatory subunit of phosphatidylinositol 3-kinase (PI 3-kinase), was also found to associate with all of these docking molecules, showing that EGF activated PI 3-kinase pools that were additional to those of insulin. |
| 644 | 12138086 | EGF and/or insulin increased protein kinase B/Akt serine phosphorylation to a similar extent, whereas mitogen-activated protein kinase phosphorylation was more pronounced for EGF than for insulin. |
| 645 | 12138086 | The impaired insulin-stimulated downstream signaling, measured as protein kinase B/Akt serine phosphorylation, in insulin-resistant cells (Type 2 diabetes) was improved by the addition of EGF. |
| 646 | 12138086 | EGF mimics the effects of insulin on both the metabolic and mitogenic pathways but utilize in part different signaling pathways. |
| 647 | 12138086 | Both insulin and EGF increase the tyrosine phosphorylation and activation of IRS-1 and IRS-2, whereas EGF is also capable of activating additional PI 3-kinase pools and, thus, can augment the downstream signaling of insulin in insulin-resistant states like Type 2 diabetes. |
| 648 | 12138086 | Epidermal growth factor and transforming growth factor alpha mimic the effects of insulin in human fat cells and augment downstream signaling in insulin resistance. |
| 649 | 12138086 | The ability of the growth factors epidermal growth factor (EGF), transforming growth factor alpha, and platelet-derived growth factor to exert insulin-like effects on glucose transport and lipolysis were examined in human and rat fat cells. |
| 650 | 12138086 | No effects were found in rat fat cells, whereas EGF (EC(50) for glucose transport approximately 0.02 nm) and transforming growth factor alpha (EC(50) approximately 0.2 nm), but not platelet-derived growth factor, mimicked the effects of insulin (EC(50) approximately 0.2 nm) on both pathways. |
| 651 | 12138086 | EGF increased the tyrosine phosphorylation of several proteins (the EGF receptor, insulin receptor substrate (IRS)-1, IRS-2, and Grb2-associated binder 1), whereas Shc and Gab2 were only weakly and inconsistently phosphorylated. p85, the regulatory subunit of phosphatidylinositol 3-kinase (PI 3-kinase), was also found to associate with all of these docking molecules, showing that EGF activated PI 3-kinase pools that were additional to those of insulin. |
| 652 | 12138086 | EGF and/or insulin increased protein kinase B/Akt serine phosphorylation to a similar extent, whereas mitogen-activated protein kinase phosphorylation was more pronounced for EGF than for insulin. |
| 653 | 12138086 | The impaired insulin-stimulated downstream signaling, measured as protein kinase B/Akt serine phosphorylation, in insulin-resistant cells (Type 2 diabetes) was improved by the addition of EGF. |
| 654 | 12138086 | EGF mimics the effects of insulin on both the metabolic and mitogenic pathways but utilize in part different signaling pathways. |
| 655 | 12138086 | Both insulin and EGF increase the tyrosine phosphorylation and activation of IRS-1 and IRS-2, whereas EGF is also capable of activating additional PI 3-kinase pools and, thus, can augment the downstream signaling of insulin in insulin-resistant states like Type 2 diabetes. |
| 656 | 12176727 | Insulin inhibits PDGF-directed VSMC migration via NO/ cGMP increase of MKP-1 and its inactivation of MAPKs. |
| 657 | 12176727 | Platelet-derived growth factor (PDGF) increased VSMC migration, which was inhibited by pretreatment with insulin in a dose-dependent manner. |
| 658 | 12176727 | Insulin also caused a 60% decrease in PDGF-stimulated mitogen-activated protein kinase (MAPK) phosphorylation and activation. |
| 659 | 12176727 | Insulin inhibition of MAPK was accompanied by a rapid induction of MAPK phosphatase (MKP-1), which inactivates MAPKs by dephosphorylation. |
| 660 | 12176727 | Pretreatment with inhibitors of the nitric oxide (NO)/cGMP pathway, blocked insulin-induced MKP-1 expression and restored PDGF-stimulated MAPK activation and migration. |
| 661 | 12176727 | In contrast, adenoviral infection of VSMCs with MKP-1 or cGMP-dependent protein kinase Ialpha (cGK Ialpha), the downstream effector of cGMP signaling, blocked the activation of MAPK and prevented PDGF-directed VSMC migration. |
| 662 | 12176727 | Expression of antisense MKP-1 RNA prevented insulin's inhibitory effect and restored PDGF-directed VSMC migration and MAPK phosphorylation. |
| 663 | 12176727 | We conclude that insulin inhibition of VSMC migration may be mediated in part by NO/cGMP/cGK Ialpha induction of MKP-1 and consequent inactivation of MAPKs. |
| 664 | 12196513 | High glucose stimulates synthesis of fibronectin via a novel protein kinase C, Rap1b, and B-Raf signaling pathway. |
| 665 | 12196513 | This investigation describes the effect of high glucose (HG) on a small GTP-binding protein, Rap1b, expression and activation, and the relevance of protein kinase C (PKC) and Raf pathways in fibronectin synthesis in cultured renal glomerular mesangial cells (MCs). |
| 666 | 12196513 | B-Raf and Raf-1 expression was investigated to assess whether Rap1b effects are mediated via the Raf pathway. |
| 667 | 12196513 | B-Raf, and not Raf-1, expression was increased in MCs transfected with Rap1b. |
| 668 | 12196513 | HG also caused activation of Rap1b, which was largely unaffected by anti-platelet-derived growth factor (PDGF) antibodies. |
| 669 | 12196513 | HG-induced activation of Rap1b was specific, since Rap2b activation and expression of Rap2a and Rap2b were unaffected by HG. |
| 670 | 12196513 | This effect appears to be PKC-dependent and PDGF-independent, but involves B-Raf, suggesting a novel PKC-Rap1b-B-Raf pathway responsible for HG-induced increased mesangial matrix synthesis, a hallmark of diabetic nephropathy. |
| 671 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 672 | 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). |
| 673 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 674 | 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. |
| 675 | 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. |
| 676 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 677 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 678 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 679 | 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. |
| 680 | 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. |
| 681 | 12213733 | Independent regulation of transforming growth factor-beta1 transcription and translation by glucose and platelet-derived growth factor. |
| 682 | 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). |
| 683 | 12213733 | The aim of the current study was to characterize the mechanism by which glucose and PDGF synergistically stimulate the generation of TGF-beta1. |
| 684 | 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. |
| 685 | 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. |
| 686 | 12213733 | PDGF at low dose did not influence TGF-beta1 transcription, but led to alteration in TGF-beta1 mRNA stability and translation. |
| 687 | 12213733 | Without a previous glucose-induced increase in the amount of TGF-beta1 transcript, PDGF did not stimulate significant TGF-beta1 protein synthesis. |
| 688 | 12213733 | At a high dose (100 ng/ml) PDGF stimulated TGF-beta1 synthesis independent of glucose concentration. |
| 689 | 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. |
| 690 | 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. |
| 691 | 12232532 | The place of topical growth factor like PDGF (platelet derived growth factor) and of living skin equivalents (dermagraft, apligraf) is not defined in ischaemic diabetic ulcers. |
| 692 | 12351455 | Platelet-derived growth factor (PDGF)-B is involved in pericyte recruitment, and brain capillaries of mice with a genetic ablation of PDGF-B show pericyte loss and microaneurysms. |
| 693 | 12512939 | Cultured explants from diabetic rats displayed a delay in the time-course of [3H]-thymidine incorporation as well as enhanced sensitivity to endothelin-1 (ET-1) or insulin. iSC cultured in high (25 mM) glucose-containing media also exhibited higher [3H]-thymidine incorporation, along with an enhanced activation of p38 mitogen-activated protein kinase and phospholipase C in response to ET-1 or platelet-derived growth factor as compared to controls (5.5 mM glucose). |
| 694 | 12540630 | Glucose-induced phosphatidylinositol 3-kinase and mitogen-activated protein kinase-dependent upregulation of the platelet-derived growth factor-beta receptor potentiates vascular smooth muscle cell chemotaxis. |
| 695 | 12540630 | The aim of this study was to investigate the effects of elevated D-glucose concentrations on vascular smooth muscle cell (VSMC) expression of the platelet-derived growth factor (PDGF)beta receptor and VSMC migratory behavior. |
| 696 | 12540630 | Immunoprecipitation, immunofluorescent staining, and RT-PCR of human VSMCs showed that elevated D-glucose induced an increase in the PDGFbeta receptor that was inhibited by phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathway inhibitors. |
| 697 | 12540630 | Exposure to 25 mmol/l D-glucose (HG) induced increased phosphorylation of protein kinase B (PKB) and extracellular-regulated kinase (ERK). |
| 698 | 12540630 | An anti-PDGFbeta receptor antibody inhibited glucose-potentiated VSMC chemotaxis, as did the inhibitors for the PI3K and MAPK pathways. |
| 699 | 12540630 | Glucose-induced phosphatidylinositol 3-kinase and mitogen-activated protein kinase-dependent upregulation of the platelet-derived growth factor-beta receptor potentiates vascular smooth muscle cell chemotaxis. |
| 700 | 12540630 | The aim of this study was to investigate the effects of elevated D-glucose concentrations on vascular smooth muscle cell (VSMC) expression of the platelet-derived growth factor (PDGF)beta receptor and VSMC migratory behavior. |
| 701 | 12540630 | Immunoprecipitation, immunofluorescent staining, and RT-PCR of human VSMCs showed that elevated D-glucose induced an increase in the PDGFbeta receptor that was inhibited by phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathway inhibitors. |
| 702 | 12540630 | Exposure to 25 mmol/l D-glucose (HG) induced increased phosphorylation of protein kinase B (PKB) and extracellular-regulated kinase (ERK). |
| 703 | 12540630 | An anti-PDGFbeta receptor antibody inhibited glucose-potentiated VSMC chemotaxis, as did the inhibitors for the PI3K and MAPK pathways. |
| 704 | 12540630 | Glucose-induced phosphatidylinositol 3-kinase and mitogen-activated protein kinase-dependent upregulation of the platelet-derived growth factor-beta receptor potentiates vascular smooth muscle cell chemotaxis. |
| 705 | 12540630 | The aim of this study was to investigate the effects of elevated D-glucose concentrations on vascular smooth muscle cell (VSMC) expression of the platelet-derived growth factor (PDGF)beta receptor and VSMC migratory behavior. |
| 706 | 12540630 | Immunoprecipitation, immunofluorescent staining, and RT-PCR of human VSMCs showed that elevated D-glucose induced an increase in the PDGFbeta receptor that was inhibited by phosphatidylinositol 3-kinase (PI3K) and mitogen-activated protein kinase (MAPK) pathway inhibitors. |
| 707 | 12540630 | Exposure to 25 mmol/l D-glucose (HG) induced increased phosphorylation of protein kinase B (PKB) and extracellular-regulated kinase (ERK). |
| 708 | 12540630 | An anti-PDGFbeta receptor antibody inhibited glucose-potentiated VSMC chemotaxis, as did the inhibitors for the PI3K and MAPK pathways. |
| 709 | 12560158 | High glucose potentiates mitogenic responses of cultured ovine coronary smooth muscle cells to platelet derived growth factor and transforming growth factor-beta1. |
| 710 | 12560158 | Transforming growth factor-beta1 (1 ng/ml) caused a 100% increase of the PDGF-bb response in both normal and high glucose media. |
| 711 | 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. |
| 712 | 12574158 | The extracellular domain of receptor activity-modifying protein 1 is sufficient for calcitonin receptor-like receptor function. |
| 713 | 12574158 | A functional calcitonin gene-related peptide (CGRP) receptor requires dimerization of calcitonin receptor-like receptor (CRLR) with receptor activity-modifying protein 1 (RAMP 1). |
| 714 | 12574158 | To determine the function of the three domains (extracellular, ECD; transmembrane, TM; and tail domains) of human RAMP 1, three mutants were constructed: RAMP 1 without the cytoplasmic tail, a chimera consisting of the ECD of RAMP 1 and the TM and tail of the platelet-derived growth factor receptor, and the ECD of RAMP 1 alone. |
| 715 | 12574158 | These RAMP 1 mutants were examined for their ability to associate with CRLR to effect CGRP-stimulated cAMP accumulation, CGRP binding, CRLR trafficking, and cell surface expression. |
| 716 | 12574158 | All RAMP 1 mutants were able to associate with CRLR with full efficacy for CGRP-stimulated cAMP accumulation. |
| 717 | 12574158 | However, the RAMP 1/platelet-derived growth factor receptor chimera demonstrated a 10-fold decrease in potency for CGRP signaling and binding, and the RAMP 1-ECD mutant had a 4000-fold decrease in potency. |
| 718 | 12574158 | The extracellular domain of receptor activity-modifying protein 1 is sufficient for calcitonin receptor-like receptor function. |
| 719 | 12574158 | A functional calcitonin gene-related peptide (CGRP) receptor requires dimerization of calcitonin receptor-like receptor (CRLR) with receptor activity-modifying protein 1 (RAMP 1). |
| 720 | 12574158 | To determine the function of the three domains (extracellular, ECD; transmembrane, TM; and tail domains) of human RAMP 1, three mutants were constructed: RAMP 1 without the cytoplasmic tail, a chimera consisting of the ECD of RAMP 1 and the TM and tail of the platelet-derived growth factor receptor, and the ECD of RAMP 1 alone. |
| 721 | 12574158 | These RAMP 1 mutants were examined for their ability to associate with CRLR to effect CGRP-stimulated cAMP accumulation, CGRP binding, CRLR trafficking, and cell surface expression. |
| 722 | 12574158 | All RAMP 1 mutants were able to associate with CRLR with full efficacy for CGRP-stimulated cAMP accumulation. |
| 723 | 12574158 | However, the RAMP 1/platelet-derived growth factor receptor chimera demonstrated a 10-fold decrease in potency for CGRP signaling and binding, and the RAMP 1-ECD mutant had a 4000-fold decrease in potency. |
| 724 | 12598306 | To identify new markers for pericytes, we have taken advantage of the platelet-derived growth factor (PDGF)-B knockout mouse model, in which developing blood vessels in the central nervous system are almost completely devoid of pericytes. |
| 725 | 12598306 | Absence of RGS5 expression in PDGF-B and PDGFR beta-null embryos correlated with pericyte loss in these mice. |
| 726 | 12598306 | To identify new markers for pericytes, we have taken advantage of the platelet-derived growth factor (PDGF)-B knockout mouse model, in which developing blood vessels in the central nervous system are almost completely devoid of pericytes. |
| 727 | 12598306 | Absence of RGS5 expression in PDGF-B and PDGFR beta-null embryos correlated with pericyte loss in these mice. |
| 728 | 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. |
| 729 | 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. |
| 730 | 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). |
| 731 | 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. |
| 732 | 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. |
| 733 | 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). |
| 734 | 12606528 | Role of protein kinase C on the expression of platelet-derived growth factor and endothelin-1 in the retina of diabetic rats and cultured retinal capillary pericytes. |
| 735 | 12606528 | The effects of high glucose and protein kinase C (PKC) activation on platelet-derived growth factor (PDGF)-BB and of ET-1 expression in the retina of streptozotocin (STZ)-induced diabetic rats and bovine retinal pericytes (BRPC) were examined. |
| 736 | 12606528 | Treatment with PKC-beta isoform-specific inhibitor (LY333531) or insulin normalized retinal ET-1 and PDGF-B expression. |
| 737 | 12606528 | The addition of PDGF-BB but not PDGF-AA increased expression of ppET-1 and vascular endothelial growth factor mRNA by 1.6- and 2.1-fold, respectively, with both inhibited by AG1296, a selective PDGF receptor kinase inhibitor. |
| 738 | 12606528 | Thus, increased ET-1 expression in diabetic retina could be due to increased expression of PDGF-BB, mediated via PDGF-beta receptors in part by PKC activation. |
| 739 | 12606528 | Role of protein kinase C on the expression of platelet-derived growth factor and endothelin-1 in the retina of diabetic rats and cultured retinal capillary pericytes. |
| 740 | 12606528 | The effects of high glucose and protein kinase C (PKC) activation on platelet-derived growth factor (PDGF)-BB and of ET-1 expression in the retina of streptozotocin (STZ)-induced diabetic rats and bovine retinal pericytes (BRPC) were examined. |
| 741 | 12606528 | Treatment with PKC-beta isoform-specific inhibitor (LY333531) or insulin normalized retinal ET-1 and PDGF-B expression. |
| 742 | 12606528 | The addition of PDGF-BB but not PDGF-AA increased expression of ppET-1 and vascular endothelial growth factor mRNA by 1.6- and 2.1-fold, respectively, with both inhibited by AG1296, a selective PDGF receptor kinase inhibitor. |
| 743 | 12606528 | Thus, increased ET-1 expression in diabetic retina could be due to increased expression of PDGF-BB, mediated via PDGF-beta receptors in part by PKC activation. |
| 744 | 12606528 | Role of protein kinase C on the expression of platelet-derived growth factor and endothelin-1 in the retina of diabetic rats and cultured retinal capillary pericytes. |
| 745 | 12606528 | The effects of high glucose and protein kinase C (PKC) activation on platelet-derived growth factor (PDGF)-BB and of ET-1 expression in the retina of streptozotocin (STZ)-induced diabetic rats and bovine retinal pericytes (BRPC) were examined. |
| 746 | 12606528 | Treatment with PKC-beta isoform-specific inhibitor (LY333531) or insulin normalized retinal ET-1 and PDGF-B expression. |
| 747 | 12606528 | The addition of PDGF-BB but not PDGF-AA increased expression of ppET-1 and vascular endothelial growth factor mRNA by 1.6- and 2.1-fold, respectively, with both inhibited by AG1296, a selective PDGF receptor kinase inhibitor. |
| 748 | 12606528 | Thus, increased ET-1 expression in diabetic retina could be due to increased expression of PDGF-BB, mediated via PDGF-beta receptors in part by PKC activation. |
| 749 | 12606528 | Role of protein kinase C on the expression of platelet-derived growth factor and endothelin-1 in the retina of diabetic rats and cultured retinal capillary pericytes. |
| 750 | 12606528 | The effects of high glucose and protein kinase C (PKC) activation on platelet-derived growth factor (PDGF)-BB and of ET-1 expression in the retina of streptozotocin (STZ)-induced diabetic rats and bovine retinal pericytes (BRPC) were examined. |
| 751 | 12606528 | Treatment with PKC-beta isoform-specific inhibitor (LY333531) or insulin normalized retinal ET-1 and PDGF-B expression. |
| 752 | 12606528 | The addition of PDGF-BB but not PDGF-AA increased expression of ppET-1 and vascular endothelial growth factor mRNA by 1.6- and 2.1-fold, respectively, with both inhibited by AG1296, a selective PDGF receptor kinase inhibitor. |
| 753 | 12606528 | Thus, increased ET-1 expression in diabetic retina could be due to increased expression of PDGF-BB, mediated via PDGF-beta receptors in part by PKC activation. |
| 754 | 12740486 | Contribution of Rho A and Rho kinase to platelet-derived growth factor-BB-induced proliferation of vascular smooth muscle cells. |
| 755 | 12740486 | In order to identify small G protein (s) which contributes to the proliferation of vascular smooth muscle cells (VSMCs), we examined the effect of an HMG-CoA reductase inhibitor (cerivastatin), a farnesyltransferase inhibitor (FTI-277), a geranyl geranyl transferase inhibitor (GGTI-286) and a Rho kinase inhibitor (Y-27632) on the proliferation of cultured rat VSMCs stimulated with 20ng/ml platelet-derived growth factor (PDGF)-BB. |
| 756 | 12740486 | Contribution of Rho A and Rho kinase to platelet-derived growth factor-BB-induced proliferation of vascular smooth muscle cells. |
| 757 | 12740486 | In order to identify small G protein (s) which contributes to the proliferation of vascular smooth muscle cells (VSMCs), we examined the effect of an HMG-CoA reductase inhibitor (cerivastatin), a farnesyltransferase inhibitor (FTI-277), a geranyl geranyl transferase inhibitor (GGTI-286) and a Rho kinase inhibitor (Y-27632) on the proliferation of cultured rat VSMCs stimulated with 20ng/ml platelet-derived growth factor (PDGF)-BB. |
| 758 | 12768220 | In addition to decreasing angiotensin II and increasing bradykinin levels, ramipril increases the levels of vasodilatory renal medullary neutral lipids and inhibits platelet-derived growth factor-induced proliferation of glomerulus cells. |
| 759 | 12845621 | These include increased synthesis of type IV collagen following hyperglycaemia-induced alteration of the pattern of podocyte-integrin expression, decreased expression of matrix metalloproteinases (MMP-2 and 3), and increased expression of tissue inhibitor of metalloproteinase (TIMP). |
| 760 | 12845621 | Other factors which may contribute to renal matrix accumulation include vascular endothelial growth factor (VEGF), since treatment with anti-VEGF antibodies attenuates glomerular basement membrane thickening, platelet-derived growth factor (PDGF) (B chain) and its receptor, which appear to be highly expressed in mesangial and visceral epithelial cells and might play a role in the development of diabetic nephropathy. |
| 761 | 14514641 | The mechanisms by which insulin exerts these contrasting effects were examined using alpha-smooth muscle actin (alpha-SMA) as a marker of VSMC phenotype because alpha-SMA is highly expressed in quiescent but not migratory VSMC. |
| 762 | 14514641 | Wortmannin, a phosphatidylinositol 3-kinase (PI3K) inhibitor, decreased insulin-stimulated expression of alpha-SMA mRNA by 26% and protein by 48% but had no effect on VSMC migration. |
| 763 | 14514641 | PD98059, a mitogen-activated protein kinase (MAPK) kinase inhibitor, decreased insulin-induced VSMC migration by 52% but did not affect alpha-SMA levels. |
| 764 | 14514641 | Platelet-derived growth factor (PDGF) promoted dedifferentiation of VSMC, and insulin counteracted this effect. |
| 765 | 14514641 | Furthermore, insulin increased alpha-SMA mRNA and protein levels to 111 and 118%, respectively, after PDGF-induced dedifferentiation, an effect inhibited by wortmannin. |
| 766 | 14514641 | In conclusion, insulin's ability to maintain VSMC quiescence and reverse the dedifferentiating influence of PDGF is mediated via the PI3K pathway, whereas insulin promotes VSMC migration via the MAPK pathway. |
| 767 | 14514641 | Thus, with impaired PI 3-kinase signaling and intact MAPK signaling, as seen in insulin resistance, insulin may lose its ability to maintain VSMC quiescence and instead promote VSMC migration. |
| 768 | 14516785 | The present studies were designed to investigate the signal transduction pathways controlling the expression of MCM6 and MCM7 in VSMC in response to mitogenic stimuli. |
| 769 | 14516785 | MCM6 and MCM7 expression was substantially increased after stimulation with platelet-derived growth factor-BB and insulin. |
| 770 | 14516785 | Pretreatment with PD98059, a specific inhibitor of the extracellular signal-regulated kinases (ERK)-mitogen-activated protein kinase (MAPK), competely inhibited the mitogen-induced MCM6 and MCM7 mRNA and protein expression, demonstrating a critical role for this pathway in transmitting transmembrane signals required for the initiation of DNA replication. |
| 771 | 14516785 | The p38MAPK inhibitor SB203580, the phosphatidylinositol 3 kinase (PI3-kinase) pathway inhibitor wortmannin, and the protein kinase C pathway (PKC) inhibitor Gö 6976 did not significantly affect mitogen-induced MCM6 and MCM7 expression. |
| 772 | 14516785 | Transient transfection experiments revealed that PD98059 inhibited mitogen-induced MCM6 and MCM7 transcriptional activation. |
| 773 | 14516785 | Inhibition of mitogen-induced MCM6 and MCM7 expression by PD98059 was reversed by ectopic overexpression of E2F, indicating that ERK/MAPK signaling is required for events that occur upstream of E2F release from phosphorylated Rb. |
| 774 | 14669155 | To examine possible mechanisms for this effect, we studied nuclear factor-kappa B (NF-kappaB) activation and the tyrosine phosphorylation pathway; AGE stimulated NF-kappaB activity, but phosphorylation of the platelet-derived growth factor (PDGF) receptor was unchanged. |
| 775 | 14669155 | In Chinese hamster ovary (CHO) cells overexpressing galectin-3, an AGE receptor related to atherosclerosis, AGE increased thymidine uptake. |
| 776 | 15067514 | Glomerular expression of platelet-derived growth factor (PDGF)-A, -B chain and PDGF receptor-alpha, -beta in human diabetic nephropathy. |
| 777 | 15127326 | Differential regulation of ANG2 and VEGF-A in human granulosa lutein cells by choriogonadotropin. |
| 778 | 15127326 | In this study we investigated by RT PCR if the growth factors PGF, PDGF-A, PDGF-B, VEGF-A, VEGF-B, VEGF-C, VEGF-D, ANG1, ANG2, ANG3 and ANG4 are expressed in granulosa cells. |
| 779 | 15127326 | We show the expression of VEGF-A, VEGF-B, PDGF-A, ANG1 and ANG2 in granulosa cells. |
| 780 | 15127326 | Using RT-PCR and Real-Time PCR we demonstrate that angiopoietin 2 is downregulated in human granulosa cells in vitro after choriogonadotropin treatment whereas the expression of angiopoietin 1 is not significantly altered. |
| 781 | 15127326 | In total these findings suggests that in granulosa cells the mRNA of various growth factors is detectable by RT-PCR and that VEGF-A and ANG2 is regulated by the gonadotropic hormone choriogonadotropin. |
| 782 | 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). |
| 783 | 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. |
| 784 | 15131119 | These data suggest an intrinsic heterogeneity of adipocytes with differences in gene expression related to adipocyte size and insulin signaling. |
| 785 | 15140748 | We investigated the effects of angiotensin II (ANG II) and platelet-derived growth factor (PDGF)-BB on VSMC-monocyte interactions. |
| 786 | 15140748 | Using specific signal transduction inhibitors, we demonstrated the involvement of Src, phosphoinositide 3-kinase, and MAPKs in ANG II- or PDGF-BB-induced binding. |
| 787 | 15161630 | Analysis of gene expression by real-time reverse transcriptase-polymerase chain reaction demonstrates a significant up-regulation of platelet-derived growth factor-B and fibroblast growth factor-2 in VEGF-treated wounds, which corresponds with the increased granulation tissue in these wounds. |
| 788 | 15161630 | We observed increased numbers of circulating VEGFR2(+)/CD11b(-) cells in the VEGF-treated mice by fluorescence-activated cell sorting analysis, which likely represent an endothelial precursor population. |
| 789 | 15161630 | In diabetic mice with bone marrow replaced by that of tie2/lacZ mice we demonstrate that the local recruitment of bone marrow-derived endothelial lineage lacZ+ cells was augmented by topical VEGF. |
| 790 | 15176000 | While there are several mechanisms that regulate IFP in tumors, activation of platelet-derived growth factor receptor, which is expressed in various cell types within the tumor microenvironment, has been observed to play an important role in elevating IFP. |
| 791 | 15176000 | In preclinical studies, treatment with imatinib, which inhibits both alpha- and beta-platelet-derived growth factor receptors, as well as KIT, ABL, ARG, and BCR-ABL tyrosine kinases, has been shown to decrease tumor IFP and concomitantly augment uptake of chemotherapeutic drugs, thereby enhancing the efficacy of chemotherapy. |
| 792 | 15176000 | While there are several mechanisms that regulate IFP in tumors, activation of platelet-derived growth factor receptor, which is expressed in various cell types within the tumor microenvironment, has been observed to play an important role in elevating IFP. |
| 793 | 15176000 | In preclinical studies, treatment with imatinib, which inhibits both alpha- and beta-platelet-derived growth factor receptors, as well as KIT, ABL, ARG, and BCR-ABL tyrosine kinases, has been shown to decrease tumor IFP and concomitantly augment uptake of chemotherapeutic drugs, thereby enhancing the efficacy of chemotherapy. |
| 794 | 15229188 | It regulates both insulin and leptin signaling, and interacts with the epidermal- and platelet-derived growth factor receptors. |
| 795 | 15240344 | In wild-type VSMCs, exogenously added L-PGDS delayed serum-induced cell cycle progression from the G1 to S phase, as determined by gene array analysis and the decreased protein expressions of cyclin-dependent kinase-2, p21(Cip1), and cyclin D1. |
| 796 | 15240344 | Cyclin D3 protein expression was unaffected by L-PGDS, although its gene expression was stimulated by L-PGDS in wild-type cells. |
| 797 | 15240344 | In addition, platelet-derived growth factor-induced VSMC migration was inhibited by L-PGDS in wild-type cells. |
| 798 | 15331555 | Müller cells, the principal glia of the retina, generate tractional forces in response to IGF-I and platelet-derived growth factor and are present in diabetic fibro-vascular scar tissues causing traction retinal detachment. |
| 799 | 15336602 | Calcium-sensing receptor activation stimulates parathyroid hormone-related protein secretion in prostate cancer cells: role of epidermal growth factor receptor transactivation. |
| 800 | 15336602 | We have previously reported that high extracellular Ca2+ stimulates parathyroid hormone-related protein (PTHrP) release from human prostate and breast cancer cell lines as well as from H-500 rat Leydig cancer cells, an action mediated by the calcium-sensing receptor (CaR). |
| 801 | 15336602 | Activating the CaR leads to phosphorylation of mitogen-activated protein kinases (MAPKs) that participate in PTHrP synthesis and secretion. |
| 802 | 15336602 | Because the CaR is a G protein-coupled receptor (GPCR), it is likely to transactivate the epidermal growth factor receptor (EGFR) or the platelet-derived growth factor receptor (PDGFR). |
| 803 | 15336602 | In this study, we hypothesized that activation of the CaR transactivates the EGFR or PDGFR, and examined whether transactivation affects PTHrP secretion in PC-3 human prostate cancer cells. |
| 804 | 15336602 | Using Western analysis, we observed that an increase in extracellular Ca2+ resulted in delayed activation of extracellular signal-regulated kinase (ERK) in PC-3 cells. |
| 805 | 15336602 | Pre-incubation with AG1478 (an EGFR kinase inhibitor) or an EGFR neutralizing antibody inhibited the high Ca2+ -induced phosphorylation of ERK1/2. |
| 806 | 15336602 | GM6001, a pan matrix metalloproteinase (MMP) inhibitor, also partially suppressed the ERK activation, but AG1296 (a PDGFR kinase inhibitor) did not. |
| 807 | 15336602 | When cells were preincubated with AG1478, GM6001, or an antihuman heparin-binding EGF (HB-EGF) antibody, PTHrP secretion was significantly inhibited under basal as well as high Ca2+ conditions, while AG1296 had no effect on PTHrP secretion. |
| 808 | 15336602 | Taken together, these findings indicate that activation of the CaR transactivates the EGFR, but not the PDGFR, leading to phosphorylation of ERK1/2 and resultant PTHrP secretion, although CaR-EGFR-ERK might not be the only signaling pathway for PTHrP secretion. |
| 809 | 15336602 | This transactivation is most likely mediated by activation of MMP and cleavage of proheparin-binding EGF (proHB-EGF) to HB-EGF. |
| 810 | 15370072 | One mechanism by which ROS exert their cellular effects involves their ability to modulate the expression and function of vascular genes, such as vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), and platelet-derived growth factor (PDGF), which play key atherogenic roles by their regulation of cell growth, differentiation, and fibroproliferative responsiveness. |
| 811 | 15467196 | Choroidal explants in the early diabetic stage released vascular endothelial growth factor (VEGF) and tended to increase tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B, and concomitantly facilitated growth of sprout and buds, compared to the normal control. |
| 812 | 15467196 | When choroidal explants were stimulated with CML-human serum albumin (HSA), its releasing effect was in the order VEGF>TNFalpha>PDGF-B. |
| 813 | 15467196 | In conclusion, CML adducts were accumulated and over-produced the actions of VEGF, TNFalpha and PDGF-B in the choroidal explant during diabetes in an age-dependent manner. |
| 814 | 15467196 | TNFalpha and VEGF are likely to play a predominant role for the CML-induced choroidal neovascularization. |
| 815 | 15467196 | Choroidal explants in the early diabetic stage released vascular endothelial growth factor (VEGF) and tended to increase tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B, and concomitantly facilitated growth of sprout and buds, compared to the normal control. |
| 816 | 15467196 | When choroidal explants were stimulated with CML-human serum albumin (HSA), its releasing effect was in the order VEGF>TNFalpha>PDGF-B. |
| 817 | 15467196 | In conclusion, CML adducts were accumulated and over-produced the actions of VEGF, TNFalpha and PDGF-B in the choroidal explant during diabetes in an age-dependent manner. |
| 818 | 15467196 | TNFalpha and VEGF are likely to play a predominant role for the CML-induced choroidal neovascularization. |
| 819 | 15467196 | Choroidal explants in the early diabetic stage released vascular endothelial growth factor (VEGF) and tended to increase tumor necrosis factor (TNF) alpha and platelet-derived growth factor (PDGF)-B, and concomitantly facilitated growth of sprout and buds, compared to the normal control. |
| 820 | 15467196 | When choroidal explants were stimulated with CML-human serum albumin (HSA), its releasing effect was in the order VEGF>TNFalpha>PDGF-B. |
| 821 | 15467196 | In conclusion, CML adducts were accumulated and over-produced the actions of VEGF, TNFalpha and PDGF-B in the choroidal explant during diabetes in an age-dependent manner. |
| 822 | 15467196 | TNFalpha and VEGF are likely to play a predominant role for the CML-induced choroidal neovascularization. |
| 823 | 15504957 | Platelet-derived growth factor stimulates glucose transport in skeletal muscles of transgenic mice specifically expressing platelet-derived growth factor receptor in the muscle, but it does not affect blood glucose levels. |
| 824 | 15504957 | Insulin stimulates the disposal of blood glucose into skeletal muscle and adipose tissues by the translocation of GLUT4 from intracellular pools to the plasma membrane, and consequently the concentration of blood glucose levels decreases rapidly in vivo. |
| 825 | 15504957 | Phosphatidylinositol (PI) 3-kinase and Akt play a pivotal role in the stimulation of glucose transport by insulin, but detailed mechanisms are unknown. |
| 826 | 15504957 | We and others reported that not only insulin but also platelet-derived growth factor (PDGF) and epidermal growth factor facilitate glucose uptake through GLUT4 translocation by activation of PI 3-kinase and Akt in cultured cells. |
| 827 | 15504957 | We generated transgenic mice that specifically express the PDGF receptor in skeletal muscle. |
| 828 | 15504957 | Thus, PDGF apparently shares with insulin some of the signaling molecules needed for the stimulation of glucose transport. |
| 829 | 15504957 | The degree of glucose uptake in vivo reached approximately 60% of that by insulin injection in skeletal muscle, but blood glucose levels were not decreased by PDGF in these mice. |
| 830 | 15504957 | Platelet-derived growth factor stimulates glucose transport in skeletal muscles of transgenic mice specifically expressing platelet-derived growth factor receptor in the muscle, but it does not affect blood glucose levels. |
| 831 | 15504957 | Insulin stimulates the disposal of blood glucose into skeletal muscle and adipose tissues by the translocation of GLUT4 from intracellular pools to the plasma membrane, and consequently the concentration of blood glucose levels decreases rapidly in vivo. |
| 832 | 15504957 | Phosphatidylinositol (PI) 3-kinase and Akt play a pivotal role in the stimulation of glucose transport by insulin, but detailed mechanisms are unknown. |
| 833 | 15504957 | We and others reported that not only insulin but also platelet-derived growth factor (PDGF) and epidermal growth factor facilitate glucose uptake through GLUT4 translocation by activation of PI 3-kinase and Akt in cultured cells. |
| 834 | 15504957 | We generated transgenic mice that specifically express the PDGF receptor in skeletal muscle. |
| 835 | 15504957 | Thus, PDGF apparently shares with insulin some of the signaling molecules needed for the stimulation of glucose transport. |
| 836 | 15504957 | The degree of glucose uptake in vivo reached approximately 60% of that by insulin injection in skeletal muscle, but blood glucose levels were not decreased by PDGF in these mice. |
| 837 | 15517944 | [The role of platelet-derived growth factor A (PDGF-A) in hypertension and renal diseases. |
| 838 | 15517944 | Many studies have suggested deleterious effects of platelet-derived growth factor (PDGF) released by intrinsic renal cells during glomerulonephritis (GN). |
| 839 | 15517944 | Increase in PDGF B chain expression has particularly been noted in glomeruli of patients with GN. |
| 840 | 15517944 | [The role of platelet-derived growth factor A (PDGF-A) in hypertension and renal diseases. |
| 841 | 15517944 | Many studies have suggested deleterious effects of platelet-derived growth factor (PDGF) released by intrinsic renal cells during glomerulonephritis (GN). |
| 842 | 15517944 | Increase in PDGF B chain expression has particularly been noted in glomeruli of patients with GN. |
| 843 | 15517944 | [The role of platelet-derived growth factor A (PDGF-A) in hypertension and renal diseases. |
| 844 | 15517944 | Many studies have suggested deleterious effects of platelet-derived growth factor (PDGF) released by intrinsic renal cells during glomerulonephritis (GN). |
| 845 | 15517944 | Increase in PDGF B chain expression has particularly been noted in glomeruli of patients with GN. |
| 846 | 15539012 | Altered local gene expression of humoral factors (eg, transforming growth factor-b, connective tissue growth factor, and platelet-derived growth factor) can lead to increased production of ECM components (eg, fibronectin and collagen IV) or decreased degradation through matrix metalloproteinases (eg, MMP-1, MMP-2). |
| 847 | 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. |
| 848 | 15583025 | Finally, the respective roles of TGF-beta, GH and IGFs, vascular endothelial growth factor, and platelet-derived growth factor are covered. |
| 849 | 15625075 | The objectives of this study were first to assess whether PDGF-dependent pathways are involved in the development of diabetic nephropathy and second to determine the effects of PDGF receptor antagonism on this disorder and associated molecular and cellular processes. |
| 850 | 15625075 | This model of accelerated renal disease with albuminuria as well as glomerular and tubulointerstitial injury was associated with increased renal expression of PDGF-B, proliferating cells, and alpha-smooth muscle actin-positive cells. |
| 851 | 15684477 | The CML-enhanced neovascularization activity is associated with the actions of tumor necrosis factor (TNF) alpha, vascular endothelial growth factor and platelet-derived growth factor released from the choroidal explant (Kobayashi et al., Biol. |
| 852 | 15953049 | When exposed to transforming growth factor-beta2 (1-10,000 pg/ml) and platelet-derived growth factor-BB (0.5-500 ng/ml) under both normo- and hyperglycemic conditions, there was a dose-related increase in proliferation of both diabetic and nondiabetic controls. |
| 853 | 15953049 | Western blot analysis did not show any apparent difference in the expression of platelet-derived growth factor receptor alpha, mitogen-activated protein kinase/ERK2, or transforming growth factor-beta receptor II to account for the reduced proliferation of diabetic hTCF. |
| 854 | 15953049 | When exposed to transforming growth factor-beta2 (1-10,000 pg/ml) and platelet-derived growth factor-BB (0.5-500 ng/ml) under both normo- and hyperglycemic conditions, there was a dose-related increase in proliferation of both diabetic and nondiabetic controls. |
| 855 | 15953049 | Western blot analysis did not show any apparent difference in the expression of platelet-derived growth factor receptor alpha, mitogen-activated protein kinase/ERK2, or transforming growth factor-beta receptor II to account for the reduced proliferation of diabetic hTCF. |
| 856 | 16103269 | Platelet-derived growth factor (PDGF)-BB (25 ng/mL) increased DNA synthesis ([3H]thymidine incorporation), cellular proliferation (cell number), collagen synthesis ([3H]proline incorporation), and mitogen-activated protein kinase (MAPK) activity, and these effects were attenuated by 2-chloroadenosine (nonselective AR agonist) and 5'-N-methylcarboxamidoadenosine (MECA; nonselective AR agonist), but not by N6-cyclopentyladenosine (selective A1 AR agonist), AB-N-MECA (selective A3 AR agonist), or CGS21680 (selective A(2A) AR agonist). |
| 857 | 16103269 | Antisense, but not sense or scrambled, oligonucleotides to the A(2B) receptor increased both basal and PDGF-induced DNA synthesis, cell proliferation, and collagen synthesis, and the growth-inhibitory effects of 2-chloroadenosine, 5'-N-MECA, and erythro-9-(2-hydroxy-3-nonyl)adenine (inhibitor of adenosine deaminase) plus iodotubercidin (inhibitor of adenosine kinase) were abolished by antisense, but not scrambled or sense, oligonucleotides to the A(2B) receptor. |
| 858 | 16149463 | [Platelet derived growth factor (PDGF)]. |
| 859 | 16156274 | This study sought to assess the effects of Quercetin and Enalapril on urinary protein excretion and amount of platelet-derived growth factor-B (PDGF-B) and vascular endothelial growth factor-1 (VEGF-1) in renal tissue of diabetic rats. 29 streptozotocin-induced diabetic rats were divided into 3 groups, diabetic control group (group D, n=12); Enalapril group (group E, n=10); Quercetin group (group Q, n=7). |
| 860 | 16165393 | In these situations, retinal dysfunction has been linked to angiotensin-mediated induction of growth factors including vascular endothelial growth factor, platelet-derived growth factor and connective tissue growth factor. |
| 861 | 16215210 | Formation of the deep capillary layers at p8 was associated with a combined up-regulation of angiopoietin-1 and PDGF-B, while VEGF was almost unchanged during the transition from a susceptible to a resistant capillary network. |
| 862 | 16249442 | Stimulation of patients' skin fibroblast cells with platelet-derived growth factor (PDGF) resulted in a lower-level tyrosine phosphorylation of cytosolic proteins compared with that seen in normal cells. |
| 863 | 16249442 | We further showed that the lower-level tyrosine phosphorylation in response to growth factors results from the downregulation of an NADPH oxidase, Nox4, which in turn results in the reduction of ROS generation. |
| 864 | 16249442 | Ectopic expression of Nox4 in the patient fibroblast cells consistently restored PDGF-induced ROS production and regulation of PTPase activities. |
| 865 | 16306442 | Diabetic microangiopathy in ischemic limb is a disease of disturbance of the platelet-derived growth factor-BB/protein kinase C axis but not of impaired expression of angiogenic factors. |
| 866 | 16306442 | Supplementation of the PDGF-B gene resulted in the prevention of autoamputation, and, furthermore, a protein kinase C (PKC) inhibitor restored the PDGF-BB expression and also resulted in complete rescue of the limbs of the STZ-DM mice. |
| 867 | 16306442 | Diabetic microangiopathy in ischemic limb is a disease of disturbance of the platelet-derived growth factor-BB/protein kinase C axis but not of impaired expression of angiogenic factors. |
| 868 | 16306442 | Supplementation of the PDGF-B gene resulted in the prevention of autoamputation, and, furthermore, a protein kinase C (PKC) inhibitor restored the PDGF-BB expression and also resulted in complete rescue of the limbs of the STZ-DM mice. |
| 869 | 16339836 | To assess the contribution of diabetic changes in the local vasculature, diabetic mice were treated with pinnal injections of platelet-derived growth factor (PDGF)-AB, which promotes cardiac angiogenesis in wild-type mice. |
| 870 | 16489846 | Other topics covered include the role of HMG-CoA reductase inhibitors and fibric acid derivatives with respect to their lipid-altering ability, as well as their emerging pleiotropic anti-atherogenic actions; the effect of inhibiting the renin-angiotensin system by either ACE inhibition or angiotensin II receptor antagonism; the effect of glycemic control and, in particular, the promising role of thiazolidinediones with respect to their direct anti-atherogenic actions; and newly emerging mediators of diabetes-associated atherosclerosis, such as advanced glycation end products, vascular endothelial growth factor and platelet-derived growth factor. |
| 871 | 16503870 | In this review the effect of inhibiting the renin-angiotensin system with angiotensin converting enzyme inhibition and a comparison to angiotensin II receptor antagonism is discussed, with the results of clinical trails reflecting the more recently discovered, non-haemodynamic, proatherogenic actions of angiotensin II. |
| 872 | 16503870 | Finally, growth factors, including vascular endothelial growth factor and platelet-derived growth factor are discussed in detail. |
| 873 | 16566566 | Platelet-derived growth factor (PDGF) is released by activated platelets to recruit inflammatory cells toward the wound bed. |
| 874 | 16569213 | Angiotensin II stimulates phosphorylation of an ectodomain-truncated platelet-derived growth factor receptor-beta and its binding to class IA PI3K in vascular smooth muscle cells. |
| 875 | 16569213 | PI3K (phosphoinositide 3-kinase) activity is involved in Ang (angiotensin) II-stimulated VSMC (vascular smooth muscle cell) growth and hypertrophy. |
| 876 | 16569213 | In the present study, we demonstrate that the inhibition of PI3K in VSMCs by expression of a dominant-negative p85alpha mutant lacking the p110-binding domain (Deltap85), or by treatment of cells with LY294002, inhibited Ang II-stimulated PAI-1 (plasminogen activator inhibitor-1) mRNA expression. |
| 877 | 16569213 | Using a GST (glutathione S-transferase) fusion protein containing the p85 N-terminal SH2 (Src homology 2) domain as 'bait' followed by MS/MS (tandem MS), we identified a 70 kDa fragment of the p70 PDGFR-beta (platelet-derived growth factor receptor-beta) as a signalling adapter that is phosphorylated and recruits the p85 subunit of PI3K after Ang II stimulation of AT1 (Ang II subtype 1) receptors on VSMCs. |
| 878 | 16569213 | Stimulation of VSMCs with Ang II increased tyrosine-phosphorylation of p70 PDGFR-beta at Tyr751 and Tyr1021 and increased its binding to p85. |
| 879 | 16569213 | PDGF also induced phosphorylation of p70 PDGFR-beta, a response inhibited by the PDGF tyrosine kinase selective inhibitor, AG1296. |
| 880 | 16569213 | Ang II-stimulated phosphorylation of the p70 PDGFR-beta was blocked by the AT1 receptor antagonist, candesartan (CV 11974) and was partially inhibited by PP2 {4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine}, an Src family kinase inhibitor. |
| 881 | 16569213 | Our result suggests that the p70 PDGFR-beta functions as an adapter that recruits PI3K to the membrane upon AT1 receptor stimulation. |
| 882 | 16569213 | Angiotensin II stimulates phosphorylation of an ectodomain-truncated platelet-derived growth factor receptor-beta and its binding to class IA PI3K in vascular smooth muscle cells. |
| 883 | 16569213 | PI3K (phosphoinositide 3-kinase) activity is involved in Ang (angiotensin) II-stimulated VSMC (vascular smooth muscle cell) growth and hypertrophy. |
| 884 | 16569213 | In the present study, we demonstrate that the inhibition of PI3K in VSMCs by expression of a dominant-negative p85alpha mutant lacking the p110-binding domain (Deltap85), or by treatment of cells with LY294002, inhibited Ang II-stimulated PAI-1 (plasminogen activator inhibitor-1) mRNA expression. |
| 885 | 16569213 | Using a GST (glutathione S-transferase) fusion protein containing the p85 N-terminal SH2 (Src homology 2) domain as 'bait' followed by MS/MS (tandem MS), we identified a 70 kDa fragment of the p70 PDGFR-beta (platelet-derived growth factor receptor-beta) as a signalling adapter that is phosphorylated and recruits the p85 subunit of PI3K after Ang II stimulation of AT1 (Ang II subtype 1) receptors on VSMCs. |
| 886 | 16569213 | Stimulation of VSMCs with Ang II increased tyrosine-phosphorylation of p70 PDGFR-beta at Tyr751 and Tyr1021 and increased its binding to p85. |
| 887 | 16569213 | PDGF also induced phosphorylation of p70 PDGFR-beta, a response inhibited by the PDGF tyrosine kinase selective inhibitor, AG1296. |
| 888 | 16569213 | Ang II-stimulated phosphorylation of the p70 PDGFR-beta was blocked by the AT1 receptor antagonist, candesartan (CV 11974) and was partially inhibited by PP2 {4-amino-5-(4-chlorophenyl)-7-(t-butyl)pyrazolo[3,4-d]pyrimidine}, an Src family kinase inhibitor. |
| 889 | 16569213 | Our result suggests that the p70 PDGFR-beta functions as an adapter that recruits PI3K to the membrane upon AT1 receptor stimulation. |
| 890 | 16682971 | We previously mapped the type 2 diabetes mellitus-2 locus (T2dm2), which affects fasting insulin levels, to distal chromosome 19 in a leptin-deficient obese F2 intercross derived from C57BL/6 (B6) and BTBR T+ tf/J (BTBR) mice. |
| 891 | 16682971 | SorCS1 binds platelet-derived growth factor, a growth factor crucial for pericyte recruitment to the microvasculature, and may thus have a role in expanding or maintaining the islet vasculature. |
| 892 | 16785777 | PL 14736 tended to have a greater effect than becaplermin on the formation of granulation tissue containing mature collagen. |
| 893 | 16807374 | Microarray analysis of blood microvessels from PDGF-B and PDGF-Rbeta mutant mice identifies novel markers for brain pericytes. |
| 894 | 16807374 | Here we describe an approach to identify pericyte markers based on transcription profiling of pericyte-deficient brain microvessels isolated from platelet-derived growth factor (PDGF-B)-/- and PDGF beta receptor (PDGFRbeta)-/- mouse mutants. |
| 895 | 16807374 | Of candidates for novel pericyte markers, we selected ATP-sensitive potassium-channel Kir6.1 (also known as Kcnj8) and sulfonylurea receptor 2, (SUR2, also known as Abcc9), both part of the same channel complex, as well as delta homologue 1 (DLK1) for in situ hybridization, which demonstrated their specific expression in brain pericytes of mouse embryos. |
| 896 | 16807374 | Microarray analysis of blood microvessels from PDGF-B and PDGF-Rbeta mutant mice identifies novel markers for brain pericytes. |
| 897 | 16807374 | Here we describe an approach to identify pericyte markers based on transcription profiling of pericyte-deficient brain microvessels isolated from platelet-derived growth factor (PDGF-B)-/- and PDGF beta receptor (PDGFRbeta)-/- mouse mutants. |
| 898 | 16807374 | Of candidates for novel pericyte markers, we selected ATP-sensitive potassium-channel Kir6.1 (also known as Kcnj8) and sulfonylurea receptor 2, (SUR2, also known as Abcc9), both part of the same channel complex, as well as delta homologue 1 (DLK1) for in situ hybridization, which demonstrated their specific expression in brain pericytes of mouse embryos. |
| 899 | 16842933 | Recent study indicated that reduction of platelet derived growth factor (PDGF) expression was indeed critical, in causing functional and morphological vascular changes, namely the dissociation of pericytes from the capillaries in muscles. |
| 900 | 17003476 | Platelet-derived growth factor, fibroblast growth factor-2, and vascular endothelial growth factor mRNA levels were increased in AdCMV.PlGF-treated wounds, possibly enhancing PlGF-mediated effects. |
| 901 | 17134386 | Synergistic actions of platelet-derived growth factor and the insulin-like growth factors in vivo. |
| 902 | 17134386 | Topical application of platelet-derived growth factor, insulin-like growth factor-I, or insulin-like growth factor-II enhances healing in this model. |
| 903 | 17134386 | Marked synergism was found when platelet-derived growth factor and insulin-like growth factor-II were combined to produce augmentation in wound closure beyond that achieved by application of the individual growth factors. |
| 904 | 17134386 | The synergistic effect allowed for improved tissue repair at doses of platelet-derived growth factor and insulin-like growth factor-II that were ineffective when applied individually. |
| 905 | 17134386 | The addition of insulin-like growth factor-I or insulin to platelet-derived growth factor produced no significant synergism. |
| 906 | 17134386 | Synergistic actions of platelet-derived growth factor and the insulin-like growth factors in vivo. |
| 907 | 17134386 | Topical application of platelet-derived growth factor, insulin-like growth factor-I, or insulin-like growth factor-II enhances healing in this model. |
| 908 | 17134386 | Marked synergism was found when platelet-derived growth factor and insulin-like growth factor-II were combined to produce augmentation in wound closure beyond that achieved by application of the individual growth factors. |
| 909 | 17134386 | The synergistic effect allowed for improved tissue repair at doses of platelet-derived growth factor and insulin-like growth factor-II that were ineffective when applied individually. |
| 910 | 17134386 | The addition of insulin-like growth factor-I or insulin to platelet-derived growth factor produced no significant synergism. |
| 911 | 17134386 | Synergistic actions of platelet-derived growth factor and the insulin-like growth factors in vivo. |
| 912 | 17134386 | Topical application of platelet-derived growth factor, insulin-like growth factor-I, or insulin-like growth factor-II enhances healing in this model. |
| 913 | 17134386 | Marked synergism was found when platelet-derived growth factor and insulin-like growth factor-II were combined to produce augmentation in wound closure beyond that achieved by application of the individual growth factors. |
| 914 | 17134386 | The synergistic effect allowed for improved tissue repair at doses of platelet-derived growth factor and insulin-like growth factor-II that were ineffective when applied individually. |
| 915 | 17134386 | The addition of insulin-like growth factor-I or insulin to platelet-derived growth factor produced no significant synergism. |
| 916 | 17134386 | Synergistic actions of platelet-derived growth factor and the insulin-like growth factors in vivo. |
| 917 | 17134386 | Topical application of platelet-derived growth factor, insulin-like growth factor-I, or insulin-like growth factor-II enhances healing in this model. |
| 918 | 17134386 | Marked synergism was found when platelet-derived growth factor and insulin-like growth factor-II were combined to produce augmentation in wound closure beyond that achieved by application of the individual growth factors. |
| 919 | 17134386 | The synergistic effect allowed for improved tissue repair at doses of platelet-derived growth factor and insulin-like growth factor-II that were ineffective when applied individually. |
| 920 | 17134386 | The addition of insulin-like growth factor-I or insulin to platelet-derived growth factor produced no significant synergism. |
| 921 | 17134386 | Synergistic actions of platelet-derived growth factor and the insulin-like growth factors in vivo. |
| 922 | 17134386 | Topical application of platelet-derived growth factor, insulin-like growth factor-I, or insulin-like growth factor-II enhances healing in this model. |
| 923 | 17134386 | Marked synergism was found when platelet-derived growth factor and insulin-like growth factor-II were combined to produce augmentation in wound closure beyond that achieved by application of the individual growth factors. |
| 924 | 17134386 | The synergistic effect allowed for improved tissue repair at doses of platelet-derived growth factor and insulin-like growth factor-II that were ineffective when applied individually. |
| 925 | 17134386 | The addition of insulin-like growth factor-I or insulin to platelet-derived growth factor produced no significant synergism. |
| 926 | 17168853 | The role of growth hormone, insulin-like growth factor and somatostatin in diabetic retinopathy. |
| 927 | 17168853 | Growth hormone (GH) and insulin-like growth factor-I (IGF-I) are implicated in the aberrant cell growth and pathological neovascularization that characterises proliferative diabetic retinopathy. |
| 928 | 17168853 | IGF-I may exert its cell growth promoting properties by stimulating a number of pathways including protein-kinase B (Akt), nuclear factor kB (NF-kappaB)/AP-1 and hypoxic-inducible factor-1alpha (HIF-1alpha). |
| 929 | 17168853 | In addition, other growth factors may participate in IGF-I induced cell growth including vascular endothelial growth factor (VEGF), platelet derived growth factor (PDGF) and fibroblast growth factor (FGF). |
| 930 | 17168853 | GH receptor antagonists, GH receptor antisense oligonucleotides, somatostatin analogues and receptor neutralising antibodies to IGF-I reduce hypoxic-induced retinal neovascularization. |
| 931 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 932 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 933 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 934 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 935 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 936 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 937 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 938 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 939 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 940 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 941 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 942 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 943 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 944 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 945 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 946 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 947 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 948 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 949 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 950 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 951 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 952 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 953 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 954 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 955 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 956 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 957 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 958 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 959 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 960 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 961 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 962 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 963 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 964 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 965 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 966 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 967 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 968 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 969 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 970 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 971 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 972 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 973 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 974 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 975 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 976 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 977 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 978 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 979 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 980 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 981 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 982 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 983 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 984 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 985 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 986 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 987 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 988 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 989 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 990 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 991 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 992 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 993 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 994 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 995 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 996 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 997 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 998 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 999 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 1000 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 1001 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 1002 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 1003 | 17173561 | Combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone in stimulating complete healing of full-thickness wounds in "older" diabetic mice. |
| 1004 | 17173561 | Platelet-derived growth factor and insulin-like growth factor-I have been shown to interact synergistically to enhance repair of skin wounds in normal healing swine. |
| 1005 | 17173561 | The objective of this study was to compare the wound healing effects of platelet-derived growth factor-BB alone with those of a combination of platelet-derived growth factor-BB and insulin-like growth factor-I in an improved model with the use of "older" animals with diabetes. |
| 1006 | 17173561 | Treatment groups included the following: 4.0 microg/cm(2) of platelet-derived growth factor-BB, 40.0 microg/cm(2) of platelet-derived growth factor-BB, 4.0 microg/cm(2) of both platelet-derived growth factor-BB and insulin-like growth factor-I or vehicle. |
| 1007 | 17173561 | The median time to complete healing for animals receiving the platelet-derived growth factor-BB/insulin-like growth factor-I combination was 38% and 33% faster (p < 0.001) than animals receiving 4.0 microg/cm(2) and 40.0 microg/cm(2) of platelet-derived growth factor-BB, respectively. |
| 1008 | 17173561 | The mean time to complete healing for platelet-derived growth factor/insulin-like growth factor-I treated animals was 31% and 29% faster (p < 0.001) than 4.0 microg/cm(2) and 40.0 microg/cm(2) platelet-derived growth factor-BB treated animals, respectively. |
| 1009 | 17173561 | Wounds treated with 4.0 microg/cm(2) platelet-derived growth factor-BB/insulin-like growth factor-I healed, on average, in 22 days compared with 31 days for 40.0 microg/cm(2) platelet-derived growth factor-BB alone and 38 days for vehicle. |
| 1010 | 17173561 | Also, platelet-derived growth factor-BB/insulin-like growth factor-I significantly improved the rate of wound closure throughout the duration of the studies compared with either dose of platelet-derived growth factor-BB alone (p < 0.005) or vehicle (p < 0.001). |
| 1011 | 17173561 | In conclusion, the data show that the combination of platelet-derived growth factor-BB and insulin-like growth factor-I is more effective than platelet-derived growth factor-BB alone at the doses tested or vehicle treatment in stimulating cutaneous wound healing in older, diabetic mice. |
| 1012 | 17191576 | Recombinant human platelet-derived growth factor enhances repair of cutaneous full-thickness excision by increasing the phosphorylation of extracellular signal-regulated kinase in diabetic rat. |
| 1013 | 17259386 | The Rab GTPase-activating protein AS160 integrates Akt, protein kinase C, and AMP-activated protein kinase signals regulating GLUT4 traffic. |
| 1014 | 17259386 | Insulin-dependent phosphorylation of Akt target AS160 is required for GLUT4 translocation. |
| 1015 | 17259386 | Insulin and platelet-derived growth factor (PDGF) (Akt activators) or activation of conventional/novel (c/n) protein kinase C (PKC) and 5' AMP-activated protein kinase (AMPK) all promote a rise in membrane GLUT4 in skeletal muscle and cultured cells. |
| 1016 | 17259386 | Here we explore the hypothesis that AS160 is a molecular link among diverse signaling cascades converging on GLUT4 translocation. |
| 1017 | 17259386 | PDGF and insulin increased AS160 phosphorylation in CHO-IR cells. |
| 1018 | 17259386 | Stimuli that activate c/n PKC or AMPK also elevated AS160 phosphorylation. |
| 1019 | 17259386 | We therefore examined if these signaling pathways engage AS160 to regulate GLUT4 traffic in muscle cells. |
| 1020 | 17259386 | Nonphosphorylatable AS160 (4P-AS160) virtually abolished the net surface GLUT4myc gains elicited by insulin, PDGF, K(+) depolarization, or 5-aminoimidazole-4-carboxamide-1-beta-d-ribofuranoside but partly, yet significantly, inhibited the effects of 4-phorbol-12-myristate-13-acetate. |
| 1021 | 17259386 | RK-AS160 (GTPase-activating protein [GAP] inactive) or 4PRK-AS160 (GAP inactive, nonphosphorylatable) had no effect on surface GLUT4myc elicited by all stimuli. |
| 1022 | 17259386 | Collectively, these results indicate that activation of Akt, c/n PKC, or alpha2-AMPK intersect at AS160 to regulate GLUT4 traffic, as well as highlight the potential of AS160 as a therapy target to increase muscle glucose uptake. |
| 1023 | 17270401 | Recombinant human platelet-derived growth factor enhanced dermal wound healing by a pathway involving ERK and c-fos in diabetic rats. |
| 1024 | 17344201 | The most important of growth factors are recombinant human platelet-derived growth factor-BB and granulocyte colony-stimulating factor. |
| 1025 | 17403678 | The Lipoxin A4 receptor is coupled to SHP-2 activation: implications for regulation of receptor tyrosine kinases. |
| 1026 | 17403678 | Using site-directed mutagenesis of the cytosolic domain of the platelet-derived growth factor receptor beta (PDGFRbeta), we report that mutation of the sites for phosphatidylinositol 3-kinase (Tyr(740) and Tyr(751)) and SHP-2 (Tyr(763) and Tyr(1009)) recruitment specifically inhibit the effect of LXA(4) on the PDGFRbeta signaling; furthermore inhibition of SHP-2 expression with short interfering RNA constructs blocked the effect of LXA(4) on PDGFRbeta phosphorylation. |
| 1027 | 17403678 | We demonstrate that association of the PDGFRbeta with lipid raft microdomains renders it susceptible to LXA(4)-mediated dephosphorylation by possible reactivation of oxidatively inactivated SHP-2. |
| 1028 | 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. |
| 1029 | 17477023 | In addition, direct interaction between monocyte-macrophage CD18 and PTC cell surface ICAM-1 stimulates TGF-beta1 synthesis. |
| 1030 | 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. |
| 1031 | 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). |
| 1032 | 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. |
| 1033 | 17650100 | Here, we extend the model to include equations for platelet-derived growth factor concentration, fibroblast density, collagen density, and hyaluronan concentration. |
| 1034 | 17941874 | Several factors are contemplated to be engaged in pericyte conscription including angiopoietin-1 and its receptor tyrosine kinase Tie-2, vascular endothelial growth factor-A and its receptor flk-1 and the platelet-derived growth factor PDGF-B/PDGF-beta system. |
| 1035 | 18158592 | Involvement of the Rho/Rho kinase signaling pathway in platelet-derived growth factor BB-induced vascular endothelial growth factor expression in diabetic rat retina. |
| 1036 | 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. |
| 1037 | 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. |
| 1038 | 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. |
| 1039 | 18292357 | One of the crucial biological factors responsible for reparative osseous activity is platelet-derived growth factor (PDGF). |
| 1040 | 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. |
| 1041 | 18318812 | Wound fluid was analyzed for insulin-like growth factor-1 (IGF-1), platelet-derived growth factor, and transforming growth factor. |
| 1042 | 18356692 | Proliferation was assessed by [H]-thymidine incorporation and cell counting and proteoglycan synthesis by [S]-sulfate incorporation using human vSMCs stimulated with platelet-derived growth factor (PDGF; 50 ng/mL) and transforming growth factor (TGF)-beta (2 ng/mL). |
| 1043 | 18481030 | More recently, LXs have emerged as potential anti-fibrotic mediators that may influence pro-fibrotic cytokines and matrix-associated gene expression in response to platelet-derived growth factor (PDGF). |
| 1044 | 18506785 | Expression of mRNAs encoding the angiogenic cytokines vascular endothelial growth factor (VEGF), angiopoietin 1 (ANGPT1), ANGPT2, platelet-derived growth factor B (PDGF-B), and placental growth factor (PLGF) was also impaired in wounds of older db/db mice. |
| 1045 | 18506785 | Intradermal injection of plasmid gWIZ-CA5, which encodes a constitutively active form of HIF-1alpha, followed by electroporation, induced increased levels of HIF-1alpha mRNA at the injection site on day 3 and increased levels of VEGF, PLGF, PDGF-B, and ANGPT2 mRNA on day 7. |
| 1046 | 18506785 | Expression of mRNAs encoding the angiogenic cytokines vascular endothelial growth factor (VEGF), angiopoietin 1 (ANGPT1), ANGPT2, platelet-derived growth factor B (PDGF-B), and placental growth factor (PLGF) was also impaired in wounds of older db/db mice. |
| 1047 | 18506785 | Intradermal injection of plasmid gWIZ-CA5, which encodes a constitutively active form of HIF-1alpha, followed by electroporation, induced increased levels of HIF-1alpha mRNA at the injection site on day 3 and increased levels of VEGF, PLGF, PDGF-B, and ANGPT2 mRNA on day 7. |
| 1048 | 18561944 | High glucose-induced upregulation of Rho/Rho-kinase via platelet-derived growth factor receptor-beta increases migration of aortic smooth muscle cells. |
| 1049 | 18561944 | Platelet-derived growth factor (PDGF) is known to stimulate the migration of SMCs. |
| 1050 | 18561944 | PDGF stimulated the activation and the protein level of Rho. |
| 1051 | 18561944 | The protein level of PDGF receptor-beta (PDGFR-beta) was increased under the high glucose condition concomitant with the increased protein level and activation of Rho. |
| 1052 | 18561944 | The increased protein level and activity of Rho were suppressed by an anti-PDGF neutralizing antibody or a PDGFR-beta inhibitor, AG1433, under the high glucose condition. |
| 1053 | 18561944 | The protein levels of Rho were increased in aortae of diabetic rats, which were abolished by the treatment of Imatinib, the inhibitor of PDGFR. |
| 1054 | 18561944 | These observations indicate that the upregulation of the PDGFR-beta / Rho / Rho-kinase pathway increases the migration of SMCs under the high glucose condition. |
| 1055 | 18561944 | High glucose-induced upregulation of Rho/Rho-kinase via platelet-derived growth factor receptor-beta increases migration of aortic smooth muscle cells. |
| 1056 | 18561944 | Platelet-derived growth factor (PDGF) is known to stimulate the migration of SMCs. |
| 1057 | 18561944 | PDGF stimulated the activation and the protein level of Rho. |
| 1058 | 18561944 | The protein level of PDGF receptor-beta (PDGFR-beta) was increased under the high glucose condition concomitant with the increased protein level and activation of Rho. |
| 1059 | 18561944 | The increased protein level and activity of Rho were suppressed by an anti-PDGF neutralizing antibody or a PDGFR-beta inhibitor, AG1433, under the high glucose condition. |
| 1060 | 18561944 | The protein levels of Rho were increased in aortae of diabetic rats, which were abolished by the treatment of Imatinib, the inhibitor of PDGFR. |
| 1061 | 18561944 | These observations indicate that the upregulation of the PDGFR-beta / Rho / Rho-kinase pathway increases the migration of SMCs under the high glucose condition. |
| 1062 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1063 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1064 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1065 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1066 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1067 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1068 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1069 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1070 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1071 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1072 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1073 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1074 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1075 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1076 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1077 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1078 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1079 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1080 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1081 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1082 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1083 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1084 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1085 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1086 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1087 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1088 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1089 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1090 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1091 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1092 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1093 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1094 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1095 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1096 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1097 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1098 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1099 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1100 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1101 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1102 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1103 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1104 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1105 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1106 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1107 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1108 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1109 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1110 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1111 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1112 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1113 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1114 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1115 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1116 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1117 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1118 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1119 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1120 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1121 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1122 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1123 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1124 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1125 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1126 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1127 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1128 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1129 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1130 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1131 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1132 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1133 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1134 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1135 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1136 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1137 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1138 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1139 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1140 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1141 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1142 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1143 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1144 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1145 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1146 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1147 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1148 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1149 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1150 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1151 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1152 | 18600092 | Association of platelet-derived growth factor-D gene polymorphism with ischemic stroke in a Chinese case-control study. |
| 1153 | 18600092 | Platelet-derived growth factor-D has been found to be involved in the pathogenesis of atherosclerosis, suggesting possible association between platelet-derived growth factor-D and the development of ischemic stroke. |
| 1154 | 18600092 | However, little information on the relationship between platelet-derived growth factor-D and stroke is currently available. |
| 1155 | 18600092 | The aim of this study was to investigate the association between platelet-derived growth factor-D genetic variation and the risk of ischemic stroke in a Chinese population. |
| 1156 | 18600092 | Platelet-derived growth factor-D C/G polymorphism at position +3166 (rs7950273) was detected by TaqMan SNP genotyping assay. |
| 1157 | 18600092 | Overall, the combined rates of platelet-derived growth factor- D CG and GG are 51% in patients in contrast with 46% in controls. |
| 1158 | 18600092 | There were no significant differences in the genotype frequencies of platelet-derived growth factor-D +3166 polymorphisms between the patients and controls with history or family history of hypertension or diabetes (P = 0.770). |
| 1159 | 18600092 | However, among people without history or family history of hypertension or diabetes, platelet-derived growth factor-D CG/GG is significantly more frequently expressed in patients (60%) than in controls (43%) (odds ratio 1.97; 95% confidence interval 1.19-3.26). |
| 1160 | 18600092 | Our study found that the G allele of rs7950273 of the platelet-derived growth factor-D gene is associated with higher risk of ischemic stroke in a Chinese population without history or family history of hypertension or diabetes. |
| 1161 | 18600092 | Future studies with larger and ethnically diverse populations are needed to further evaluate the platelet-derived growth factor-D polymorphism and stroke association, as well as its pathophysiological mechanisms. |
| 1162 | 18804536 | Simvastatin was reported to attenuate platelet-derived growth factor (PDGF)-induced vascular smooth muscle proliferation by up-regulation of cyclin dependent kinase (CDK) inhibitor p27, but had no effect on p16, p21, p53 expression. |
| 1163 | 18804536 | We also found that simvastatin inhibited phosphorylation of Rb, promoted expression of p53, p16, p21, p27 and decreased CDK2/4 activity. |
| 1164 | 18804536 | In conclusion, simvastatin inhibits VSMC proliferation in high glucose status, mimicking diabetes, inducing a G0/G1 phase cell cycle growth arrest by acting on multiple steps upstream of pRb, including inhibition of CDK2/4 expression and up-regulation of p53, p21, p16, and p27. |
| 1165 | 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). |
| 1166 | 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. |
| 1167 | 18923384 | Addition of active MMP-7 degraded this excess tenascin-C in vitro, a process that could be prevented by an exogenous MMP inhibitor. |
| 1168 | 18973985 | Angiopoietin-1, but not platelet-derived growth factor-AB, is a cooperative stimulator of vascular endothelial growth factor A-accelerated endothelial cell scratch closure. |
| 1169 | 18973985 | Human umbilical vein endothelial cells were isolated, cultured to confluence, and subjected to a scratch wound assay with the addition of vascular endothelial growth factor (VEGF)-A(165), platelet-derived growth factor (PDGF)-AB, angiopoietin-1 (ANG1), or ANG2 and all of their 16 possible combinations. |
| 1170 | 18973985 | VEGF-A(165) plus ANG1 was most effective at accelerating endothelial scratch closure. |
| 1171 | 18973985 | Thus, with respect to their effects on endothelial cells, a combination of VEGF-A with ANG1 is the most promising and is superior to combinations with PDGF-AB. |
| 1172 | 18973985 | Angiopoietin-1, but not platelet-derived growth factor-AB, is a cooperative stimulator of vascular endothelial growth factor A-accelerated endothelial cell scratch closure. |
| 1173 | 18973985 | Human umbilical vein endothelial cells were isolated, cultured to confluence, and subjected to a scratch wound assay with the addition of vascular endothelial growth factor (VEGF)-A(165), platelet-derived growth factor (PDGF)-AB, angiopoietin-1 (ANG1), or ANG2 and all of their 16 possible combinations. |
| 1174 | 18973985 | VEGF-A(165) plus ANG1 was most effective at accelerating endothelial scratch closure. |
| 1175 | 18973985 | Thus, with respect to their effects on endothelial cells, a combination of VEGF-A with ANG1 is the most promising and is superior to combinations with PDGF-AB. |
| 1176 | 19033819 | Platelet-derived growth factor (PDGF) stimulates proteoglycan synthesis and is strongly implicated in atherogenesis. |
| 1177 | 19105210 | The Marburg I variant (G534E) of the factor VII-activating protease determines liver fibrosis in hepatitis C infection by reduced proteolysis of platelet-derived growth factor BB. |
| 1178 | 19170096 | Recombinant human platelet-derived growth factor BB (rhPDGF-BB) and beta-tricalcium phosphate/collagen matrix enhance fracture healing in a diabetic rat model. |
| 1179 | 19170096 | Indeed, previous studies have found reduced platelet-derived growth factor (PDGF) levels in the fracture callus of diabetic rats, suggesting that local application of PDGF may overcome the negative effects of diabetes and promote fracture healing. |
| 1180 | 19170096 | Recombinant human platelet-derived growth factor BB (rhPDGF-BB) and beta-tricalcium phosphate/collagen matrix enhance fracture healing in a diabetic rat model. |
| 1181 | 19170096 | Indeed, previous studies have found reduced platelet-derived growth factor (PDGF) levels in the fracture callus of diabetic rats, suggesting that local application of PDGF may overcome the negative effects of diabetes and promote fracture healing. |
| 1182 | 19373754 | Platelet-derived growth factor (PDGF) and PDGF receptor expression and function in folliculostellate pituitary cells. |
| 1183 | 19373754 | Homo- and heterodimers of platelet-derived growth factor-A (PDGF-A) and PDGF-B chains are involved through PDGF alpha- and beta-receptors in the growth regulation of multiple normal and tumoural cell types as well as in tumour neovascularization. |
| 1184 | 19373754 | Rat somatotroph MtT-S and mouse corticotroph AtT20 tumor cells expressed only a part of the PDGF/PDGF receptor components whereas mouse gonadotroph alphaT3-1 and rat lactosomatotroph GH3 pituitary tumour cells contained neither PDGF nor PDGF receptors. |
| 1185 | 19373754 | To further characterize the role of PDGF in TtT/GF cells, the effect of PDGF-AB and -BB on growth and vascular endothelial growth factor-A (VEGF-A) release was studied. |
| 1186 | 19373754 | The PI3 kinase inhibitor LY 294002 blocked the increase in VEGF-A. |
| 1187 | 19373754 | Western immunoblotting confirmed the participation of key components of the PI3 kinase/Akt signal pathway (PDK1, Akt-Ser476) in PDGF-stimulated VEGF production. |
| 1188 | 19373754 | Thus the PDGF/PDGF receptor system is expressed in folliculostellate cells and is involved in VEGF regulation. |
| 1189 | 19373754 | Platelet-derived growth factor (PDGF) and PDGF receptor expression and function in folliculostellate pituitary cells. |
| 1190 | 19373754 | Homo- and heterodimers of platelet-derived growth factor-A (PDGF-A) and PDGF-B chains are involved through PDGF alpha- and beta-receptors in the growth regulation of multiple normal and tumoural cell types as well as in tumour neovascularization. |
| 1191 | 19373754 | Rat somatotroph MtT-S and mouse corticotroph AtT20 tumor cells expressed only a part of the PDGF/PDGF receptor components whereas mouse gonadotroph alphaT3-1 and rat lactosomatotroph GH3 pituitary tumour cells contained neither PDGF nor PDGF receptors. |
| 1192 | 19373754 | To further characterize the role of PDGF in TtT/GF cells, the effect of PDGF-AB and -BB on growth and vascular endothelial growth factor-A (VEGF-A) release was studied. |
| 1193 | 19373754 | The PI3 kinase inhibitor LY 294002 blocked the increase in VEGF-A. |
| 1194 | 19373754 | Western immunoblotting confirmed the participation of key components of the PI3 kinase/Akt signal pathway (PDK1, Akt-Ser476) in PDGF-stimulated VEGF production. |
| 1195 | 19373754 | Thus the PDGF/PDGF receptor system is expressed in folliculostellate cells and is involved in VEGF regulation. |
| 1196 | 19443196 | Ferulic acid augments angiogenesis via VEGF, PDGF and HIF-1 alpha. |
| 1197 | 19443196 | Using Western blot analysis and quantitative real-time polymerase chain reaction, we found that ferulic acid increased vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) expression in HUVECs. |
| 1198 | 19443196 | Furthermore, the amounts of hypoxic-induced factor (HIF) 1 alpha mRNA and protein, the major regulator of VEGF and PDGF, also showed up-regulation by ferulic acid. |
| 1199 | 19443196 | Moreover, inhibitors of extracellular-signal-regulated kinase 1/2 and phosphoinositide-3 kinase (PI3K) abolished the binding activity of HIF-1 alpha and the subsequent activation of VEGF and PDGF production by ferulic acid. |
| 1200 | 19443196 | This effect might be observed through the modulation of VEGF, PDGF and HIF-1 alpha. |
| 1201 | 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. |
| 1202 | 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. |
| 1203 | 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). |
| 1204 | 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. |
| 1205 | 19799585 | Vitreous and serum levels of vascular endothelial growth factor and platelet-derived growth factor and their correlation in patients with non-proliferative diabetic retinopathy and clinically significant macula oedema. |
| 1206 | 19881493 | In the retina, pericyte apoptosis and the formation of acellular capillaries, the most specific vascular pathologies attributed to hyperglycemia, is linked to the loss of platelet-derived growth factor (PDGF)-mediated survival actions owing to unknown mechanisms. |
| 1207 | 19881493 | Here we show that hyperglycemia persistently activates protein kinase C-delta (PKC-delta, encoded by Prkcd) and p38alpha mitogen-activated protein kinase (MAPK) to increase the expression of a previously unknown target of PKC-delta signaling, Src homology-2 domain-containing phosphatase-1 (SHP-1), a protein tyrosine phosphatase. |
| 1208 | 19881493 | This signaling cascade leads to PDGF receptor-beta dephosphorylation and a reduction in downstream signaling from this receptor, resulting in pericyte apoptosis independently of nuclear factor-kappaB (NF-kappaB) signaling. |
| 1209 | 19881493 | Unlike diabetic age-matched wild-type mice, diabetic Prkcd(-/-) mice did not show activation of p38alpha MAPK or SHP-1, inhibition of PDGF signaling in vascular cells or the presence of acellular capillaries. |
| 1210 | 19881493 | We also observed PKC-delta, p38alpha MAPK and SHP-1 activation in brain pericytes and in the renal cortex of diabetic mice. |
| 1211 | 20091922 | The objective of this study was to assess the effects of three specific concentrations of silicone resin particles (12 mum average diameter) in conjunction with either platelet-derived growth factor (PDGF-BB) or basic fibroblast growth factor (bFGF) on fibroblast cell proliferation, collagen synthesis, cell morphology, and migration through in vitro assays and a monolayer scratch wound model. |
| 1212 | 20091922 | PDGF and bFGF enhanced the proliferation of fibroblasts 5.7-fold and fivefold, respectively, while the addition of silicone particles had no significant effect on proliferation. |
| 1213 | 20091922 | Fibroblast migration was enhanced by the addition of both PDGF and bFGF compared to controls, although slower scratch wound closure rates were observed in the presence of particles compared to controls without particles. |
| 1214 | 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. |
| 1215 | 20610572 | PDGF beta-receptor kinase activity and ERK1/2 mediate glycosaminoglycan elongation on biglycan and increases binding to LDL. |
| 1216 | 20610572 | Structural characteristics of glycosaminoglycan (GAG) chains on PGs influence lipoprotein binding and are altered adversely by platelet-derived growth factor (PDGF). |
| 1217 | 20610572 | The signaling pathway for PDGF-mediated GAG elongation via the PDGF receptor (PDGFR) was investigated. |
| 1218 | 20610572 | Knockdown of PDGFRbeta using small interfering RNA demonstrated that PDGF mediated changes in PGs via PDGFRbeta. |
| 1219 | 20610572 | Downstream signaling to GAG hyperelongation was mediated through ERK MAPK and not phosphatidylinositol-3 kinase or phospholipase Cgamma. |
| 1220 | 20610572 | In high-fat-fed apolipoprotein E(-/-) mice, inhibition of PDGFRbeta activity by imatinib reduced aortic total lipid staining area by 35% (P < 0.05). |
| 1221 | 20659357 | Among them, keratinocyte growth factor and platelet-derived growth factor were highly expressed in the EPCs and were present at substantial levels in the EPC-injected dermal tissue. |
| 1222 | 20705622 | Oxidative stress is one of the major markers of inflammatory response and oxidative stress markers such as lipid peroxidation, thiobarbituric acid reactive substance (TBARS), Superoxide Dismutase (SOD), Catalase, G Peroxidase, G-S Peroxidase and plasma total antioxidant play a major role in the nonhealing of diabetic foot ulcers. |
| 1223 | 20705622 | Growth factors such as platelet-derived growth factor (PDGF), transforming growth factor (VEGF), and epidermal growth factor (EGF) are needed for normal wound repair, while proteases such as matrix metalloproteinase (MMP) and serine proteases found in chronic wounds delay the healing process. |
| 1224 | 20800279 | To examine if DAPT would interfere with vessel maturation, DAPT was also delivered with a combination of VEGF and platelet derived growth factor (PDGF). |
| 1225 | 20946955 | Epidermal growth factor (EGF) and platelet-derived growth factor (PDGF) signal through EGF and PDGF receptors, which are important receptor tyrosine kinases (RTKs). |
| 1226 | 20946955 | Growth hormone (GH) and prolactin (PRL) are four helical bundle peptide hormones that signal via GHR and PRLR, members of the cytokine receptor superfamily. |
| 1227 | 20946955 | We find that GH and EGF specifically synergize for activation of ERK in murine preadipocytes. |
| 1228 | 20946955 | The locus of this synergy resides at the level of MEK activation, but not above this level (i.e., not at the level of EGFR, SHC, or Raf activation). |
| 1229 | 20946955 | Furthermore, dephosphorylation of the scaffold protein, KSR, at a critical serine residue is also synergistically promoted by GH and EGF, suggesting that GH sensitizes these cells to EGF-induced ERK activation by augmenting the actions of KSR in facilitating MEK-ERK activation. |
| 1230 | 20946955 | Similarly specific synergy in ERK activation is also detected in human T47D breast cancer cells by cotreatment with PRL and PDGF. |
| 1231 | 20946955 | Consistent with this synergy, PRL and PDGF also synergized for c-fos-dependent transactivation of a luciferase reporter gene in T47D cells, indicating that events downstream of ERK activation reflect this signaling synergy. |
| 1232 | 21537407 | However, vascular complications result from imbalances caused by increases in systemic toxic metabolites, such as those that occur under conditions of hyperglycemia and dyslipidemia, and by reductions in endogenous protective factors such as insulin, vascular endothelial growth factor, and platelet derived growth factor. |
| 1233 | 21559360 | Platelet-derived growth factor induces Rad expression through Egr-1 in vascular smooth muscle cells. |
| 1234 | 21833587 | Deletion of platelet-derived growth factor receptor-β improves diabetic nephropathy in Ca²⁺/calmodulin-dependent protein kinase IIα (Thr286Asp) transgenic mice. |
| 1235 | 21969604 | Insulin exerts many of its metabolic actions via the canonical phosphatidylinositide 3 kinase (PI3K)/Akt pathway, leading to phosphorylation and 14-3-3 binding of key metabolic targets. |
| 1236 | 21969604 | We previously identified a GTPase-activating protein (GAP) for Rac1 called RhoGAP22 as an insulin-responsive 14-3-3 binding protein. |
| 1237 | 21969604 | Insulin increased 14-3-3 binding to RhoGAP22 fourfold, and this effect was PI3K dependent. |
| 1238 | 21969604 | Mutation of the catalytic arginine of the GAP domain of RhoGAP22 potentiated growth factor-stimulated Rac1 GTP loading. |
| 1239 | 21969604 | We propose that insulin and possibly growth factors such as platelet-derived growth factor may play a novel role in regulating cell migration and motility via the Akt-dependent phosphorylation of RhoGAP22, leading to modulation of Rac1 activity. |
| 1240 | 21993628 | Here we show that platelet-derived growth factor receptor (Pdgfr) signalling controls age-dependent β-cell proliferation in mouse and human pancreatic islets. |
| 1241 | 21993628 | With age, declining β-cell Pdgfr levels were accompanied by reductions in β-cell enhancer of zeste homologue 2 (Ezh2) levels and β-cell replication. |
| 1242 | 22048734 | On day 7 after treatment, AMD3100 was associated with higher circulating EPC and macrophage counts, and with significantly upregulated mRNA levels of stromal cell-derived factor 1 and platelet-derived growth factor B in the wound bed. |
| 1243 | 22076171 | Immunohistochemical results of the tumor were as follows: α-methylacyl-coenzyme A rasemase (AMACR) +++, vimentin +++, cytokeratin (CK) 18 +++, CD10 +++, S-100 protein +, MUC1 ++, MUC2 ++, MUC5AC ++, MUC6 ++, panCK Cam5.2 +, CK7 +, CK8 +, CK14 +, CK19 +, CK20 +, p53 +, HepPar1 +, CD68 +, platelet-derived growth factor-α (PDGFRA) +, PanCK AE1/3 -, PanCK WSS -, PanCK MNF115 -, CK 35BE12 -, CK5/6 -, EMA -, desmin -, smooth muscle antigen -, α-fetoprotein -, CEA -, estrogen receptor -, progesterone receptor -, HER2 -, p63 -, and KIT -. |
| 1244 | 22076171 | These results suggest that OPRCC can express colloidal iron, low molecular weight CKs, S100 protein, MUC1, MUC2, MUC5AC, MUC6, p53, PDGFRA, and HepPar1. |
| 1245 | 22092796 | Controls were db/db mice receiving platelet-derived growth factor + insulin-like growth factor-1 (group 5), topical placebo (NaCl 9 mg/mL) and insulin (group 6), placebo (group 7), and a nondiabetic group receiving placebo (group 8). |
| 1246 | 22859860 | Addition of adiponectin to quiescent porcine coronary artery SMCs increased both protein and DNA synthesis and concurrently activated ERK1/2 and Akt. |
| 1247 | 22859860 | By contrast, globular adiponectin, a truncated form of this protein, exhibited anti-mitogenic properties as indicated by the inhibition of protein and DNA synthesis in SMCs stimulated with platelet-derived growth factor (PDGF). |
| 1248 | 22859860 | Whereas globular adiponectin did not stimulate growth-related signal transduction pathways, it was able to block the PDGF-dependent phosphorylation of eukaryotic elongation factor 2 kinase, a regulator of protein synthesis. |
| 1249 | 23239217 | LAD; SIS; SSS; CT-LeSc) were also significantly higher in diabetic patients. |
| 1250 | 23239217 | In the per segment analysis, diabetics had a higher percentage of segments with plaque in every vessel (2.6/13.1/7.5/10.5% for diabetics vs. 1.4/7.1/3.3/4.4% for nondiabetics for LM, LAD, LCx, RCA respectively; p < 0.001 for all) and of both calcified (19.3 vs. 9.2%, p < 0.001) and noncalcified or mixed types (14.4 vs. 7.0%; p < 0.001); the ratio of proximal-to-distal relative plaque distribution (calculated as LM/proximal vs. mid/distal/branches) was lower for diabetics (0.75 vs. 1.04; p = 0.009). |
| 1251 | 23421427 | Treatment of VSMCs with PDGF (platelet-derived growth factor)-BB resulted in decreased expression of the contractile phenotype markers calponin and α-smooth muscle actin and up-regulation of the synthetic phenotype markers osteopontin and vimentin. |
| 1252 | 23421427 | Autophagy, as assessed by LC3 (microtubule-associated protein light chain 3 α; also known as MAP1LC3A)-II abundance, LC3 puncta formation and electron microscopy, was activated by PDGF exposure. |
| 1253 | 23494241 | As an illustration, we applied ROR to assess an association between HLA-DRB1 and type 1 diabetes (T1D), discovering SSVs of HLA-DRB1 with sequence data from the Wellcome Trust Case Control Consortium. |
| 1254 | 23557702 | Hyperglycemia is known to activate protein kinase C (PKC), affecting the expression and activity of growth factors such as vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF). |
| 1255 | 23557702 | VEGF and PDGF mRNA and protein expression were decreased in the muscles of diabetic Prkcd(+/+) mice and were normalized in diabetic Prkcd(-/-) mice. |
| 1256 | 23557702 | Furthermore, phosphorylation of VEGF receptor 2 (VEGFR2) and PDGF receptor-β (PDGFR-β) were blunted in diabetic Prkcd(+/+) mice but elevated in diabetic Prkcd(-/-) mice. |
| 1257 | 23557702 | The inhibition of VEGFR2 and PDGFR-β activity was associated with increased SHP-1 expression. |
| 1258 | 23577003 | We have provided an overview of functional BRET studies associated with the RTK superfamily involving: neurotrophic receptors [e.g., tropomyosin-related kinase (Trk) and p75 neurotrophin receptor (p75NTR)]; insulinotropic receptors [e.g., insulin receptor (IR) and insulin-like growth factor receptor (IGFR)] and growth factor receptors [e.g., ErbB receptors including the EGFR, the fibroblast growth factor receptor (FGFR), the vascular endothelial growth factor receptor (VEGFR) and the c-kit and platelet-derived growth factor receptor (PDGFR)]. |
| 1259 | 23577003 | In addition, we review BRET-mediated studies of other tyrosine kinase-associated receptors including cytokine receptors, i.e., leptin receptor (OB-R) and the growth hormone receptor (GHR). |
| 1260 | 23583575 | GPCR signalling is well known to proceed through several linear pathways involving activation of G proteins and their downstream signalling pathways such as activation of phospholipase C. |
| 1261 | 23583575 | In addition, GPCRs signal via transactivation of Protein Tyrosine Kinase receptors such as that for Epidermal Growth Factor (EGF) and Platelet-Derived Growth Factor (PDGF) where GPCR agonists mediate increase levels of phosphorylated Erk (pErk) the immediate downstream product of the activation of EGF receptor. |
| 1262 | 23583575 | It has recently been shown that this paradigm can be extended to include the GPCR transactivation of a Protein Serine/Threonine Kinase receptor, specifically the Transforming Growth Factor β Type I receptor (also known as Alk V) (TβRI) in which case GPCR activation leads to the formation of carboxy terminal polyphosphorylated Smad2 (phosphoSmad2) being the immediate downstream product of the activation of TβRI. |
| 1263 | 23583575 | In the example of proteoglycan synthesis stimulated by GPCR agonists such as thrombin and endothelin-1, the transactivation pathways for the EGF receptor and TβRI are both active and together account for essentially all of the response to the GPCRs. |
| 1264 | 23583575 | In contrast, signalling downstream of GPCRs such as increased inositol 1,4,5 trisphosphate (IP3) and intracellular calcium do not have any effect on GPCR stimulated proteoglycan synthesis. |
| 1265 | 23606982 | In particular, the effects of tight glucose control, ultrasound therapy, platelet-rich plasma (PRP), platelet-derived growth factor (PDGF), bone morphogenetic protein 2 (BMP-2), and allograft bone incorporation have been studied extensively. |
| 1266 | 23856609 | Platelet-derived growth factor C promotes revascularization in ischemic limbs of diabetic mice. |