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Gene Information
Gene symbol: VEGFA
Gene name: vascular endothelial growth factor A
HGNC ID: 12680
Synonyms: VEGF-A, VPF
Related Genes
Related Sentences
| # | PMID | Sentence |
| 1 | 22043302 | Here, we show that N-CAM ablation results in reduced vascular tuft formation due to reduced endothelial cell proliferation despite an elevation in VEGFA mRNA expression, whereas retinal developmental angiogenesis was unaffected. |
| 2 | 9374757 | In this study, we examined the regulation of VEGF expression in vascular smooth muscle cells (VSMC) by hyperglycemia as well as by angiotensin II (ANG II). |
| 3 | 9374757 | We also examined whether the 12-lipoxygenase (12-LO) product 12-hydroxyeicosatetraenoic acid (12-HETE) can alter VEGF expression, since 12-LO products of arachidonic acid have angiogenic properties, and ANG II as well as high glucose (HG, 25 mM) can increase 12-LO activity and expression in VSMC. |
| 4 | 10643294 | VEGF stimulates vascular endothelial cell proliferation by binding to a specific receptor named kinase insert domain-containing receptor/fetal liver kinase (KDR/FIk-1, KDR). |
| 5 | 10977134 | VEGF receptor expression was examined by RT-PCR, and activation of MAP kinase was examined with antibody against phospho-Elk-1 (Ser383). |
| 6 | 11018037 | Since connective tissue growth factor (CTGF) is a potent mitogen for fibrosis, extracellular matrix production, and angiogenesis, we have studied the effects and mechanism by which vascular endothelial growth factor (VEGF) regulates CTGF gene expression in retinal capillary cells. |
| 7 | 11018037 | In our study, VEGF increased CTGF mRNA levels in a time- and concentration-dependent manner in bovine retinal endothelial cells and pericytes, without the need of new protein synthesis and without altering mRNA stability. |
| 8 | 11018037 | VEGF activated the tyrosine receptor phosphorylation of KDR and Flt1 and increased the binding of phosphatidylinositol 3-kinase (PI3-kinase) p85 subunit to KDR and Flt1, both of which could mediate CTGF gene induction. |
| 9 | 11018037 | VEGF-induced CTGF expression was mediated primarily by PI3-kinase activation, whereas PKC and ERK pathways made only minimal contributions. |
| 10 | 11018037 | Furthermore, overexpression of constitutive active Akt was sufficient to induce CTGF gene expression, and inhibition of Akt activation by overexpressing dominant negative mutant of Akt abolished the VEGF-induced CTGF expression. |
| 11 | 11018037 | These data suggest that VEGF can increase CTGF gene expression in bovine retinal capillary cells via KDR or Flt receptors and the activation of PI3-kinase-Akt pathway independently of PKC or Ras-ERK pathway, possibly inducing the fibrosis observed in retinal neovascular diseases. |
| 12 | 11126403 | We sought to determine the effects of ACE inhibition on retinal VEGF expression and permeability in experimental diabetic retinopathy. |
| 13 | 11126403 | Angiotensin converting enzyme inhibitor treatment of diabetic rats reduced diabetes-associated changes in VEGF gene expression and vascular permeability. |
| 14 | 11274084 | This finding is important for three reasons: First, the decrease may result in reduced excitability of inner retinal neurons, as both peptides are known to modulate the excitability of these neurons; second, the decrease may be the consequence of a depressing and/or damaging effect by excitotoxins; and third, it may help explain why neovascularizations do not occur in this animal model, although VEGF is massively upregulated, as substance P is a very potent vascular growth factor. |
| 15 | 11290536 | In this study we report that hyperglycemic insult results in reduced levels of VEGF-A in the conceptus, which in turn, leads to abnormal VEGF receptor signaling, ultimately resulting in embryonic (vitelline) vasculopathy. |
| 16 | 11437859 | To determine whether circulating plasma vascular endothelial growth factor (VEGF) is elevated in the presence of diabetic microvascular complications, and whether the impact of angiotensin-converting enzyme (ACE) inhibitors on these complications can be accounted for by changes in circulating VEGF. |
| 17 | 11437859 | Changes in circulating VEGF cannot account for the beneficial effect of ACE inhibition on retinopathy. |
| 18 | 11571295 | Insulin and Alb-AGE stimulate VEGF mRNA and protein expression in retinal epithelial cells (ARPE-19). |
| 19 | 11571295 | Alb-AGE-induced VEGF expression is not modulated by the use of antioxidants, N-acetyl-l-cysteine or pyrrolidinedithiocarbamate, or by an inhibitor of phosphatidylinositol 3-kinase (PI3K), wortmannin. |
| 20 | 11571295 | Thus, stimulation of VEGF expression by Alb-AGE, through the activation of HIF-1, could play an important role in the development of diabetic retinopathy. |
| 21 | 11824650 | VEGF concentrations were lower and ACE activity was significantly higher in the sera of patients with type 1 diabetes than in the sera of those with type 2 diabetes. |
| 22 | 11694503 | We present novel findings demonstrating that stretch-induced VEGF expression in retinal capillary pericytes is mediated by phosphatidylinositol (PI) 3-kinase and protein kinase C (PKC)-zeta but is not mediated by ERK1/2, classical/novel isoforms of PKC, Akt, or Ras despite their activation by stretch. |
| 23 | 11694503 | Overexpression of DN ERK and Ras had no effect on VEGF expression in these cells. |
| 24 | 11694503 | Although stretch-induced PI 3-kinase activation increased both Akt phosphorylation and activity of PKC-zeta, VEGF expression was dependent on PKC-zeta but not Akt. |
| 25 | 11694503 | These results suggest that stretch-induced expression of VEGF involves a novel mechanism dependent upon PI 3-kinase-mediated activation of PKC-zeta that is independent of stretch-induced activation of ERK1/2, classical/novel PKC isoforms, Ras, or Akt. |
| 26 | 11935151 | Treatment with ACE-inhibitors attenuates retinal overexpression of VEGF-A in patients with proliferative diabetic retinopathy, probably by interference with a local effect of angiotensin II. |
| 27 | 11937295 | Promoter assay showed that the induction of VEGF was dependent on AP-1. |
| 28 | 12368225 | Cerivastatin, a hydroxymethylglutaryl CoA reductase inhibitor; pyrrolidinedithiocarbamate; or curcumin was found to completely prevent the AGE-induced increase in NF-kB and AP-1 activity, VEGF mRNA up-regulation, and the resultant increase in DNA synthesis in microvascular EC. |
| 29 | 12368225 | These results suggest that the AGE-RAGE interaction elicited angiogenesis through the transcriptional activation of the VEGF gene via NF-kB and AP-1 factors. |
| 30 | 12689920 | Furthermore, vascular endothelial growth factor receptor-1 (flt-1) and plasminogen activator inhibitor-1, two known Egr-1-responsive genes, were also upregulated in the presence of insulin or glucose. |
| 31 | 12775712 | The effects of insulin on vascular endothelial growth factor (VEGF) expression in cultured vascular cells and in angiogenesis were characterized. |
| 32 | 12775712 | Insulin increased VEGF mRNA levels in mouse aortic smooth muscle cells from 10(-9) to 10(-7) m with an initial peak of 3.7-fold increases at 1 h and a second peak of 2.8-fold after 12 h. |
| 33 | 12775712 | In contrast, the chronic effect of insulin on VEGF expression was partially inhibited by both LY294002 or PD98059 as well as by the overexpression of dominant negatives of PI 3-kinase or Ras. |
| 34 | 12775712 | Thus, unlike other cells, insulin can regulate VEGF expression by both IRS-1/PI 3-kinase-Akt cascade and Ras-MAPK pathways in aortic smooth muscle cells. |
| 35 | 12775712 | The in vivo results provide direct evidence that insulin can modulate hypoxia-induced angiogenesis via reduction in VEGF expression in vivo. |
| 36 | 12920663 | In seven diabetic patients with proliferative retinopathy, the most profound finding was a significant decrease of the PEDF level (mean value: 237 ng/ml), whereas VEGF levels were comparable to diabetic patients without proliferation (mean value: 3153; p = 0.003). |
| 37 | 15154937 | Urinary excretion of VEGF increased during the earlier stage of diabetic nephropathy and was significantly correlated with urinary albumin excretion. |
| 38 | 15245384 | Most have been associated with obesity, hyperinsulinaemia, type 2 diabetes, and chronic vascular disease; in addition, six adipocytokines--vascular endothelial growth factor, hepatocyte growth factor, leptin, tumour necrosis factor-alpha, heparin-binding epidermal growth factor-like growth factor, and interleukin-6--promote angiogenesis while one, adiponectin, is inhibitory. |
| 39 | 15258030 | It has a role in the pathogenesis of diabetic nephropathy and possibly in diabetic retinopathy (DR): in cultured retinal vascular cells CTGF is induced by VEGF-A. |
| 40 | 15259294 | To investigate (1) the mechanism of blood-retinal barrier breakdown induced by protein kinase C (PKC) activation (2) the relationship between PKC activation and vascular endothelial growth factor (VEGF) in 2-week streptozotocin-induced diabetes. |
| 41 | 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. |
| 42 | 15467196 | When choroidal explants were stimulated with CML-human serum albumin (HSA), its releasing effect was in the order VEGF>TNFalpha>PDGF-B. |
| 43 | 15555528 | EPA depresses vascular endothelial growth factor (VEGF)-specific tyrosine kinase receptor activation and expression. |
| 44 | 15774928 | Angiopoietin 1 and 2 interact with vascular endothelial growth factor (VEGF) to promote angiogenesis in animal and in vitro models. |
| 45 | 15812560 | Insulin-like growth factor-I is a growth factor for KSIMM cells with a maximum increase of 3H-thymidine incorporation of 130 +/- 27.6% (P < 0.05) similar to that induced by VEGF and with which it is additive (281 +/- 13%) (P < 0.05). |
| 46 | 15806157 | In addition, we show that the reduction in tumor angiogenesis is correlated with a reduced association of VEGF-A with its receptor VEGF-R2 on the tumor endothelium, implicating heparanase in the mobilization of matrix-associated VEGF. |
| 47 | 15840669 | Podocyte expression of alpha3(IV) collagen may involve the transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF) systems. |
| 48 | 15840669 | Cultured mouse podocytes were treated with various doses of AngII for selected periods of time, with or without inhibitors of TGF-beta and VEGF signalling, SB-431542 and SU5416, respectively. |
| 49 | 15840669 | Blockade of the endogenous VEGF activity by SU5416 prevented AngII-stimulated alpha3(IV) collagen production. |
| 50 | 15940042 | Moreover, we used a transgene mouse model with human vascular endothelial growth factor (VEGF) production in beta-cells under the control of the rat insulin promoter (RIP) to stimulate islet EC proliferation. |
| 51 | 15914522 | The aim of the study was to assess the effect of insulin treatment and glycemic control on plasma VEGF levels in children with new-onset diabetes. |
| 52 | 15914522 | Presence of hyperglycemia and/ or insulin deficiency in children with new-onset of diabetes is associated with plasma VEGF elevation, even at the outset of disease, and this can be mitigated by insulin therapy. |
| 53 | 16178982 | The expression of Ki67 was not correlated with microvessel number or VEGF expression. |
| 54 | 16186390 | Increase in the renal expression of VEGF-A, flk-1, Ang-2, an antagonist of angiopoietin-1, transforming growth factor-beta1, interleukin-6, and monocyte chemoattractant protein-1 was inhibited by endostatin peptide in diabetic mice. |
| 55 | 16186390 | Endogenous renal levels of endostatin were decreased in endostatin peptide-treated groups in parallel with VEGF-A. |
| 56 | 16299147 | High glucose stimulated a striking increase in BRPC gremlin mRNA levels in parallel with increases in mRNA for the growth factors vascular endothelial growth factor (VEGF), transforming growth factor beta (TGFbeta), and connective tissue growth factor (CTGF) and changes in other genes including fibronectin and plasminogen activator inhibitor-1 (PAI-1). |
| 57 | 16054135 | Earlier studies showed that the level of PEDF was decreased and VEGF was increased in proliferative diabetic retinopathy in human eyes. |
| 58 | 16368716 | Intravitreal injection of PEDF significantly reduced vascular hyper-permeability in rat models of diabetes and oxygen-induced retinopathy, correlating with the decreased levels of retinal inflammatory factors, including VEGF, VEGF receptor-2, MCP-1, TNF-alpha, and ICAM-1. |
| 59 | 16368716 | Moreover, down-regulation of PEDF expression by siRNA resulted in significantly increases of VEGF and TNF-alpha secretion in retinal Müller cells. |
| 60 | 16421022 | However, no study has yet reported concerning the effects of ET-1 receptor antagonist on the upregulated VEGF and ICAM-1 in morphologically intact diabetic retina. |
| 61 | 16421022 | The current study investigated the effect of ET(A) receptor antagonist (TA-0201; 1 mg kg(-1) day(-1)) on the expressions of VEGF and ICAM-1 in rat diabetic retina. |
| 62 | 16421022 | Thus, ET(A) receptor antagonist might be useful in preventing the progression of diabetic retinopathy, as evidenced by suppressing the increase in VEGF and ICAM-1 levels as well as leukostasis in morphologically intact diabetic retina. |
| 63 | 16428460 | While ATF3 failed to induce expressions of VEGF and VEGFR, it regulated those of CDK2, CDK4, p8, plasminogen activator inhibitor 1, integrin alpha1, subunit and matrix metalloprotease MMP13. |
| 64 | 16433046 | Vascular endothelial growth factor (VEGF), basic fibroblast growth factor (bFGF), transforming growth factor-beta1 (TGF-beta1), endothelin-1 (ET-1) and soluble c-kit ligand (sKL) are cytokines involved in embryogenesis. |
| 65 | 16436494 | These data suggest that the uncoupling of VEGF with NO enhances endothelial cell proliferation via the KDR pathway. |
| 66 | 16436494 | In addition, a VEGF mutant, which binds only KDR, induced extracellular signal-regulated kinase (ERK) activation, and inhibition of ERK completely blocked endothelial cell proliferation under this condition, suggesting a role of the KDR-ERK1/2 pathway on endothelial cell proliferation. |
| 67 | 16505232 | Overexpression of PKCbeta1 and -beta2, but not PKCalpha or -delta, also decreased Akt phosphorylation stimulated by vascular endothelial growth factor (VEGF). |
| 68 | 16505232 | Thus, activation of PKCbeta in endothelial cells and vascular tissue inhibits Akt activation by insulin and VEGF, inhibits Akt-dependent eNOS regulation by insulin, and causes endothelial dysfunction in obesity-associated insulin resistance. |
| 69 | 16506055 | We previously demonstrated that insulin stimulates vascular endothelial growth factor (VEGF) synthesis and secretion via phosphatidylinositol-3 kinase (PI3-K) and mitogen-activated protein kinase (MAPK) pathways in vascular smooth muscle cells (VSMC) from humans and from insulin-sensitive lean Zucker fa/+ rats. |
| 70 | 16506055 | As it is not known whether the effects of insulin on VEGF involve activation of hypoxia-inducible factor-1 (HIF-1), we aimed to evaluate: (1) whether insulin modulates HIF-1alpha protein synthesis and activity; (2) the insulin signalling pathways involved; and (3) the role of insulin resistance. |
| 71 | 16506055 | Using aortic VSMC taken from humans and Zucker rats and cultured in normoxia, the following were evaluated: (1) dose-dependent (0.5, 1, 2 nmol/l) and time-dependent (2, 4, 6 h) effects exerted by insulin on HIF-1alpha content in both nucleus and cytosol, measured by Western blots; (2) insulin effects on HIF-1 DNA-binding activity on the VEGF gene, measured by electrophoretic mobility shift assay; and (3) involvement of the insulin signalling molecules in these insulin actions, by using the following inhibitors: LY294002 (PI3-K), PD98059 (extracellular signal regulated kinase [ERK]), SP600125 (Jun N terminal kinase [JNK]), SB203580 (p38 mitogen-activated protein kinase) and rapamycin (mammalian target of rapamycin), and by detecting the insulin signalling molecules by Western blots. |
| 72 | 16506055 | In aortic VSMC from humans and Zucker fa/+ rats cultured in normoxia insulin increases the HIF-1alpha content in cytosol and nucleus via dose- and time-dependent mechanisms, and HIF-1 DNA-binding activity on the VEGF gene. |
| 73 | 16520919 | R-(+)-alpha-lipoic acid treatment reduced oxidative stress, normalised NFkappaB activation and angiopoietin-2 expression, and reduced vascular endothelial growth factor in the diabetic retina by 43% (p<0.0001). |
| 74 | 16873687 | In the matrigel, proangiogenic VEGF expression was decreased, while antiangiogenic thrombospondin-1 was upregulated in diabetic mice, regardless of the presence of RAGE. |
| 75 | 16891410 | Matrix metalloprotease type 9 (MMP-9) has been functionally implicated in VEGF activation, the induction and maintenance of chronic angiogenesis, and early stage tumor growth in a number of mouse models of cancer. |
| 76 | 16891410 | Transient depletion of neutrophils significantly suppressed VEGF:VEGF-receptor association, a signature of MMP-9 activity, and markedly reduced the frequency of initial angiogenic switching in dysplasias. |
| 77 | 16906650 | Here, we report that down-regulated VEGF expression in the diabetic rat heart is normalized by an endothelin ETA receptor antagonist, suggesting that endothelin antagonism may be a novel therapeutic strategy for diabetic heart. |
| 78 | 16955284 | The aims of this study were to determine effects of diabetes duration on myocardial ischemia/reperfusion (I/R) injury and test whether time-dependent differences in sensitivity of the streptozotocin diabetic rat heart to I/R are related to differences in vascular density, levels of vascular endothelial growth factor (VEGF) or endothelial nitric oxide synthase (eNOS) expression, NO formation, activation of Akt, and/or oxidative stress. |
| 79 | 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. |
| 80 | 17046555 | In the present study, we investigated the role of nicotinamide adenine dinucleotide phosphate (reduced form) (NADPH) oxidase in AGE-induced ROS intracellular generation and vascular endothelial growth factor (VEGF) expression in bovine retinal endothelial cells (BRECs). |
| 81 | 17046555 | Overall, these results demonstrate that AGEs induce intracellular ROS generation and VEGF expression in retinal endothelial cells through a PKC-dependent activation of NADPH oxidase. |
| 82 | 17049056 | In addition, significant activation of vascular endothelial growth factor in islet grafts on POD 7 correlated with development of massive newly formed microvessels, whose maturation is advanced on POD 14 with gradual diminution of HIF-1alpha. |
| 83 | 17065333 | In spite of normal pancreatic insulin content and beta-cell mass, mice with beta-cell-reduced VEGF-A expression had impaired glucose-stimulated insulin secretion. |
| 84 | 17065333 | Factors modulating VEGF-A expression may influence islet vascularity and, consequently, the amount of insulin delivered into the systemic circulation. |
| 85 | 17065350 | Increased expression of endothelin-1 (ET-1), vascular endothelial growth factor (VEGF), transforming growth factor (TGF)-beta, connective tissue growth factor (CTGF), and collagens IV and VI found in diabetic wild-type mice was attenuated in diabetic PKC-beta(-/-) mice. |
| 86 | 17065350 | Lack of PKC-beta can protect against diabetes-induced renal dysfunction, fibrosis, and increased expressions of Nox2 and -4, ET-1, VEGF, TGF-beta, CTGF, and oxidant production. |
| 87 | 17065523 | In addition, SK inhibitors were shown to block TNFalpha-induced expression of adhesion proteins, suppress VEGF-induced vascular leakage in an in vivo mouse model, and reduce retinal vascular leakage in the rat diabetic retinopathy model. |
| 88 | 17065527 | Retinal mRNA expression of VEGF, angiopoietin-1 and -2, and PDGF was examined at days P14 and P20. |
| 89 | 17065532 | This study was conducted to examine how VEGF and diabetes alter occludin phosphorylation and endothelial cell permeability. |
| 90 | 17065532 | VEGF stimulated the phosphorylation of occludin in primary retinal endothelial cells. |
| 91 | 17072586 | Defective EPC mobilisation in diabetes was associated with altered release of SDF-1 and VEGF and inability to upregulate muscle HIF-1alpha. |
| 92 | 16753211 | On the other hand, expression of vascular endothelial growth factor (VEGF), the other important factor in placental development, has been demonstrated to be regulated by PPARgamma in vascular smooth muscle cells. |
| 93 | 17303801 | Nevertheless, CTGF promoted vascular endothelial growth factor (VEGF) gene expression by hyalocytes and BRPEs. |
| 94 | 17437639 | The levels of interleukin-1beta (IL-1beta) and vascular endothelial growth factor (VEGF) were elevated by 30% and 110% respectively, and the nuclear transcription factor (NF-kB) was activated by 2 fold. |
| 95 | 17445799 | Here, we investigate the role of Hepatocyte growth factor-Regulated tyrosine kinase Substrate (Hrs), a regulator of RTK trafficking, in VEGF and insulin signaling. |
| 96 | 17445799 | We show that the UIM domain is required for Hrs phosphorylation in response to VEGF, but not to insulin. |
| 97 | 17470563 | Conversely, RARalpha decreases expression of vascular endothelial growth factor (VEGF)/vascular permeability factor. |
| 98 | 17229797 | To investigate the expression of the hypoxia-inducible factor-1alpha (HIF-1alpha) and the protein products of its target genes vascular endothelial growth factor (VEGF), erythropoietin (Epo) and angiopoietins (Angs), and the antiangiogenic pigment epithelium-derived factor (PEDF) in proliferative diabetic retinopathy (PDR) epiretinal membranes. |
| 99 | 17586470 | Metallothionein (MT) is effective in the prevention of diabetic cardiomyopathy, and hypoxia-inducible factor-1 (HIF-1) is known to control vascular endothelial growth factor (VEGF) gene expression and regulate angiogenesis in diabetic hearts. |
| 100 | 17641742 | Gal-3(-/-) mice showed significantly less diabetes-mediated iBRB dysfunction, junctional disruption, and VEGF expression changes than their WT counterparts. |
| 101 | 17653050 | To investigate the effect of PEDF and vascular endothelial growth factor (VEGF) on leukostasis, the adhesion of monocytes to human umbilical vein endothelial cells (HUVECs) was assayed in vitro. |
| 102 | 17653050 | In vitro studies showed that exposure of HUVECs to VEGF increased the number of adhering monocytes, and PEDF inhibited the VEGF-induced leukostasis in a dose-dependent manner. |
| 103 | 17578883 | The detailed analysis of molecular markers revealed fibroblast growth factor-4 and vascular endothelial growth factor as possible mediators of the systemic effect of Wnt10b transgene expression. |
| 104 | 17823371 | In the absence of ischemia, DM mice had increased VEGF (NC versus DM: 26.6+/-2.6 versus 53.5+/-8.8 pg/mg protein; P<0.05), decreased soluble and membrane-bound VEGFR-1 (NC versus DM: 1.44+/-0.30 versus 0.85+/-0.08 and 1.03+/-0.10 versus 0.72+/-0.10, respectively; P<0.05), decreased phospho-AKT/AKT and phospho-endothelial NO synthase/endothelial NO synthase (NC versus DM: 0.76+/-0.2 versus 0.38+/-0.1 and 0.36+/-0.06 versus 0.25+/-0.04, respectively; P<0.05), and no change in VEGFR-2. |
| 105 | 17971009 | Reduction in Hif-1alpha levels results in decreased DNA-binding activity and in decreased expression of several Hif-1 target genes, including vascular endothelial growth factor, heme oxygenase-1, and inducible nitric oxide synthase. |
| 106 | 18318806 | Mice were killed 3, 6, and 12 days after skin injury to measure vascular endothelial growth factor (VEGF) mRNA expression and protein synthesis, to assay angiogenesis and tissue remodeling through histological evaluation, and to study CD31, Angiopoietin-1 and Transglutaminase-II. |
| 107 | 18056916 | Arterial hypertension (HT) has been reported in all studies involving bevacizumab, an antiangiogenic agent designed to target vascular endothelial growth factor (VEGF). |
| 108 | 18268046 | In addition, PPAR alpha- and PPAR gamma-induced in vitro and in vivo angiogenesis may be significantly decreased by inhibiting VEGF activity. |
| 109 | 18268046 | These findings demonstrate that PPAR alpha and PPAR gamma activation stimulates neoangiogenesis through a VEGF-dependent mechanism. |
| 110 | 18322021 | In cultured primary human renal mesangial cells (HMC), the high-glucose medium-induced upregulation of VEGF and MCP-1 was largely blocked by PEDF. |
| 111 | 18387670 | Moreover, we found that maternal diabetes causes decreased expression of genes involved in the oxidative stress defense system (CuZnSOD in non-malformed D11 embryos, MnSOD at all gestational time points, ECSOD and Gpx-1 at GD11-GD15, CAT and Gpx-2 at GD15), decreased expression of Pax-3 at GD11, and increased expression of Vegf-A at all gestational time points. |
| 112 | 18078386 | Finally, we investigated VEGF (vascular endothelial growth factor) mRNA and protein levels, eNOS (endothelial NO synthase) expression and VEGFR-1 and VEGFR-2 (VEGF receptor-1 and -2 respectively) immunostaining. |
| 113 | 18078386 | In conclusion, our results provide strong evidence that Ang-1 gene transfer improves the delayed wound repair in diabetes by inducing angiogenesis in a VEGF-independent manner. |
| 114 | 18452614 | Of the proangiogenic factors, VEGF-A and VEGF receptor-2 (VEGFR-2) mRNA expression increased significantly (P < 0.05) in healthy skeletal muscle 6 h post exercise. |
| 115 | 18465359 | On the other hand, acute abundance of (exogenously administered) insulin and IGF-1 enhances ischaemia-induced VEGF expression. |
| 116 | 18525005 | Expression of endothelial nitric oxidase synthase was reduced and that of VEGF was markedly elevated in CaMTg mice kidney compared with nontransgenic mice. |
| 117 | 18599600 | Inhibitor studies revealed a strong functional dependence of troglitazone- and L165,041-induced VEGF expression on p38 and p42/44 mitogen-activated protein kinase (MAPK) activation in keratinocytes. |
| 118 | 18599600 | Functional ablation of PPARbeta/delta and PPARgamma from keratinocytes by small interfering RNA did not abrogate L165,041- and troglitazone-induced VEGF biosynthesis and suggested VEGF induction as a pleiotropic, PPAR-independent effect of both drugs in the cells. |
| 119 | 18599600 | In accordance with the in vitro situation, we found activated p38 MAPK in wound keratinocytes from acute wounds of rosiglitazone- and troglitazone-treated diabetic obese/obese mice, whereas keratinocyte-specific VEGF protein signals were only prominent upon troglitazone treatment. |
| 120 | 18563560 | With supplementation of taurine in diet, lower expression of GFAP and VEGF while higher expression of GLAST, GS and GAD in retina of diabetic rats were determinated by RT-PCR, Western-blotting and immunofluorescence (P < 0.05). |
| 121 | 19107135 | In this study, we showed that blockade of Ang II attenuates vascular endothelial growth factor (VEGF)-mediated BRB breakdown in DR. |
| 122 | 19107135 | Ang II induced VEGF expression in retinal endothelial cells accompanied by loss of tight junction proteins. |
| 123 | 19107135 | However, the blockade of Ang II by perindopril, an angiotensin converting enzyme (ACE) inhibitor, inhibited upregulation of VEGF, and prevented the loss of tight junction proteins. |
| 124 | 19150609 | It significantly inhibited angiogenesis induced by vascular endothelial growth factor in a rabbit cornea model as well as the swelling of mouse feet in an anti-type II collagen antibody-induced arthritis model. |
| 125 | 19236815 | Although the VEGF is expressed in an early-stage diabetic retina, whether it directly up-regulates ICAM-1 in retinal endothelial cells (ECs) is unknown. |
| 126 | 19236815 | In this study, we provided a new mechanism to explain that VEGF does up-regulate the expression of ICAM-1 in retinal ECs. |
| 127 | 19236815 | When eNOS was blocked by L-NAME or PI3K was blocked by LY294002, the basal level of NO production and the increment of NO caused by VEGF could be significantly decreased. |
| 128 | 19236815 | ROS-NO coupling in the retinal endothelium may be a new mechanism that could help to explain why VEGF induces ICAM-1 expression and the resulting leukostasis in diabetic retinopathy. |
| 129 | 19188426 | Furthermore, we investigated other possible mechanisms involved in this pathogenesis: alterations in the levels of vascular endothelial growth factor (VEGF) or phosphorylated Smad2 (the latter can be induced by both glycation products and VEGF). |
| 130 | 19286667 | Knockdown of either DHFR or GTPCH1 attenuated vascular endothelial growth factor (VEGF)-induced eNOS activity and NO production; these effects were recovered by supplementation with BH4. |
| 131 | 19286667 | DHFR but not GTPCH1 knockdown inhibited VEGF-induced dephosphorylation of eNOS at the inhibitory site serine 116; these effects were recovered by supplementation with BH4. |
| 132 | 19404486 | Rat retinal capillary endothelial cells (RRCECs) were infected with rAAV2-NTF2, or with a vector expressing siRNA targeted against NTF2, to assess the effects of overexpression and inhibition of NTF2 on vascular endothelial growth factor (VEGF) expression (mRNA and protein). |
| 133 | 19319465 | BCAA treatment significantly suppressed glucose- and insulin-induced in vitro angiogenesis in the presence of VEGF. |
| 134 | 19398755 | In contrast to VEGF blockade, interruption of M-CSF inhibition did not promote rapid vascular regrowth. |
| 135 | 19389828 | PRRB suppressed the activation of ERK and the production of VEGF, but not ICAM-1, in AT1-R-deficient diabetic mice. |
| 136 | 19539633 | This diabetic milieu accelerates cell proliferation, at least in part, through TGFbeta/Alk1-smad1/5 and probably involving VEGF as well as pro-migratory MMP2 downstream of Alk1. |
| 137 | 19553613 | Retinal VEGF and TNF-alpha levels and NF-kappaB activity were measured by ELISA. |
| 138 | 19685553 | Further, retinal 8-OHdG, p22phox and VEGF levels and NADPH oxidase activity were increased, and BRB was broken in diabetic rats. |
| 139 | 19558529 | Diabetic mice also showed impaired ischaemia-induced upregulation of vascular endothelial growth factor (VEGF), hypoxia-inducible factor (HIF)-1 alpha and interleukin-1 beta, an exaggerated increase in matrix metalloproteinase (MMP)-2 and -9 and a suppressed increase in tissue inhibitor of matrix metalloproteinase (TIMP)-1. |
| 140 | 19675133 | Our results demonstrated that systemic blockade of VEGF by dRK6 had deleterious effects on the heart in an animal model of type 2 diabetes; dRK6 induced downregulation of the VEGFR-2 and Akt-eNOS axis and enhancement of oxidative stress. |
| 141 | 19848322 | VEGF receptor 2 mRNA expression was tested with RT-PCR. |
| 142 | 19376168 | We co-expressed human vascular endothelial growth factor (hVEGF) and human interleukin-1 receptor antagonist (hIL-1Ra) after transduction of human islets with Adv-hVEGF-hIL-1Ra. |
| 143 | 19376168 | There was dose and time dependent expression of hVEGF and hIL-1Ra or hHGF and hIL-1Ra by islets, which led to decrease in caspase-3 activity and apoptosis induced by a cocktail of TNF-alpha, IL-1beta and IFN-gamma. |
| 144 | 19694557 | As determined by immunohistochemistry, VEGF-A(165) significantly increased the number and size of the capillaries in various compartments of the eyes. 15-LO-1 efficiently inhibited VEGF-A(165)-induced neovascularization and pathological changes by reducing VEGF-A(165) mRNA and protein expression, determined by RT-PCR, ELISA, and immunohistochemistry. 15-LO-1, which produces endogenous ligands for peroxisome proliferator-activated receptor-gamma (PPARgamma), also prevented VEGF-A(165)-induced expression of PPARgamma and VEGF receptor-2, as measured by quantitative RT-PCR. |
| 145 | 19997642 | In PDR patients, the elevation of VEGF was significantly correlated with the three factors: IL-6, IL-8, and MCP-1, while no significant correlation was observed in CRVO patients. |
| 146 | 20011081 | In HUVECs, EC-SOD at 100 ng/ml significantly suppressed VEGF-induced proliferation and tube formation, but not VEGF-induced migration. |
| 147 | 19626038 | This increased rate of closure of the two EPO-treated wounds in diabetic rats was associated with increased MVD, VEGF, and HP contents, and a reduced extent of apoptosis. |
| 148 | 19862499 | In diabetic mice, high-dose avosentan treatment significantly attenuated the glomerulosclerosis index, mesangial matrix accumulation, glomerular accumulation of the matrix proteins collagen IV, and renal expression of genes encoding connective tissue growth factor, vascular endothelial growth factor, transforming growth factor beta and nuclear factor kappaB (p65 subunit). |
| 149 | 19373754 | The PI3 kinase inhibitor LY 294002 blocked the increase in VEGF-A. |
| 150 | 19216096 | VEGF may potently promote growth of endothelial cells and formation of new vessels implicated in proliferative retinopathy. s-Fas could be involved in advancement of apoptotic changes in retinopathy and high levels of b-FGF, and ADM may be compensatorily neuroprotective and vasculoprotective. |
| 151 | 19436948 | Only TAFI correlated with VEGF in MAU. |
| 152 | 19759273 | Chronic high-glucose-based PDF exposure resulted in increased vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) expression, accumulation of advanced glycation end-products (AGEs), and up-regulation of the receptor for AGE (RAGE), which were ameliorated in the icodextrin-based PDF group. |
| 153 | 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. |
| 154 | 20375116 | Taken together, increased podocyte GLUT1 expression in diabetic mice does not contribute to early diabetic nephropathy; surprisingly, it protects against mesangial expansion and fibronectin accumulation possibly by blunting podocyte VEGF increases. |
| 155 | 20515763 | Exogenous EPO at pharmacologic levels leads to suppression of VEGF and in turn, restoration of the normal functions of BRB in a time-dependent manner. |
| 156 | 20515763 | In the diabetic retina, the same level of exogenous EPO that inhibits VEGF also exerted neuronal protection. |
| 157 | 19903865 | HUVECs in 25 mmol/l glucose showed increased p300 production accompanied by increased binding of p300 to ET-1 and FN promoters, augmented histone acetylation, H2AX phosphorylation, activation of multiple transcription factors, and increased mRNA expression of vasoactive factors and ECM proteins. p300 overexpression showed a glucose-like effect on the mRNA expression of ET-1, VEGF, and FN. |
| 158 | 20445124 | AP-1, the downstream transcription factor of ERK1/2, was also activated, and VEGF became highly regulated in a similar trend. |
| 159 | 20445124 | U0126, an inhibitor of ERK1/2, also downregulated VEGF expression, in addition to ERK1/2 and AP-1 activity. |
| 160 | 20538658 | The decreased levels of blood VEGF after an intravitreal injection of bevacizumab indicate that bevacizumab enters the general circulation and may also affect the PEDF levels. |
| 161 | 20547975 | The effect of 4E-BP1 and 4E-BP2 gene deletion on VEGF expression was examined in mice and in mouse embryo fibroblasts (MEFs). |
| 162 | 20547975 | Hyperglycemia induces VEGF expression through cap-independent mRNA translation mediated by increased expression of 4E-BP1. |
| 163 | 20566666 | Simvastatin significantly upregulated PGC-1alpha (P < 0.01), subsequently decreased Deltapsim (P < 0.05) and ROS generation (P < 0.01), inhibited PARP activation (P < 0.01), and further reduced VEGF expression (P < 0.01) and p38 MAPK activity (P < 0.01). |
| 164 | 20570185 | Immunohistochemistry for endothelial cell markers (CD34 and von Willebrand Factor); real-time reverse transcription polymerase chain reaction (RT-PCR) to quantify arterial wall expression of vascular endothelial growth factor (VEGF); enzyme-linked immunosorbent assay (ELISA) to assess blood VEGF; flow cytometry to detect circulating endothelial cells (CECs). |
| 165 | 20599775 | The PKCbeta/HuR activation was accompanied by enhanced VEGF protein expression that was, again, blunted by the PKCbeta inhibitor. |
| 166 | 18303668 | Strict control of blood glucose by insulin could decrease VEGF expression in retina and protect retinal vessels from impairing in early STZ-diabetic rats. |
| 167 | 18378570 | Prior studies have implicated oxidative stress and NADPH oxidase-mediated activation of signal transducer and activator of transcription 3 (STAT3) in diabetes-induced increases in expression of vascular endothelial growth factor (VEGF) and intercellular adhesion molecule (ICAM)-1 and breakdown of the blood-retinal barrier (BRB). |
| 168 | 18378570 | These studies showed that simvastatin blocks diabetes or high-glucose-induced increases in VEGF and ICAM-1 and preserves the BRB by a process involving blockade of diabetes/high-glucose-induced activation of STAT3 and NADPH oxidase. |
| 169 | 18709948 | SDF-1 may be correlated with VEGF in angiogenesis in PDR. |
| 170 | 19234337 | Apocynin also blocked CCL2 production in endothelial cells (ECs), retinal microglia, and Müller cells stimulated with TNF-alpha, VEGF, or LPS. |
| 171 | 19557019 | BRECs were then treated with 100 nM insulin for 24 h or not, and cells were prepared for the determination of VEGF mRNA expression by real-time PCR. |
| 172 | 19557019 | Insulin or high glucose alone markedly increased VEGF mRNA and protein levels in BRECs (P<0.05, two-way ANOVA). |
| 173 | 19557019 | However, the combination of insulin and high glucose displayed a weaker effect in promoting VEGF expression than did insulin alone (P<0.05, t-test). |
| 174 | 19557019 | Pretreatment of cells with PI3-K inhibitor significantly (P<0.05, one-way ANOVA) suppressed the insulin-induced VEGF expression; neither pretreatment with the PKC inhibitor nor with the P42/p44 MAPK inhibitor showed an effect on the expression of VEGF at the mRNA or protein level (P>0.05, one-way ANOVA). |
| 175 | 19557019 | Both insulin and high glucose can markedly increase VEGF expression in BRECs at the mRNA and protein level. |
| 176 | 20667614 | We produced a fusion protein (CBD-VEGF) consisting of VEGF and a collagen-binding domain (CBD), which allowed VEGF to bind to collagen. |
| 177 | 20674013 | In this study, we analised the expression of VEGF and its receptors VEGFR-1 (Flt-1) and VEGFR-2 (KDR) in placentas from mildly hyperglycemic women. |
| 178 | 20667471 | Blockade of AT2, but not AT1, prevented increase in VEGF synthesis by inhibiting translation of VEGF mRNA in renal cortex. |
| 179 | 20667471 | Acute hyperglycemia increased VEGF expression in wild type but not in AT2 knockout mice. |
| 180 | 20667471 | To confirm results obtained with PD123319, we induced hyperglycemia in AT2 knockout mice and found that in the absence of AT2, translational control of VEGF expression by hyperglycemia was abolished. |
| 181 | 20667471 | Our data show that acute hyperglycemia stimulates Ang II synthesis in murine kidney cortex, this leads to AT2 activation and stimulation of VEGF mRNA translation, via the Akt-mTOR-p70(S6K) signaling pathway. |
| 182 | 20039857 | These results suggest that the diabetes-mediated increase in CTGF upregulates VEGF and TGF-?(2) expression and induces apoptosis in the retina. |
| 183 | 20626511 | Expression of ERK protein, an activator of VEGF-induced cell proliferation, was decreased. |
| 184 | 20408853 | A mouse model of incisional wound treated with NAC resulted in lower levels of tissue oxidative stress, higher levels of tissue glutathione, and downregulation of iNOS expression coupled with upregulation of VEGF expression, producing an overall favourable clinical outcome of higher WBS and a shorter wound-healing period both in diabetic and nondiabetic mice. |
| 185 | 20876710 | Treatment with salsalate significantly decreased the intima-to-media ratio and upregulated the expression of aortic endothelial nitric oxide synthase (eNOS), phosphorylated eNOS (p-eNOS) (ser 1177), and manganese superoxide dismutase (MnSOD) and reduced serum interleukin (IL)-6 with concomitant downregulation of nuclear factor (NF) ?B subunit p65 and vascular endothelial growth factor (VEGF) expression in the balloon-injured carotid artery of female Zucker fatty rats. |
| 186 | 20876710 | The beneficial effect of salsalate on vascular injury was associated with upregulation of eNOS, p-eNOS, and MnSOD, which reduce oxidative stress and have anti-inflammatory properties, as evidenced by reduction in serum IL-6 and the downregulation of VEGF and NF?B, which promote inflammation without changing glucose levels. |
| 187 | 20653693 | Retinal expression of VEGF was inhibited 1 week and 1 month after injection (P < 0.01, paired t-test), and the expression of CD34 was not obviously inhibited until 2 months after injection (P < 0.05, paired t-test). |
| 188 | 21139695 | Retinal transfection with the hPEDF gene construct led to sustained hPEDF gene expression for 6 months, significantly suppressing VEGF mRNA expression in the retina after 1, 3, and 6 months of diabetes induced by STZ compared with paired controls. |
| 189 | 21139695 | The effect is associated with downregulation of retinal VEGF mRNA and ICAM-1 expression and a reduction in the loss of retinal occludin induced by diabetes. |
| 190 | 20501654 | Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo. |
| 191 | 20501654 | We identified VEGF-A as a putative target of miR-93 in the kidney with a perfect complementarity between miR-93 and the 3'-untranslated region of vegfa in several species. |
| 192 | 20501654 | When cotransfected with a luciferase reporter construct containing the mouse vegfa 3'-untranslated region, expression of miR-93 markedly decreased the luciferase activity. |
| 193 | 21151599 | FDP-lysine accumulation was associated with the induction of HO-1, no change in GFAP, a decrease in protein levels of the potassium channel subunit Kir4.1, and upregulation of transcripts for VEGF, IL-6, and TNF-?. |
| 194 | 20564543 | Most studies reviewed have focused on vascular endothelial growth factor (VEGF)/vascular endothelial growth factor receptor 2 (VEGFR-2) signaling for endothelial response processes and have led to the identification of many potential antiangiogenic agents. |
| 195 | 19765632 | These data show that: (1) HG increases AGT synthesis and activation of renin and ACE by MCTs, leading to local production of Ang I and Ang II. (2) Ang II activates endogenous AT1 and stimulates synthesis of VEGF. (3) HG activation of ERK starts within minutes and lasts for up to 24h. |
| 196 | 19765632 | Early ERK activation is involved in AGT upregulation and sustained ERK activation, mediated via AT1, is responsible for VEGF synthesis. |
| 197 | 21245960 | Both mRNA and protein levels of CHOP, TNF-?, and VEGF in the retina of diabetic rats were remarkably reduced in P58(IPK)-transfected rats. |
| 198 | 19404567 | The data obtained in this study indicate that activation of Rac1 GTPase contributes to VEGF-induced endothelial cell hyperpermeability. |
| 199 | 20144181 | Liver tissue was recovered at the same time points for correlative histology, including: hematoxylin and eosin, hypoxia-inducible factor (HIF1?), Terminal deoxynucleotidyl transferase (TdT)-mediated dUTP-biotin nick end labeling (TUNEL), vascular endothelial growth factor (VEGF), and von Willebrand Factor immunohistochemistry. |
| 200 | 21189286 | In cultured lung epithelial cells, insulin reduced VEGF expression and transcriptional activity of HIF-2 on VEGF promoter in an mTOR-dependent manner. |
| 201 | 20070983 | The results showed that pretreatment of MSCs with a recombinant netrin-1 protein markedly augmented the angiographic score and capillary density, improved function of the ischemic limb, and increased levels of VEGF in the plasma and damaged tissues. |
| 202 | 21193740 | Increased glucose augmented expression of BMP-2 and BMP-4; the BMP inhibitors matrix Gla protein (MGP) and Noggin; activin-like kinase receptor (ALK)1, -2, -3 and -6; the BMP type 2 receptor; and the vascular endothelial growth factor in human aortic endothelial cells (HAECs). |
| 203 | 20890241 | Intravitreal bevacizumab injection may lead to a decrease in the intraocular and systemic concentrations of VEGF, suggesting a local and potentially a systemic effect on VEGF but may have no effect on apelin. |
| 204 | 20890241 | Apelin may be associated with the development of epiretinal membranes in proliferative diabetic retinopathy and may not directly correlate with VEGF. |
| 205 | 21437112 | Curcumin has been reviewed for its multiple molecular action on inhibiting tumor angiogenesis via its mechanisms of cyclooxygenase (COX)-2, and vascular endothelial growth factor (VEGF) inhibition. |
| 206 | 21242957 | VHL-knockout islets had decreased GLUT2, but increased glucose transporter 1 and vascular endothelial growth factor expression. |
| 207 | 17522264 | Ruboxistaurin is an inhibitor of the beta isoform of protein kinase C (PKC-beta) that reduces the actions of vascular endothelial growth factor (VEGF) and attenuates the progression of diabetic retinopathy. |
| 208 | 21286681 | We investigated the association of diabetes and sepsis with various endothelial activation biomarkers of cell adhesion (E-selectin, vascular cell adhesion molecule 1 [VCAM-1] and intercellular adhesion molecule 1 [ICAM-1]), coagulation (plasminogen activator inhibitor 1 [PAI-1]) and VEGF signalling (soluble fms-like tyrosine kinase-1 [sFLT-1]). |
| 209 | 21318407 | It also led to increased VEGF receptor 2 and semaphorin3a levels, as well as nephrin and matrix metalloproteinase-2 downregulation, whereas circulating VEGF-A levels were similar to those in control diabetic mice. |
| 210 | 21329734 | Visfatin induced the expression of hypoxia-inducible factor 1? (HIF1?) and vascular endothelial growth factor (VEGF) in human endothelial cells. |
| 211 | 21329734 | The visfatin-induced increase in VEGF expression was also eliminated by RNA interference-mediated knockdown of the 70-kDa ribosomal protein S6 kinase (p70S6K), a downstream target of mTOR. |
| 212 | 21296064 | It also inhibited degradation of occludin, an important tight junction protein, and blocked VEGF-induced disruption of its linear pattern at the cell border. |
| 213 | 12574231 | An IGFBP-3 mutant, which binds IGFs normally but has a substituted mid-region domain, lost the ability to inhibit VEGF actions. |
| 214 | 20185806 | CD11c(+) eATMPhis expressed a mixed M1/M2 profile, with some M1 transcripts upregulated (IL-12p40 and IL-1beta), others downregulated (iNOS, caspase-1, MCP-1, and CD86), and multiple M2 and matrix remodeling transcripts upregulated (arginase-1, IL-1Ra, MMP-12, ADAM8, VEGF, and Clec-7a). |
| 215 | 21409414 | AGEs reduced the production of claudin-5 in PnMECs by increasing autocrine signalling through vascular endothelial growth factor (VEGF) secreted by the PnMECs themselves. |
| 216 | 21409414 | Furthermore, AGEs increased the amount of fibronectin, collagen type IV and TIMP-1 in pericytes through a similar upregulation of autocrine VEGF and transforming growth factor (TGF)-? released by pericytes. |
| 217 | 20671964 | Furthermore, siRNA mediated ERK5 gene knockdown suppressed MEF2C and KLF2 expression and increased VEGF expression and angiogenesis. |
| 218 | 20671964 | On the other hand, constitutively active MEK5, an activator of ERK5, increased ERK5 activation and ERK5 and KLF2 mRNA expression and attenuated basal- and glucose-induced VEGF mRNA expression. |
| 219 | 20671964 | These results indicated that ERK5 depletion contributes to glucose induced increased VEGF production and angiogenesis. |
| 220 | 20200317 | Furthermore, we observed that HMGB1 administration restored the blood flow recovery and capillary density in the ischemic muscle of diabetic mice, that this process was associated with the increased expression of vascular endothelial growth factor (VEGF), and that HMGB1-induced angiogenesis was significantly reduced by inhibiting VEGF activity. |
| 221 | 20332345 | Overexpression of Nox4 increased basal level of ROS generation, HIF-1alpha, and VEGF expression in RCECs. |
| 222 | 20332345 | Finally, depletion of Nox4 by adenovirus-delivered Nox4 small interfering RNA significantly decreased retinal NADPH oxidase activity and VEGF expression and reduced retinal vascular premeability in db/db mice. |
| 223 | 20332345 | Activation of Nox4 plays an important role in high-glucose- and hypoxia-mediated VEGF expression and diabetes-induced BRB breakdown. |
| 224 | 21196299 | Intravitreal injection of EPO performed 24 h prior to sacrifice significantly reduced TNF-alpha and IL-1beta production while moderately attenuating IL-6 and VEGF in the retinas of streptozotocin-induced diabetic rats. |
| 225 | 21293011 | Tissue kallikrein inhibited vascular endothelial growth factor-165 (VEGF165)-induced tube formation, proliferation, and migration in vitro angiogenesis model via suppression of the VEGF165-induced phosphorylation of VEGF receptor-2. |
| 226 | 20179357 | Studies using RIP-Cre:Vegf(fl/fl) mice revealed that defects in the normal vascular structure are associated with abnormal insulin secretion and concluded that the islet vascular system is essential for normal insulin secretion into the blood stream. |
| 227 | 21527748 | Exposure to acrolein blocked vascular endothelial growth factor (VEGF)/AMD3100-stimulated mobilization of Flk-1(+)/Sca-1(+) but not Sca-1(+)-only cells and prevented VEGF-induced phosphorylation of Akt and endothelial nitric oxide synthase in the aorta. |
| 228 | 21538000 | In addition to inflammatory cytokines and neurotrophic factors such as VEGF, anti-inflammatory cytokines such as IL-10 and IL-13 may be involved more in the pathogenesis of DR and CRVO than in other diseases; cytokines and chemokines may also be correlated to VEGF in the vitreous fluid. |
| 229 | 16816123 | For example, levels of proangiogenic VEGF-A, VEGF-B, neuropilin-1, VEGFR-1, and VEGFR-2 were reduced and the levels of antiangiogenic thrombospondin-1 and retinoblastoma like-2 were increased. |
| 230 | 18323518 | Vascular endothelial growth factor (VEGF) stimulates proangiogenic signal transduction and cell function in part through activation of protein kinase C (PKC). |
| 231 | 18323518 | Consistent with an effect on several pathways of VEGF signaling, VEGF receptor-2 (VEGFR2) tyrosine phosphorylation and expression of VEGFR2 protein and mRNA was decreased by 81, 90, and 84%, respectively, during knockdown of PKC-epsilon, but increased during PKC-alpha knockdown. |
| 232 | 18323518 | By regulating VEGFR2 expression and activation, PKC-epsilon expression is critical for activation of Akt and eNOS by VEGF and contributes to VEGF-stimulated Erk activation, whereas PKC-alpha has opposite effects. |
| 233 | 10199138 | In addition, we have reported that reactive oxygen intermediates, advanced glycation end products and insulin-like growth factor-1, also all, may participate in the pathogenesis of DR through their ability to increase VEGF production. |
| 234 | 17402563 | We found that retinal vascular cells have a characteristic pattern in VEGF receptor expression, which causes vascular pathology more frequently in the retina than in other organs. |
| 235 | 17402563 | Finally, we found that erythropoietin is an ischemia-induced angiogenic factor that acts independently and as potently as VEGF in proliferative diabetic retinopathy (PDR). |
| 236 | 19348185 | We have demonstrated the contribution of RAPS to the pathogenesis of CNV and dual regulation of VEGF and MCP-1 by signal transduction via (pro) renin receptor and AT1-R. |
| 237 | 21744772 | Monoclonal antibodies against VEGF and TNF-alpha such as bevacizumab, ranibizumab, infliximab and adalimumab have been used to control neovascularization and inflammation in eye with significant positive results whereas others have been used to target CD20, CD52, CD11a, and IL-2. |
| 238 | 12000720 | These changes coincided with reductions in retinal eNOS, nitric oxide, Akt (protein kinase B), and MAP kinase activity, known mediators of VEGF bioactivity and leukocyte adhesion. |
| 239 | 19958114 | RT-PCR revealed that the expression of VEGF, VEGF receptors, STAT3, erythropoietin, erythropoietin receptor, STAT5, angiopoietin 2, and Tie2 mRNA increased in the DM group, whereas angiopoietin 1 expression decreased. |
| 240 | 21660636 | Circulating concentrations of angiogenin, angiopoietin-1, platelet derived endothelial factor (PDGF)-AA, matrix metalloproteinase (MMP) 8 and 9, endothelial growth factor (EGF) and vascular EGF (VEGF) were also measured. |
| 241 | 21756365 | The simulated effects of PAR-1, Rho GTPase, ROCK, VEGF and VEGFR2 over-expression on MLC activation, and the collective modulation by thrombin and histamine are consistent with experimental findings. |
| 242 | 21756365 | Our model was used to predict enhanced MLC activation by CPI-17 over-expression and by synergistic action of thrombin and VEGF at low mediator levels. |
| 243 | 21826596 | In the PNS-L, PNS-H and catopril groups, the expression of VEGF protein was decreased but BMP-7 protein was increased in the kidney tissue (P<0.05, P<0.01). |
| 244 | 21609243 | Likewise, qPCR performed in the whole cohort showed a 30-fold increase in haptoglobin (P = 0.005), 7-fold increase in IL-10 (P < 0.001), 8-fold decrease in VEGF (P = 0.01) and a 28-fold decrease in TBOX15 (P < 0.001) in visceral compared to subcutaneous adipose tissue. |
| 245 | 21723532 | We measured significant alterations in the vitreous concentrations of 9 cytokines-eotaxin, Flt-3 ligand, growth-related oncogene (GRO), interleukin (IL)-6, IL-8, IL-9, IFN-inducible protein-10 (IP-10), macrophage-derived cytokine (MDC), and vascular endothelial growth factor (VEGF)-in advanced proliferative diabetic retinopathy, and found that oxygen tension at the posterior pole was directly correlated with vitreous VEGF concentration. |
| 246 | 21797106 | The group 2 patients had statistically significantly higher levels of IL-1beta (p = 0.01) and IL-6 (p = 0.029) and elevated TNF-alpha and VEGF levels in comparison with group 1 patients. |
| 247 | 21819507 | EPO is locally expressed and is correlated with VEGF in eyes with diabetic macular oedema. |
| 248 | 21933615 | Four factors were independently associated with a worse disease-free survival: diabetes (hazard ratio (HR) 2.338; 95% confidence interval (CI) 1.011 - 5.407), expression of cyclooxygenase-2 (Cox-2) (HR 0.335; 95%CI 0.126 - 0.888), expression of matrix metalloproteinases 2 (MMP-2) (HR 0.233; 95%CI 0.101 - 0.541), expression of vascular endothelial growth factor (VEGF) (HR 0.295; 95%CI 0.088 - 0.996). |
| 249 | 19657716 | We found a dose-dependent increase in cell survival with VEGF or Epo, which was attenuated in the presence of PEDF. |
| 250 | 19657716 | In addition, PEDF significantly (P < 0.05) inhibited migration and in vitro tube formation in RECs in the presence of VEGF as like PI3K/Akt inhibitor. |
| 251 | 19657716 | Of interest, PEDF effectively abrogated VEGF-mediated phosphorylation of PI3K/Akt. |
| 252 | 19657716 | Further studies using RECs transfected with constitutively active and dominant-negative forms of Akt suggest that PEDF could inhibit VEGF- and also Epo-induced angiogenesis by disruption of PI3K/Akt signaling. |
| 253 | 17256873 | We have recently shown improvement in islet survival and function following ex vivo infection of islets with a mixture of adenoviral vectors encoding human vascular endothelial growth factor (Adv-hVEGF) and human interleukin-1 receptor antagonist (Adv-hIL-1Ra). |
| 254 | 17256873 | Coexpression of hVEGF and hIL-1Ra suppressed nitric oxide production, total caspases, apoptosis, and necrosis in the presence of inflammatory cytokine cocktail consisting of IL-1beta, TNFalpha, and IFNgamma. |
| 255 | 19067524 | Earlier we have shown coexpression of human vascular endothelial growth factor (hVEGF) and human interleukin-1 receptor antagonist (hIL-1Ra) after transfection of plasmid DNA encoding these two genes. |
| 256 | 19067524 | Coexpression of hVEGF and hIL-1Ra by islets showed decrease in caspase-3 activity and apoptosis induced by a cocktail of inflammatory cytokines such as TNF-alpha, IL-1beta and IFN-gamma. |
| 257 | 21610567 | Patients were stratified according to hypertension or other clinical conditions, and the differences in vitreous levels of monocyte chemotactic protein 1, interleukin 8, vascular endothelial growth factor, interferon-inducible protein 10, and monokine induced by interferon gamma were examined. |
| 258 | 21610567 | Vitreous levels of vascular endothelial growth factor, interferon-inducible protein 10, and monokine induced by interferon gamma were not affected by the coexistence of hypertension. |
| 259 | 21864757 | Moreover, insulin seems to augment cardiomyocyte contraction, while it affects favorably myocardial relaxation, increases ribosomal biogenesis and protein synthesis, stimulates vascular endothelial growth factor (VEGF) and thereby angiogenesis, suppresses apoptosis, promotes cell survival and finally ameliorates both myocardial microcirculation and coronary artery resistance, leading to increased blood perfusion of myocardium. |
| 260 | 20007836 | After treatment with IVB, vascular endothelial growth factor (VEGF) concentrations in the aqueous humor decreased (P = 0.0003), whereas the concentrations of IL-8 and transforming growth factor (TGF)-beta(2) increased after IVB (P < 0.03). |
| 261 | 21839062 | The molecular mechanism for 14S,21R-diHDHA-induced recovery of impaired prohealing functions of db/db macrophages involves enhancing their secretion of vascular endothelial growth factor and platelet-derived growth factor BB, decreasing hyperglycemia-induced generation of reactive oxygen species, and increasing IL-10 expression under inflammatory stimulation. |
| 262 | 20676049 | Interestingly, we demonstrated that ATM disruption positively regulates both expression and function of the basal glucose transporter GLUT-1 as well as the proangiogenic factor, VEGF. |