Ignet

Gene Information

Gene symbol: VEGFA

Gene name: vascular endothelial growth factor A

HGNC ID: 12680

Synonyms: VEGF-A, VPF

Related Genes

#	Gene Symbol	Number of hits
1	AGT	1 hits
2	AKT1	1 hits
3	ANGPT2	1 hits
4	ARNT	1 hits
5	COL1A1	1 hits
6	EPAS1	1 hits
7	FLT1	1 hits
8	FLT4	1 hits
9	GDNF	1 hits
10	HIF1A	1 hits
11	HTR2B	1 hits
12	JUND	1 hits
13	KDR	1 hits
14	MIRN93	1 hits
15	NPHS1	1 hits
16	NPHS2	1 hits
17	NPTX1	1 hits
18	NPTX2	1 hits
19	PLVAP	1 hits
20	SEMA3A	1 hits
21	SERPINA1	1 hits
22	SLC2A1	1 hits
23	SULF1	1 hits
24	SULF2	1 hits
25	SYNPO	1 hits
26	TEK	1 hits
27	TGFB1	1 hits
28	VEGFC	1 hits
29	WT1	1 hits

Related Sentences

#	PMID	Sentence
1	22038228	The aim of the present work was to analyze the possible relation between VEGF-C and VEGF receptor (VEGFR)-2 expressions at electron microscopy level in different INS cases.
2	11261688	Ang-2 destabilises capillary integrity, facilitating sprouting when ambient vascular endothelial growth factor (VEGF) levels are high, but causing vessel regression when VEGF levels are low.
3	12617854	To examine whether semaphorins could modulate VEGF endothelial cell guidance cues in the developing kidney, we studied the expression of semaphorin 3A and semaphorin 3F and their receptors NP-1 and NP-2 in the kidney during ontogeny using Northern blot analysis, in situ hybridization, Western blot analysis and immunohistochemistry.
4	12660327	Because VEGF is highly expressed by metanephric podocytes and collecting ducts, developing mouse kidney was examined for the presence and distribution of HIF-1alpha, HIF-2alpha, and HIF-1beta.
5	15339792	We therefore investigated whether VEGF signals to reduce apoptosis and the role of nephrin in this survival mechanism.
6	15339792	Although VEGF reduced apoptosis in human conditionally immortalized podocytes [wild-type (WT)] by 18.1% of control (P < 0.001), it was unable to do so in nephrin-deficient human conditionally immortalized podocytes.
7	15339792	Moreover, Western blotting and immunodetection with an anti-nephrin antibody showed that the phosphorylation of nephrin, compared with serum-starved WTs, was significantly increased (ratio of 3.36 +/- 1.2 to control, P < 0.05) by VEGF treatment and significantly reduced by treatment with a neutralizing VEGF monoclonal antibody (mAb) (ratio of 0.2 +/- 0.09 to control, P < 0.05).
8	15339792	We suggest therefore that both exogenous and endogenous (podocyte derived) VEGF can stimulate the phosphorylation of nephrin and through this action may prevent podocyte apoptosis.
9	15840669	Podocyte expression of alpha3(IV) collagen may involve the transforming growth factor-beta (TGF-beta) and vascular endothelial growth factor (VEGF) systems.
10	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.
11	15840669	Blockade of the endogenous VEGF activity by SU5416 prevented AngII-stimulated alpha3(IV) collagen production.
12	16060125	Enhanced circulating endothelial cells, elevated transforming growth factor beta, and depleted vascular endothelial growth factor were observed in nephrosis associated with focal segmental glomerulosclerosis (FSGS).
13	16239266	The VEGF-induced elevation of LpA/Vi was blocked by the selective VEGF-R2 inhibitor ZM323881.
14	16374431	The HIF-target gene VEGF colocalized with HIF-1alpha protein in glomeruli and medullary collecting ducts.
15	16436677	A growing body of observations, including the side effects of anti-VEGF therapies as well as the role of soluble VEGFR1 in preeclampsia, points to an important role for VEGF in maintenance of stable blood vessels.
16	16436677	Additionally, VEGFR2 was constitutively phosphorylated in the liver, lung, adipose, and kidney in vivo, providing evidence consistent with a role for VEGF in adult tissues.
17	17059890	Podocalyxin expression in leukemic blasts was coupled with the concomitant expression of VEGF-R1, -R2, -R3 and Tie-2, the capacity to release VEGF-A and angiopoietin1 and the ability to differentiate into endothelial cells under appropriate culture conditions.
18	17554151	For elucidation of the pathologic consequences of high levels of VEGF in glomeruli, transgenic (Tg) rabbits that express human VEGF(165) isoform in both kidney and liver under the control of the human alpha-1-antitrypsin promoter were generated and characterized.
19	17457373	In the puromycin and the combined models, changes in GLEPP1 expression were corticosteroid-sensitive, whereas B7.1, WT1, vascular endothelial growth factor, and most slit diaphragm genes involved later in the combined model, except podocin, were corticosteroid-resistant.
20	17667850	PAN mice also had significantly decreased Flk-1 and Tie2 mRNA expression and increased angiopoitein-1 (Ang-1) expression, without change in vascular endothelial growth factor (VEGF) at 2 dpp versus NS.
21	17715266	Immunohistochemistry and real-time RT-PCR studies also indicated that 5-HT stimulated expression of vascular endothelial growth factor in podocytes in vitro and in vivo.
22	18249526	Additional studies revealed that SEMA3A effects on ureteric bud branching involve downregulation of glial cell-line derived neurotrophic factor (GDNF) signaling, competition with vascular endothelial growth factor A (VEGF-A) and decreased activity of Akt survival pathways.
23	18287402	Moreover, VEGF blockade induced ET-1 release from endothelial cells, and in turn the conditioned medium obtained triggered nephrin loss.
24	19129259	In systemic endothelial fenestrations, the intracellular pathways through which VEGF acts to induce fenestrations include a key role for the fenestral diaphragm protein plasmalemmal vesicle-associated protein-1 (PV-1).
25	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.
26	20688931	Unlike cell culture models, enhanced expression of VEGF by podocytes in vivo caused foot process fusion and alterations in slit diaphragm-associated proteins; however, inhibition of VEGFR-2 could not rescue this defect.
27	20629321	After second injected with adriamycin,the model group nephrin presented a weak signal in the end of the first week (P < 0.05), and the expression of VEGF started to increase at the end of the eighth week (P < 0.05).
28	20629321	The expression of nephrin and the number of podocyte were negatively correlated with the 24-hour urine protein, blood urea nitrogen and serum creatinine; while the expression of VEGF was positively correlated with the 24-hour urine protein, blood urea nitrogen and serum creatinine.
29	20501654	Here, we provide evidence that microRNA-93 (miR-93) regulates VEGF expression in experimental models of diabetes both in vitro and in vivo.
30	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.
31	20501654	When cotransfected with a luciferase reporter construct containing the mouse vegfa 3'-untranslated region, expression of miR-93 markedly decreased the luciferase activity.
32	12620928	Normal human podocytes are also known to express neuropilin-1, VEGF, and are VEGF-R2 negative.
33	16525158	Vascular endothelial growth factor (VEGF)-A is an autocrine survival factor for podocytes, which express two VEGF receptors, VEGF-R1 and VEGF-R3.
34	16525158	As VEGF-A is not a known ligand for VEGF-R3, the aim of this investigation was to examine whether VEGF-C, a known ligand for VEGF-R3, served a function in podocyte biology and whether this was VEGF-R3 dependent.
35	16525158	VEGF-C was also shown to induce a 0.5+/-0.13-fold reduction in levels of MAPK phosphorylation compared with VEGF-A and VEGF-A-Mab treatment (P<0.05, ANOVA, n=4), yet had no effect on Akt phosphorylation.
36	16597608	VEGF(165) induced a twofold increase in VEGFR2 mRNA and protein levels, whereas VEGFR1, sVEGFR1, NP1, and NP2 mRNA levels remained unchanged.
37	16597608	VEGF(165) induced VEGFR2 phosphorylation.
38	16597608	We determined that VEGF-A signaling regulates slit diaphragm proteins by inducing a dose-response podocin upregulation and increasing its interaction with CD2AP.
39	16597608	VEGF-A functions in podocytes include promoting survival through VEGFR2, inducing podocin upregulation and increasing podocin/CD2AP interaction.
40	19828679	We demonstrated that ablation of VEGF-A or VEGF-C as well as treatment with bevacizumab or a VEGFR-2/-3 tyrosine kinase inhibitor led to reduced podocyte survival.
41	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.
42	21451433	Furthermore, PAN-induced up-regulation of desmin, down-regulation of synaptopodin and nephrin, and disruption of glomerular morphology were significantly attenuated in VEGF-induced transgenic mice.
43	21640331	Furthermore, cultured glomeruli from Jund(-/-) mice showed relatively increased expression of vascular endothelial growth factor A (Vegfa), Cxcr4, and Cxcl12, well-known HIF target genes.
44	21640331	Accordingly, small-interfering RNA-mediated JUND knockdown in conditionally immortalized human podocyte cell lines led to increased VEGFA and HIF1A expression.
45	21640331	Our findings suggest that deficiency of Jund may cause increased oxidative stress in podocytes, leading to altered VEGFA expression and subsequent glomerular injury in Crgn.
46	21719793	Here, we found that the transcription factor Wilms' Tumor 1 (WT1) modulates VEGFA and FGF2 signaling by increasing the expression of the 6-O-endosulfatases Sulf1 and Sulf2, which remodel the heparan sulfate 6-O-sulfation pattern in the extracellular matrix.
47	21937443	We previously showed that in vivo nephrin associates with VEGF receptor-2 (VEGFR2), the signaling receptor for VEGF-A.