HCSGD entry for VEGFA


1. General information

Official gene symbolVEGFA
Entrez ID7422
Gene full namevascular endothelial growth factor A
Other gene symbolsMVCD1 VEGF VPF
Links to Entrez GeneLinks to Entrez Gene

2. Neighbors in the network

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3. Gene ontology annotation

GO ID

GO term

Evidence

Category

GO:0000122Negative regulation of transcription from RNA polymerase II promoterIDAbiological_process
GO:0001525AngiogenesisIDAbiological_process
GO:0001541Ovarian follicle developmentIEA ISSbiological_process
GO:0001569Patterning of blood vesselsIEA ISSbiological_process
GO:0001570VasculogenesisTASbiological_process
GO:0001666Response to hypoxiaIDA IEAbiological_process
GO:0001701In utero embryonic developmentIEA ISSbiological_process
GO:0001822Kidney developmentIEA ISSbiological_process
GO:0001934Positive regulation of protein phosphorylationIDAbiological_process
GO:0001938Positive regulation of endothelial cell proliferationIDA ISSbiological_process
GO:0001968Fibronectin bindingIDAmolecular_function
GO:0001974Blood vessel remodelingIEAbiological_process
GO:0002042Cell migration involved in sprouting angiogenesisIDAbiological_process
GO:0002052Positive regulation of neuroblast proliferationIEA ISSbiological_process
GO:0002053Positive regulation of mesenchymal cell proliferationIEA ISSbiological_process
GO:0002092Positive regulation of receptor internalizationIDAbiological_process
GO:0002575Basophil chemotaxisIDAbiological_process
GO:0002576Platelet degranulationTASbiological_process
GO:0002687Positive regulation of leukocyte migrationTASbiological_process
GO:0003007Heart morphogenesisISSbiological_process
GO:0003151Outflow tract morphogenesisIEA ISSbiological_process
GO:0003169Coronary vein morphogenesisIEA ISSbiological_process
GO:0005125Cytokine activityIDA ISSmolecular_function
GO:0005161Platelet-derived growth factor receptor bindingIPImolecular_function
GO:0005172Vascular endothelial growth factor receptor bindingIPImolecular_function
GO:0005515Protein bindingIPImolecular_function
GO:0005576Extracellular regionTAScellular_component
GO:0005578Proteinaceous extracellular matrixNAScellular_component
GO:0005604Basement membraneIEAcellular_component
GO:0005615Extracellular spaceIDA IEA ISScellular_component
GO:0005737CytoplasmIDA IEAcellular_component
GO:0006357Regulation of transcription from RNA polymerase II promoterIMPbiological_process
GO:0007399Nervous system developmentTASbiological_process
GO:0007498Mesoderm developmentIEA ISSbiological_process
GO:0007595LactationIEA ISSbiological_process
GO:0007596Blood coagulationTASbiological_process
GO:0008083Growth factor activityIDA IEA ISSmolecular_function
GO:0008201Heparin bindingIDA IEA IMPmolecular_function
GO:0008283Cell proliferationIEAbiological_process
GO:0008284Positive regulation of cell proliferationIDAbiological_process
GO:0008360Regulation of cell shapeIDAbiological_process
GO:0009409Response to coldIEAbiological_process
GO:0009986Cell surfaceIDAcellular_component
GO:0010469Regulation of receptor activityIPIbiological_process
GO:0010595Positive regulation of endothelial cell migrationIDAbiological_process
GO:0010628Positive regulation of gene expressionIDAbiological_process
GO:0016020MembraneIEAcellular_component
GO:0030141Secretory granuleIDAcellular_component
GO:0030168Platelet activationTASbiological_process
GO:0030212Hyaluronan metabolic processIEAbiological_process
GO:0030224Monocyte differentiationIDAbiological_process
GO:0030225Macrophage differentiationIDAbiological_process
GO:0030324Lung developmentISSbiological_process
GO:0030335Positive regulation of cell migrationIDAbiological_process
GO:0030855Epithelial cell differentiationIEA ISSbiological_process
GO:0030949Positive regulation of vascular endothelial growth factor receptor signaling pathwayIDAbiological_process
GO:0031077Post-embryonic camera-type eye developmentIEA ISSbiological_process
GO:0031093Platelet alpha granule lumenTAScellular_component
GO:0031334Positive regulation of protein complex assemblyIDAbiological_process
GO:0031954Positive regulation of protein autophosphorylationIDAbiological_process
GO:0031988Membrane-bounded vesicleIEAcellular_component
GO:0032147Activation of protein kinase activityIDAbiological_process
GO:0032793Positive regulation of CREB transcription factor activityIDAbiological_process
GO:0033138Positive regulation of peptidyl-serine phosphorylationIDAbiological_process
GO:0035148Tube formationIDAbiological_process
GO:0035767Endothelial cell chemotaxisIDAbiological_process
GO:0035924Cellular response to vascular endothelial growth factor stimulusIDAbiological_process
GO:0036303Lymph vessel morphogenesisIEA ISSbiological_process
GO:0038033Positive regulation of endothelial cell chemotaxis by VEGF-activated vascular endothelial growth factor receptor signaling pathwayIDAbiological_process
GO:0038084Vascular endothelial growth factor signaling pathwayIEAbiological_process
GO:0038091Positive regulation of cell proliferation by VEGF-activated platelet derived growth factor receptor signaling pathwayIDAbiological_process
GO:0038190VEGF-activated neuropilin signaling pathwayISSbiological_process
GO:0040007GrowthIEA ISSbiological_process
GO:0042056Chemoattractant activityIDAmolecular_function
GO:0042088T-helper 1 type immune responseIEAbiological_process
GO:0042462Eye photoreceptor cell developmentIEA ISSbiological_process
GO:0042802Identical protein bindingIPImolecular_function
GO:0042803Protein homodimerization activityIEA ISSmolecular_function
GO:0043066Negative regulation of apoptotic processIMPbiological_process
GO:0043117Positive regulation of vascular permeabilityIDA IEAbiological_process
GO:0043129Surfactant homeostasisIEA ISSbiological_process
GO:0043154Negative regulation of cysteine-type endopeptidase activity involved in apoptotic processIDAbiological_process
GO:0043183Vascular endothelial growth factor receptor 1 bindingIPImolecular_function
GO:0043184Vascular endothelial growth factor receptor 2 bindingIPImolecular_function
GO:0043406Positive regulation of MAP kinase activityIDAbiological_process
GO:0043524Negative regulation of neuron apoptotic processIEAbiological_process
GO:0043536Positive regulation of blood vessel endothelial cell migrationIDAbiological_process
GO:0045766Positive regulation of angiogenesisIDA IEA IMPbiological_process
GO:0045779Negative regulation of bone resorptionIEAbiological_process
GO:0045785Positive regulation of cell adhesionIDAbiological_process
GO:0045944Positive regulation of transcription from RNA polymerase II promoterIDA IEA IMPbiological_process
GO:0046982Protein heterodimerization activityIDAmolecular_function
GO:0048010Vascular endothelial growth factor receptor signaling pathwayIDA IEA TASbiological_process
GO:0048018Receptor agonist activityIPImolecular_function
GO:0048255MRNA stabilizationIEAbiological_process
GO:0048286Lung alveolus developmentIEAbiological_process
GO:0048469Cell maturationIEA ISSbiological_process
GO:0048593Camera-type eye morphogenesisIEA ISSbiological_process
GO:0048661Positive regulation of smooth muscle cell proliferationIEAbiological_process
GO:0048739Cardiac muscle fiber developmentIEA ISSbiological_process
GO:0048754Branching morphogenesis of an epithelial tubeISSbiological_process
GO:0048842Positive regulation of axon extension involved in axon guidanceIEA ISSbiological_process
GO:0048844Artery morphogenesisISSbiological_process
GO:0050679Positive regulation of epithelial cell proliferationIEA ISSbiological_process
GO:0050731Positive regulation of peptidyl-tyrosine phosphorylationIDAbiological_process
GO:0050840Extracellular matrix bindingICmolecular_function
GO:0050918Positive chemotaxisIDA IEAbiological_process
GO:0050927Positive regulation of positive chemotaxisIDAbiological_process
GO:0050930Induction of positive chemotaxisIDA NASbiological_process
GO:0051272Positive regulation of cellular component movementIDAbiological_process
GO:0051781Positive regulation of cell divisionIEAbiological_process
GO:0051894Positive regulation of focal adhesion assemblyIDAbiological_process
GO:0051897Positive regulation of protein kinase B signalingIEAbiological_process
GO:0060319Primitive erythrocyte differentiationIEA ISSbiological_process
GO:0060326Cell chemotaxisIEAbiological_process
GO:0060749Mammary gland alveolus developmentIEA ISSbiological_process
GO:0060754Positive regulation of mast cell chemotaxisIDAbiological_process
GO:0060948Cardiac vascular smooth muscle cell developmentIEA ISSbiological_process
GO:0060982Coronary artery morphogenesisIEA ISSbiological_process
GO:0061418Regulation of transcription from RNA polymerase II promoter in response to hypoxiaTASbiological_process
GO:0061419Positive regulation of transcription from RNA polymerase II promoter in response to hypoxiaIMPbiological_process
GO:0070374Positive regulation of ERK1 and ERK2 cascadeIEAbiological_process
GO:0071456Cellular response to hypoxiaIDA TASbiological_process
GO:0071542Dopaminergic neuron differentiationIEA ISSbiological_process
GO:0071679Commissural neuron axon guidanceIEA ISSbiological_process
GO:0090037Positive regulation of protein kinase C signalingIDAbiological_process
GO:0090050Positive regulation of cell migration involved in sprouting angiogenesisIDAbiological_process
GO:0090190Positive regulation of branching involved in ureteric bud morphogenesisIEA ISSbiological_process
GO:0090259Regulation of retinal ganglion cell axon guidanceISSbiological_process
GO:1900086Positive regulation of peptidyl-tyrosine autophosphorylationIDAbiological_process
GO:1900745Positive regulation of p38MAPK cascadeIDAbiological_process
GO:1901492Positive regulation of lymphangiogenesisIEAbiological_process
GO:1901727Positive regulation of histone deacetylase activityIDAbiological_process
GO:1902336Positive regulation of retinal ganglion cell axon guidanceIEA ISSbiological_process
GO:1902533Positive regulation of intracellular signal transductionIDAbiological_process
GO:2000273Positive regulation of receptor activityIPIbiological_process
GO:2001237Negative regulation of extrinsic apoptotic signaling pathwayIEAbiological_process
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4. Expression levels in datasets

  • Meta-analysis result

p-value upp-value downFDR upFDR down
0.00573358910.29356202650.19851176471.0000000000

  • Individual experiment result
    ( "-" represent NA in the specific microarray platform )

Data sourceUp or downLog fold change
GSE11954Down-0.8309789501
GSE13712_SHEARDown-0.4877322310
GSE13712_STATICUp0.1426021948
GSE19018Up0.2493757587
GSE19899_A1Up0.4527131272
GSE19899_A2Up1.8415313513
PubMed_21979375_A1Up1.8105154772
PubMed_21979375_A2Up0.7810819713
GSE35957Down-1.2000703813
GSE36640Down-1.4500966794
GSE54402Down-0.1305501631
GSE9593Up0.4922266102
GSE43922Up1.1591433820
GSE24585Up0.0452844200
GSE37065Up0.1225939009
GSE28863_A1Up0.7354217700
GSE28863_A2Up1.1178683229
GSE28863_A3Up0.0268011753
GSE28863_A4Down-0.3731714982
GSE48662Up0.6758711292

5. Regulation relationships with compounds/drugs/microRNAs

  • Compounds

Compound

Target

Confidence score

Uniprot

CHEMBL265885CHEMBL17834P15692
CHEMBL382044CHEMBL17834P15692
CHEMBL198643CHEMBL17834P15692
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  • Drugs

Name

Drug

Accession number

BevacizumabDB00112 BTD00087 | BIOD00087
MinocyclineDB01017 APRD00547
GliclazideDB01120 APRD00460
CarvedilolDB01136 APRD00091
RanibizumabDB01270 -
Pyroglutamic AcidDB03088 EXPT00247
TrisDB03754 EXPT03072
ABT-510DB05434 -
VEGF-ASDB05890 -
AfliberceptDB08885 -

  • MicroRNAs

  • mirTarBase

MiRNA_name

mirBase ID

miRTarBase ID

Experiment

Support type

References (Pubmed ID)

hsa-miR-200b-3pMIMAT0000318MIRT006440Luciferase reporter assay//Western blotFunctional MTI21544626
hsa-miR-373-3pMIMAT0000726MIRT000721ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-302d-3pMIMAT0000718MIRT000722ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-145-5pMIMAT0000437MIRT006215Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI22472569
hsa-miR-126-3pMIMAT0000445MIRT003428Luciferase reporter assay//Reporter assayFunctional MTI19223090
hsa-miR-126-3pMIMAT0000445MIRT003428Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI22510476
hsa-miR-126-3pMIMAT0000445MIRT003428Reporter assay;Western blotFunctional MTI21249429
hsa-miR-147aMIMAT0000251MIRT003810ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-134-5pMIMAT0000447MIRT003811ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-140-5pMIMAT0000431MIRT003812ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-29b-3pMIMAT0000100MIRT003813ELISA//Luciferase reporter assayNon-Functional MTI18320040
hsa-miR-107MIMAT0000104MIRT003814ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-16-5pMIMAT0000069MIRT003890Luciferase reporter assay//Reporter assayNon-Functional MTI15131085
hsa-miR-16-5pMIMAT0000069MIRT003890ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-16-5pMIMAT0000069MIRT003890Luciferase reporter assay//Western blotFunctional MTI19144909
hsa-miR-16-5pMIMAT0000069MIRT003890Luciferase reporter assayFunctional MTI23083510
hsa-miR-16-5pMIMAT0000069MIRT003890Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI23104180
hsa-miR-16-5pMIMAT0000069MIRT003890Luciferase reporter assayFunctional MTI23233752
hsa-miR-93-5pMIMAT0000093MIRT004055ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-17-5pMIMAT0000070MIRT004271ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-150-5pMIMAT0000451MIRT004272ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-195-5pMIMAT0000461MIRT004273ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-15b-5pMIMAT0000417MIRT004274ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-15a-5pMIMAT0000068MIRT004275ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-15a-5pMIMAT0000068MIRT004275Luciferase reporter assay//qRT-PCR//Western blotFunctional MTI23104180
hsa-miR-15a-5pMIMAT0000068MIRT004275Luciferase reporter assayFunctional MTI23233752
hsa-miR-520g-3pMIMAT0002858MIRT004276ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-378a-3pMIMAT0000732MIRT004277ELISA//Luciferase reporter assayNon-Functional MTI18320040
hsa-miR-330-3pMIMAT0000751MIRT004278ELISA//Luciferase reporter assayNon-Functional MTI18320040
hsa-miR-383-5pMIMAT0000738MIRT004443ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-125a-5pMIMAT0000443MIRT004445ELISA//Luciferase reporter assayNon-Functional MTI18320040
hsa-miR-361-5pMIMAT0000703MIRT004447ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-20a-5pMIMAT0000075MIRT004450ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-20b-5pMIMAT0001413MIRT004451ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-504-5pMIMAT0002875MIRT004457ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-520hMIMAT0002867MIRT004458ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-372-3pMIMAT0000724MIRT004461ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-106a-5pMIMAT0000103MIRT004465ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-106b-5pMIMAT0000680MIRT004466ELISA//Luciferase reporter assayFunctional MTI18320040
hsa-miR-106b-5pMIMAT0000680MIRT004466MicroarrayFunctional MTI (Weak)17242205
hsa-miR-34a-5pMIMAT0000255MIRT004513ELISA//Luciferase reporter assayNon-Functional MTI18320040
hsa-miR-205-5pMIMAT0000266MIRT004518ELISA//Luciferase reporter assayNon-Functional MTI18320040
hsa-miR-205-5pMIMAT0000266MIRT004518Luciferase reporter assay//Reporter assayFunctional MTI19238171
hsa-miR-34b-3pMIMAT0004676MIRT004519ELISA//Luciferase reporter assayNon-Functional MTI18320040
hsa-miR-200c-3pMIMAT0000617MIRT006771Luciferase reporter assay//Western blotFunctional MTI22569286
hsa-miR-503-5pMIMAT0002874MIRT007224Luciferase reporter assayFunctional MTI23352645
hsa-miR-335-5pMIMAT0000765MIRT016911MicroarrayFunctional MTI (Weak)18185580
hsa-miR-29c-3pMIMAT0000681MIRT020389SequencingFunctional MTI (Weak)20371350
hsa-miR-9-5pMIMAT0000441MIRT021401qRT-PCR;OtherNon-Functional MTI (Weak)20173740
hsa-miR-133a-3pMIMAT0000427MIRT021711Reporter assayNon-Functional MTI21249429
hsa-miR-101-3pMIMAT0000099MIRT027248SequencingFunctional MTI (Weak)20371350
hsa-miR-21-5pMIMAT0000076MIRT030717qRT-PCRFunctional MTI (Weak)19435867
hsa-miR-21-5pMIMAT0000076MIRT030717Western blot;qRT-PCRFunctional MTI21544242
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  • mirRecord

MicroRNA name

mirBase ID

Target site number

MiRNA mature ID

Test method inter

MiRNA regulation site

Reporter target site

Pubmed ID

hsa-miR-34a-5pMIMAT00002551hsa-miR-34a{ELISA}{overexpression by siRNA transfection}18320040
hsa-miR-140-5pMIMAT0000431NAhsa-miR-140-5p{ELISA}{overexpression by siRNA transfection}18320040
hsa-miR-15a-5pMIMAT00000681hsa-miR-15a{ELISA}{overexpression by siRNA transfection}18320040
hsa-miR-16-5pMIMAT0000069NAhsa-miR-16{ELISA}{overexpression by siRNA transfection}18320040
hsa-miR-147aMIMAT0000251NAhsa-miR-147{ELISA}{overexpression by siRNA transfection}18320040
hsa-miR-520hMIMAT00028671hsa-miR-520h{ELISA}{overexpression by siRNA transfection}18320040
hsa-miR-205-5pMIMAT00002661hsa-miR-205{ELISA}{overexpression by siRNA transfection}18320040
hsa-miR-126-3pMIMAT00004451hsa-miR-12619223090
hsa-miR-205-5pMIMAT00002661hsa-miR-20519238171
hsa-miR-126-3pMIMAT0000445NAhsa-miR-126{Western blot}{endogenous}21249429
hsa-miR-16-5pMIMAT00000691hsa-miR-16{Western blot}{overexpression by miRNA mimics tranfection}21885851
hsa-miR-424-5pMIMAT0001341NAhsa-miR-424{Western blot}{overexpression by miRNA mimics tranfection}21885851
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6. Text-mining results about the gene

Gene occurances in abstracts of cellular senescence-associated articles: 43 abstracts the gene occurs.


PubMed ID of the article

Sentenece the gene occurs

27917303Then, the effect of synthetic miR-146a mimetic on IL-6 and VEGF-A expression was analyzed in RPE cells treated with and without TNF-alpha
27917303Overexpression of miR-146a by miRNA mimics inhibited VEGF-A and TNF-alpha-induced IL-6 expression
27508009Furthermore, we confirmed that the expressions of endothelial nitric oxide synthase (eNOS), vascular endothelial growth factor (VEGF) and phosphoryl-Akt were augmented in SRT1720-treated senescent HUVECs
27009837Bmi-1 knockdown by Ad-Bmi-1i downregulated VEGF via inhibiting AKT activity
26654980Oxidative stress-induced premature senescence dysregulates VEGF and CFH expression in retinal pigment epithelial cells: Implications for Age-related Macular Degeneration
26654980Most important, we show for the first time that senescent ARPE-19 cells upregulated vascular endothelial growth factor (VEGF) and simultaneously downregulated complement factor H (CFH) expression
26433963In this report we show that senescent human peritoneal mesothelial cells (HPMCs) alter the secretory profile of ovarian cancer cells (A2780, OVCAR-3, SKOV-3) by increasing the release of four angiogenic agents: CXCL1, CXCL8, HGF, and VEGF
26420897Selective coexpression of VEGF receptor 2 in EGFRvIII-positive glioblastoma cells prevents cellular senescence and contributes to their aggressive nature
26105007Upon LPS treatment, SV cells also developed senescence-associated secretory phenotype (SASP), as demonstrated by the increased expression of TNFalpha, IL-1beta, IL-6, MCP-1, and VEGFalpha
26005508Initial animal studies and phase I clinical trials with vascular endothelial growth factor (VEGF) or fibroblast growth factor (FGF) demonstrated promising results, inspiring scientists to progress forward
25952632Under these conditions, the anti-senescence genes TERT, bFGF, VEGF, and ANG were increased, whereas the senescence-related genes ATM, p21, and p53 were decreased
25797700We investigated whether vascular endothelial growth factor (VEGF) signaling via its receptor, VEGFR2, regulates senescence and proliferation of tumor cells in mice with colitis-associated cancer (CAC)
25633211Pre-clinical studies and Phase I clinical trials using VEGF and fibroblast growth factor (FGF) demonstrated promising results; however, more rigorous Phase II and III clinical trials failed to demonstrate benefits for CLI patients
25633211EXPERT OPINION: Compared with VEGF and FGF, HGF has a unique molecular effect on inflammation, fibrosis and cell senescence under pathological conditions
25453983After 2 weeks, the cells were treated with either VEGF or its vehicle and their transepithelial electrical resistance (TEER) was measured
25453983RESULTS: VEGF was significantly more effective in reducing the TEER of the high PDL ARPE-19 cell layers than the low PDL layers (25% decrease vs
25453983CONCLUSIONS: The present results show that the ability of VEGF to reduce the barrier function of RPE cell layers is greater in high PDL layers, which display signs of senescence, than in low PDL layers
25388834Our data showed that both eNOS and Akt phosphorylation, VEGF expression and nitric oxide production were significantly decreased, RMVECs ageing and apoptosis increased after ox-LDL induction for 24 hrs, all of which were effectively reversed by ciglitazone pre-treatment
25192254The expression of VEGF and VEGFR2 was reduced in Sirt3KO-EPCs
25192254In post-MI mice, BMC treatment increased number of Sca1+/c-kit+ cells; enhanced VEGF expression and angiogenesis whereas Sirt3KO-BMC treatment had little effects
25158160Hepatocyte growth factor (HGF), vascular endothelial growth factor (VEGF), and fibroblast growth factor (FGF) are all potent angiogenic growth factors in animal models of ischemia, but their therapeutic effects are not the same in animal experiments and clinical trials
25158160A multicenter, double-blind, placebo-controlled phase III clinical trial in Japan and a US phase II clinical trial of HGF gene therapy for critical limb ischemia (CLI) demonstrated a significant improvement in primary end points and an increase in transcutaneous partial pressure of oxygen even after one year compared with placebo, whereas effectiveness of VEGF and FGF treatment for CLI has not yet been shown
25158160Moreover, our recent publication and another researcher demonstrated that HGF acts as an anti-inflammatory cytokine, while VEGF and FGF act as pro-inflammatory cytokine
25108204That is, DHA supplement inhibited cellular proliferation, destroyed cell membrane integrity, enhanced cellular senescence, increased vascular endothelial growth factor (VEGF) release, and decreased phagocytic function
24681605Expression of two senescence-associated cytokines (VEGFA and MCP1) was durably increased by adjuvant chemotherapy
23770676Coupling quantitative proteomics with small-molecule screens, we identified multiple SASP components mediating paracrine senescence, including TGF-beta family ligands, VEGF, CCL2 and CCL20
23758730In addition, angiogenesis and VEGF expression in CT26 colon carcinoma was significantly inhibited by TLBZT treatment
235833987-fold) and down-regulated expression of vascular endothelial growth factor-A (0
23503666The downregulation of vascular endothelial growth factor (VEGF) was observed in the irradiated HUVECs as the PN increased
23174937Potentially functional polymorphisms were found in vascular endothelial growth factor (VEGF), ABCB1, FGFR2 and PHLPP2
23174937VEGF polymorphisms were the most common and detected at four loci
22904099Compared with young EC, senescent cells displayed increased expression of senescence-associated beta-galactosidase, nitric oxide synthase (eNOS), and AKT kinase, and secreted increased amounts of growth factors (VEGF, TGF-beta), cytokines (IL-6, IL-8, MCP-1), adhesion molecules (sICAM-1), and matrix proteins (fibronectin)
22797809Atm deficiency also lowered tumor angiogenesis and enhanced the antiangiogenic action of vascular endothelial growth factor (Vegf) blockade
22470345Based on its senescence-dependent involvement in alternative splicing, we postulate that SRSF1 is a key marker of EC senescence, regulating the expression of alternative isoforms of target genes such as endoglin (ENG), vascular endothelial growth factor A (VEGFA), tissue factor (T3), or lamin A (LMNA) that integrate in a common molecular senescence program
22340562Expression of OPN, hypoxia inducible factor-1 (HIF-1) and vascular endothelial growth factor (VEGF) proteins was analyzed by Western blotting analysis
22340562RESULTS: HIF-1 and VEGF proteins in MDA-MB-343 cells were significantly downregulated upon the efficient knockdown of OPN expression under either hypoxia or normoxia environment
21793037The level of plasma vascular endothelial growth factor (VEGF) was measured by ELISA
21793037In addition, there were higher levels of plasma VEGF in CA patients compared with healthy control subjects
21622994RESULTS: Uremic MSCs showed decreased expression of vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)1 and stromal cell-derived factor (SDF)-1alpha, increased cellular senescence, decreased proliferation, defects in migration in response to VEGF and SDF-1alpha and in vitro tube formation
21622994Uremia decreased hypoxia-inducible factor-1alpha, VEGF and VEGFR1 expression under hypoxia and Akt phosphorylation in both basal and VEGF-stimulated states
21618508Vascular endothelial growth factor (VEGF) inhibitors, such as bevacizumab, have improved outcomes in metastatic colorectal cancer (CRC)
21618508Recent studies have suggested that VEGF can delay the onset of cellular senescence in human endothelial cells
21618508As VEGF receptors are known to be upregulated in CRC, we hypothesized that VEGF inhibition may directly influence cellular senescence in this disease
21618508To understand how VEGF inhibitors may regulate cellular senescence, we noted that among the two important regulators of senescent growth arrest of tumor cells, bevacizumab-associated increase in cellular senescence coincided with an upregulation of p16 but appeared to be independent of p53
21618508These findings demonstrate a novel antitumor activity of VEGF inhibitors in CRC, involving p16
21245959This study investigated the effects of short- and long-term in vitro inhibition of vascular endothelial growth factor (VEGF) Receptor-2 (VEGFR-2) signaling by SU5416 and other inhibitors of the VEGF signaling pathway in OECs
21245959Migration in vitro to VEGF and stromal cell-derived factor 1 of OECs was assessed
21245959Naturally senescent cells and cells rendered senescent by VEGFR-2 TKIs had reduced VEGFR-2 and CXCR-4 expression and demonstrated reduced migratory ability to VEGF
20713685Exposure to VAT adipocytes caused more EC senescence-associated beta-galactosidase activity than SAT adipocytes, an effect reduced in the presence of vascular endothelial growth factor A (VEGFA) neutralizing antibodies
20374652Expression of the master cell cycle regulators p53 and p21 and growth factors HGF and VEGF also declined significantly at 26 months
19047582Although both hepatocyte growth factor (HGF) and vascular endothelial growth factor (VEGF) are potent angiogenic growth factors in animal models of ischemia, their characteristics are not the same in animal experiments and clinical trials
19047582To elucidate the discrepancy between HGF and VEGF, we compared the effects of HGF and VEGF on endothelial progenitor cells under angiotensin II stimulation, which is a well-known risk factor for atherosclerosis
19047582Here, we demonstrated that HGF, but not VEGF, attenuated angiotensin II-induced senescence of endothelial progenitor cells through a reduction of oxidative stress by inhibition of the phosphatidylinositol-3,4,5-triphosphate/rac1 pathway
19047582Potent induction of neovascularization of endothelial progenitor cells by HGF, but not VEGF, under angiotensin II was also confirmed by in vivo experiments using several models, including HGF transgenic mice
19011671EC exhibited higher expression levels of markers of oxidative stress (lipid peroxydation level and caveolin-1 mRNA), inflammation (angiopoietin-like 2 mRNA), hypoxia (vascular endothelial growth factor (VEGF)-A mRNA), and cell damage (p53 mRNA)
18583712Vascular endothelial growth factor (VEGF) binds both VEGF receptor-1 (VEGFR-1) and VEGF receptor-2 (VEGFR-2)
18583712Activation of VEGFR-2 is thought to play a major role in the regulation of endothelial function by VEGF
18583712In this study, we showed that VEGFR-1 performs "fine tuning" of VEGF signaling to induce neovascularization
18583712When VEGFR-1 expression was blocked, VEGF constitutively activated Akt signals and thus induced endothelial cell senescence via a p53-dependent pathway
18583712These results suggest that VEGFR-1 plays a critical role in the maintenance of endothelial integrity by modulating the VEGF/Akt signaling pathway
17402563VEGF has been recognized as a predominant factor to induce the ischemic retinal neovascularization
17402563We 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
17402563Finally, we found that erythropoietin is an ischemia-induced angiogenic factor that acts independently and as potently as VEGF in proliferative diabetic retinopathy (PDR)
17402563Our study utilizing human vitreous samples demonstrates that the VEGF level is particularly high and strongly associated with angiogenic activity in PDR patients
17402563The potential of VEGF inhibitors has recently been recognized in clinical applications
16880208Accordingly, increased vascular endothelial growth factor (VEGF) expression was a frequent characteristic of senescent human and mouse fibroblasts in culture
16880208Increased VEGF expression was specific to the senescent phenotype and increased whether senescence was induced by replicative exhaustion, overexpression of p16(Ink4a), or overexpression of oncogenic RAS
16880208The senescence-dependent increase in VEGF production was accompanied by very little increase in hypoxic-inducible (transcription) factor 1 alpha protein levels, and hypoxia further induced VEGF in senescent cells
16880208This result suggests the rise in VEGF expression at senescence is not a hypoxic response
16827160In the immortalized HDFs, the transcriptional activity of HIF-1alpha was also evident by the accumulation of its main downstream gene targets, namely erythropoietin (EPO) and the vascular endothelial growth factor (VEGF)
16755088Angiogenic growth factors secreted by EPCs, such as vascular endothelial growth factor (VEGF), basic fibroblast growth factor (b-FGF), hepatocyte growth factor (HGF), and macrophage chemoattractant protein (MCP-1) from the culture medium were also measured by enzyme-linked immunosorbent assay
16755088There was no significant difference of angiogenic growth factors (VEGF, HGF, b-FGF, and MCP-1) secreted by EPCs between the two groups
16093915In addition, EPCs released vascular endothelial growth factor (VEGF) protein--an effect that was significantly augmented by 17beta-estradiol
16093915Finally, in a Matrigel assay, EPCs treated with both 17beta-estradiol and VEGF were shown to be more likely to integrate into the network formation than those treated with VEGF alone
16010436HUV-ST cells are capable of organizing into tubule-like networks with branching morphology in response to appropriate stimuli and migrate upon exposure to VEGF
12959928Senescent BMP4-treated cells had lower ERK activation, VEGF expression, and Bcl2 expression than wild-type cells, consistent with a less proliferative, less angiogenic phenotype with increased susceptibility to death by apoptosis
12676798In this study, we examined the relationship between telomerase activity and endothelial cell proliferation as well as the regulation of this enzyme by fibroblast growth factor-2 (FGF-2) and vascular endothelial growth factor-A (VEGF)
12676798Treatment of quiescent HUVECs with FGF-2 restored telomerase activity in a time- and dose-dependent manner, whereas VEGF had no such effect, although both factors induced comparable mitogenic responses
12676798CONCLUSIONS: FGF-2, but not VEGF, restores telomerase activity and maintains the replicative capacity of endothelial cells
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