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Knockdown of transmembrane protein 33 (tmem33) impairs multiple downstream effects of vascular endothelial growth factor (VEGF).
GDF6 promotes vascular stabilization by restraining vascular endothelial growth factor signaling.
Vegfaa role in the venous sprouting and spinal cord vascularization.
findings identify Vegfa as one of a select few known factors sufficient to activate adult cardiomyogenesis, while also illustrating how instructive factors for heart regeneration require spatiotemporal control for efficacy.
Vegfa signaling governs the formation of diverse arteries/veins by distinct cellular mechanisms in vertebrate vasculatures
vascular endothelial growth factor and Hedgehog pathways have roles in the development of the superficial system of ocular vessel patterning in zebrafish
miR-9 modulation of neuronal VEGF-A controls brain angiogenesis in vivo.
Timelapse analysis of individual cardiomyocyte trajectories reveals misdirected cells in zebrafish pdgfra mutants, suggesting that PDGF signaling steers cardiomyocytes toward the midline during cardiac fusion. Intriguingly, the ligand pdgfaa is expressed in the endoderm medial to the pdgfra-expressing myocardial precursors.
This study demonstrates the involvement of VEGF signaling in regulating sustained liver injuries after acute alcohol exposure.
we determined that radial glia control this process via the Vegf decoy receptor sFlt1: sflt1 mutants exhibit the venous over-sprouting observed in radial glia-ablated larvae, and sFlt1 overexpression rescues it. Genetic mosaic analyses show that sFlt1 function in trunk endothelial cells can limit their over-sprouting.
High VEGFA expression is associated with Ectopic Proliferation and Retinal Dysplasia in Zebrafish Optic Pathway Tumors.
Rspo1 is required for hematopoietic stem cell specification through control of parallel signaling pathways controlling HSC specification: Wnt16/DeltaC/DeltaD and Vegfa/Tgfbeta1
Tmem2 regulates hyaluronic acid turnover to promote normal Vegf signaling during developmental angiogenesis.
low levels of Vegf signaling promote overall vascular endothelial differentiation and cell survival by upregulating etv2 expression, while high levels of Vegf signaling promote arterial and inhibit venous specification.
altering the amount of VEGF signaling in endothelial cells by stimulating them with different VEGF concentrations triggered distinct and mutually exclusive dynamic Ca(2+) signaling responses that correlated with different cellular behaviors.
Bis(2,3-dibromo-4,5-dihydroxybenzyl) ether downregulate the expression of VEGF and VEGFR, and simultaneously regulates VEGF signaling pathway to prevent angiogenesis.
noncanonical function of tars regulates vascular development presumably by modulating the expression of vegfa
Methylglyoxal acts on smaller blood vessels in zebrafish via the VEGF receptor signaling cascade, thereby describing a new mechanism that can explain vascular complications under hyperglycemia and elevated MG concentrations.
The translation initiation factor eIF3i up-regulates VEGF-A, accelerates cell proliferation, and promotes angiogenesis in embryonic development.
lack of SULF1 expression downregulates VEGFA-mediated arterial marker expression, confirming that Sulf1 mediates arterial specification by regulating VegfA165 activity.
Etv6, positively regulates vegfa expression during Xenopus blood stem cell development through multiple transcriptional inputs. In agreement with its established repressive functions, Etv6 directly inhibits expression of the repressor foxo3, to prevent Foxo3 from binding to and repressing the vegfa promoter.
VEGFA produced in the somites is required to initiate adult haemangioblast programming in the adjacent dorsal lateral plate mesoderm.
sequential, isoform-specific VEGFA signaling successively induces the endothelial, arterial, and hematopoietic stem cell programs in the dorsal aorta.
VEGF induces stromal cell migration or recruitment that are required for blood vessel formation.
Functional roles of VEGF122 and VEGF170 during development were examined.
increased VEGF(170) levels disturb Hand-1 expression in the region required for normal heart morphogenesis
data for the first time demonstrate a calpain/PTP1B/VEGFR2 negative feedback loop in the regulation of VEGF-induced angiogenesis. Modulation of local PTP1B and/or calpain activities may prove beneficial in the treatment of impaired wound healing in diabetes.
Studied the effect of cyclic uniaxial stretch (20%, 1 Hz), with and without the stimulation of vascular endothelial growth factor (VEGF), on sprouting angiogenesis by employing a stretchable three-dimensional cell culture model.
Study shows that VEGFA mRNA in mammalian endothelial cells undergoes programmed translational readthrough (PTR) generating VEGF-Ax, an isoform containing a unique 22-amino-acid C terminus extension.
Data indicate that superoxide dismutase (SOD) inhibited high glucose (HG)-induced expression of uPAR and VEGF in bovine retinal microvascular endothelial cell (REC).
Exposure of endothelial cells to VEGF, high glucose, or hydrogen peroxide up-regulated the XBP1/IRE1 alpha and ATF6 arms of the unfolded protein response compared with untreated cells.
Microvascular endothelial cells are more susceptible than aortic cells to advanced glycation end products-enhanced permeability and that AGE-enhanced permeability is dependent on VEGF expression induced by reactive oxygen species.
VEGF supports germ cell survival and sperm production in bulls.
analysis of polymorphisms of bovine VEGF gene and their associations with growth traits in Chinese cattle
VEGF mRNA expression at estrus was higher than at the early I, early II and late luteal stages (P<0.05), whereas VEGF protein content was greatest at the early I luteal stage and decreased thereafter
Alterations in the expression of VEGF-A and bFGF systems suggest that angiogenic factors are involved in abnormal placental development in cloned gestations, contributing to impaired fetal development and poor survival rates.
Advanced glycation end products increase, through a protein kinase C-dependent pathway, expression in reignal endothelial cells; inhibited by gliclazide.
VEGF signaling is regulated by atrial natriuretic peptide, which preserves endothelial cell tight junction functional morphology
Airline pilots are good candidates to see if mutation in the VEGF promoter are responsible for some cases of amyotrophic lateral sclerosis.
role in dowregulating Flk-1/KDR involves Cbl-mediated ubiquitination
interaction with glucose-6-phosphate dehydrogenase is involved in angiogenesis
Results suggest that leptin might elicit angiogenesis through vascular endothelial growth factor induction as well as pigment epithelium-derived factor suppression in pericytes.
Shear stress and VEGF converge at the membrane receptor Flk-1 and these stimuli share the Flk-1/Cbl/Akt pathway in activating IKK activation.
Tumor cells activate confluent, quiescent EC, promoting survival, phenotypic, and gene expression changes. Of importance, VEGF antagonism converts tumor-conditioned medium from protective to endothelial cell-damaging effects.
MGP plays a role in endothelial cell function, by increasing transforming growth factor-beta1 activity and stimulating VEGF expression
placenta growth factor expression is regulated by both VEGF and hyperglycaemia via VEGFR-2
Vascular endothelial growth factor A (VEGF-A) serum levels increase significantly in Clostridium difficile infection patients but decrease following treatment. Toxin producing C. difficile induce the expression of VEGF-A in human colonic mucosal biopsies. Toxins-exposed human colonocytes stimulate human intestinal microvascular endothelial cells proliferation mediated by the hypoxia-inducible factor (HIF)-VEGF axis.
TNF has a role in stimulating IL-6, CXCL8 and VEGF secretion from human keratinocytes via activation of mTOR, inhibited by tetramethoxyluteolin
we outline the roles of VEGF and ANG2 in tumour immune evasion and progression, and discuss the evidence indicating that antiangiogenic agents can normalize the tumour microenvironment
Data suggest simultaneous silencing of vascular endothelial growth factor (VEGF) and Survivin using the dual siRNA may be an advantageous alternative for the development of therapeutic strategies against human osteosarcoma.
VEGF-A is considered as functional vital and direct target to miR-126 in breast cancer cell line.
The expression of VEGFR-1 and VEGFR-2 are more significant in PTC with relevant co-expression of VEGF and VEGFR-1.
This study confirms the contribution of altered VEGF secretion, resulting from genetic variation in VEGFA gene into type 2 diabetes pathogenesis.
tumor-secreted CTGF/VEGFA alone is sufficient to activate paired mammary fibroblasts from the same patient via ROCK1 and JunB signaling.
Proximal splicing that includes an exon 8a sequence results in pro-angiogenic VEGF-A165a, whereas distal splicing inclusive of exon 8b yields the anti-angiogenic isoform of VEGF-A (VEGF-A165b). This review highlights several recent preclinical and clinical studies on the role of VEGF-A165b in cardiovascular disease and chronic kidney disease as a novel function of VEGF-A. [review]
Peritoneal membrane damage in patients on peritoneal dialysis is associated with fibrosis and neoangiogenesis through the TGF-beta1-VEGF-A pathway.
Our meta-analysis suggested that rs3025039 (C>T), rs833052 (C>A) and rs25648 (C>T) polymorphisms of VEGF gene increased susceptibility to Bladder Cancer (BCa) risk. We also demonstrated homozygous TT genotype in rs3025039, homozygous AA genotype in rs833052 and homozygous TT genotype in rs25648 were significantly relevant to elevated BCa risk. rs699947 (C>A) A-allele is a protective factor for BCa.
Metastatic colorectal cancer patients with cytoplasmic E-cadherin expression had a higher level of VEGFA co-expression, a lower response rate to the first-line irinotecan-based therapy, and a poorer prognosis during the 6-year follow-up.
Overall, the study suggests that VEGF-A165b isoform might play a deleterious role after ST-segment elevation myocardial infarction as an inhibitor of angiogenesis in the myocardium.
VEGF level in the embryo culture medium can be used as one reference indicator for predicting embryo quality and pregnancy outcome. The VEGF 936 C/T gene polymorphism may be related to IVF-ET/ICSI treatment outcome, and C allele may be a susceptibility gene for IVF-ET/ICSI failure.
Plasma leptin and vascular endothelial growth factor (VEGF) in normal subjects at high altitude (5050 m).
suggest that high baseline VEGF level can be a predictor for lack of therapy response
The mean value of serum VEGF in infantile hemangioma patients was significantly higher than that in the control group.
MiR-622 inhibits CRC angiogenesis by suppressing the CXCR4-VEGFA signaling axis.
Results find the expression of VEGF-A was 60% higher in the basal ganglia of congenital heart disease fetuses compared with controls.
There was no significant difference of PD-1 and CTLA-4 expression on CD(4)(+)T cells in patients with and without OSAHS[obstructive sleep apnea hypopnea syndrome]. The expression of VEGF was elevated in OSAHS patients, and increased with the severity of OSAHS and hypoxia.
Infection with enterotoxins-producing Clostridium difficile strains but not with a TcdA(-)TcdB(-) isogenic mutant increases colonic vascular permeability in mice and elevates vascular endothelial growth factor A (VEGF-A). Both neutralization of VEGF-A and inhibition of its signalling pathway attenuated Clostridium difficile infection pathogenesis in vivo.
When miR27a expression was depleted by miR27a inhibitor, the protective effect of betaelemene on RNV was eliminated. The present study demonstrated that belemene reduced RNV in mouse oxygen-induced retinopathy (OIR) models via miR27a upregulation, leading to reduced VEGF expression.
the results of immunofluorescence staining of hepatic myeloid cells and detection of vascular growth factor A (VEGFA) in blood and liver suggested that the reduced degeneration of collagen in liver sinusoids was associated with decreased myeloid cell adhesion and the downregulation of VEGFA in the liver.
repressed Dll4-Notch1 signaling pathway but not downregulation of VEGF-A expression are responsible for hyperoxia induced pervasive vessel regression.
Here the authors have demonstrated that TGF-beta/Smad signaling plays an important role in Laser-induced choroidal neovascularization formation through down-regulation of VEGF and TNF-alpha expressions.
renal ischemia/reperfusion (I/R) induced miR-377 expression, which upregulated VEGF expression to attenuate renal I/R-induced oxidative stress and inflammation, and finally ameliorated renal dysfunction.
Mice exposed to treadmill exercise after cerebral ischemia showed a significant up-regulation in expression of VEGF compared to non-exercised animals.
At this late stage, glomerular VEGF and fibrosis-related-gene expression was also significantly increased compared with nondiabetic db/m mice. These results suggest that LRG1 plays a pivotal role in the initial development of diabetic nephropathy by promoting abnormal angiogenesis, thereby suggesting that LRG1 is a potential preemptive therapeutic target of diabetic nephropathy.
uterine endothelial cells promoted miR138 to induce exosomemediated inflammation and apoptosis in Ems through the VEGF/NFkappaB signaling pathway.
Aquaporin-4 (AQP4) is involved in the hypoxia-dependent VEGF upregulation in the retina of a mouse model of oxygen-induced retinopathy
Mechanistically, Adrb2 loss increases production of Vascular Endothelial Growth Factor-A (VEGF-A) in female neonatal beta-cells and results in hyper-vascularized islets during development, which in turn, disrupts insulin production and exocytosis.
VEGF and VEGFB counteractively regulate adipose development and function in energy metabolism.
The data suggest that TFAF6 inhibition reduces choroidal neovascularization formation via down-regulating expression of HIF-1a and VEGF and activation of macrophages and microglia.
early local misexpression of VEGF genes and abnormal decidual vasculature preceded sFlt-1 overexpression and increased complement deposition in BPH/5 placentae.
Study indicated that Stat3 was involved in the negative regulation of Vegf expression by miR20b in mouse H22 hepatocellular carcinoma cells.
Study using Hcar1-KO mice identified the lactate receptor Hcar1 as a key regulator of Vegf and angiogenesis in the brain and as an initial mediator of cerebral effects of physical exercise.
Motor neurons control blood vessel patterning by an autocrine mechanism that titrates motor neuron-derived VEGF via their own expression of sFlt1.
Targeting NLRP3 shifts the VEGF-A-induced cardiac hypertrophy from a pathologic toward a more physiologic hypertrophy.
T3 thyroid hormone stimulates the expression and secretion of VEGF by Leydig cells
Dexamethasone suppressed mRNA VEGF expression and VEGF production in cortical cells while in medullar cells only VEGF production was reduced. Introduction of IL-7, IL-1b or murine thymocytes increased while addition of Semaphorin 3A, SDF-1a or ACTH decreased VEGF production by cortical epithelial cells with no influence on medullar cells.
It regulates endometrial remodeling in the porcine endometrial tissues during follicular and luteal phase.
It was concluded that VEGF and factor VIII are important growth factors associated with fetal development in pigs and are identified in all uterine segments.
results are consistent with a participation of (VEFG) in the regulation of the dynamics of oviductal fluid secretion and the oviduct contractibility
Here we demonstrate that VEGF-165 mediates MSC differentiation into ECs via VEGFR-2-dependent induction of Sox18, which ultimately coordinates the transcriptional upregulation of specific markers of the EC phenotype.
VEGF was significantly downregulated 7 days after cryotherapy of the sclera and stayed at that level until day 14. It returned to baseline by day 21.
VEGF production, blood vessel network and follicle remodeling are impaired by the antiprogesterone RU486.
findings suggest that the augmented neovascular response seen with VEGF administration was through the VEGF-induced upregulation of Notch signaling.
interleukin-1beta-induced vascular endothelial growth factor in airway smooth muscle cells
Upregulation of VEGF during hypoxia in chondrocyte is mediated partially through HIF-1alpha.
data shows that members of the VEGF-VEGFR system are temporally and spatially well localized for playing key roles during umbilical cord formation and its intensive growth observed after day 75 of pregnancy
cardiac-specific and hypoxia-induced coexpression of VEGF and Ang1 improves the perfusion and function of porcine MI heart through the induction of angiogenesis and cardiomyocyte proliferation
The mRNA for VEGFA was expressed in early developing and in maturing glomeruli.
Data show that subventricular zone neural stem cells express VEGF and all VEGF splice variants, VEGFR1, VEGFR2 and Neuropilin-1 and -2 mRNAs.
The earlier increase in VEGF protein and mRNA expression in the Meishan versus the Yorkshire conceptus may explain the previously reported increased vascularity and increased placental efficiency of this breed compared the Yorkshire breed.
Contrast media did not affect bone marrow cell viability/VEGF secretion.
VEGF upregulation in the proliferative zone after ischemic damage may play a role in stimulating vascular invasion and granulation tissue formation in the necrotic hypertrophic zone of the epiphyseal cartilage
Data demonstrate that lipopolysaccharides evoke a heat shock response, with an increase heat shock proteins 70 and Hsp32) and of VEGF, a specific endothelial cell growth factor.
Vascular endothelial growth factor (VEGF) plays an important role in the thecal angiogenesis during follicular development.
number of preovulatory follicles and the capillary density in the theca interna increased significantly in the ovaries injected with VEGF gene
our study revealed the presence of VEGF in endothelial and smooth muscle cells of vascular subovarian plexus arteries
Peripheral Blood-Derived Mesenchymal Stromal Cells Promote Angiogenesis via Paracrine Stimulation of Vascular Endothelial Growth Factor Secretion
TNF may up-regulate VEGF and stimulate angiogenesis in the mare early corpus luteum.
After acoustic trauma, vascular endothelial growth factor was up-regulated both in the cochlea and vestibule. Expression in both structures suggests a reparative role with potentially therapeutic implications.
Studied the role of T help 17 cells (Th17) and STAT3-VEGF pathway in pathogenesis of psoriasis.
MiR-145 silencing promotes bone repair of avascular necrosis of femoral head (ANFH) via upregulating VEGF, bFGF and inhibiting the bone cells apoptosis through Wnt/beta-catenin pathway
ghrelin can inhibit intraplaque angiogenesis and promote plaque stability by down-regulating VEGF and VEGFR2 expression, inhibiting the plaque content of macrophages, and reducing MCP-1 expression at an advanced stage of atherosclerosis in rabbits
VEGF mRNA abundance was present at low levels at 16 h post-ovulation and remained low at 72 h, but the level increased at 144 h in uterus.
correlation was observed between CT perfusion parameters (BF, BV, PS, and MAV) and expression of VEGF and MVD in tumor tissue
Physiologic ischemic training stimulates VEGF-mediated mobilization of endothelial progenitor cells as well as angiogenesis.
Suggest supplemental oxygen inhibits HIF-1alpha/VEGF signaling to reduce smooth muscle proliferation in rabbit arteriovenous fistula model.
Therefore, it was reasonable to speculate that the increased expression of VEGF and MMP-9 in residual hepatic tumor cells and tumor angiogenesis post-embolization would be responsible for the increased metastatic potentiality and invasiveness.
VEGF expression peaked at 8 weeks after meniscus transplantation
Studied the biocompatibility and neovascularization of the PLGA nanospheres wrapped with vascular endothelial growth factor (VEGF).
VEGF induces TGF-beta1 expression and myofibroblast transformation after glaucoma surgery.
The results of this study are promising concerning the role of VEGF as a diagnostic marker in moderate osteoarthritis
The overexpression of VEGF increased tumor growth and vascularization, favored cyst formation, and reduced tumor necrosis.
VEGF may play a role in the blood-aqueous barrier dysfunction after retinal laser photocoagulation.
In the early stages of myocardial ischemia, bone marrow stem cells are mobilized and home to ischemic myocardium with a concomitant increase in expression of cytokines VEGF and TNFalpha.
It appears that VEGF modulates angiogenesis and osteogenesis in shockwave-promoted bone healing in rabbits.
Transplantation of mononuclear bone marrow cells promotes the expression of VEGF in acute liver injury.
The down-regulation of VEGF may play a critical role in the disease process of osteonecrosis.
Vitreous VEGF levels increase in positive correlation with plasma VEGF during pregnancy
Antenatal intratracheal VEGF administration was associated with an increase in Flk-1 immunoreactivity.
VEGF is expressed at different times and locations during bone healing.
Data suggest that microRNA-126 plays role in diabetic retinopathy; here, choroid-retinal endothelial cells exposed to high glucose exhibit down-regulation of microRNA-126 and up-regulation of VEGFA and PIK3R2; overexpression of microRNA-126 down-regulates expression of VEGFA and PIK3R2. (VEGFA = vascular endothelial growth factor A; PIK3R2 = class Ia phosphoinositol-3 kinase regulatory subunit 2)
VEGF plays an important role in choroid-retinal endothelial cell proliferation and tube formation.
Evidence of non-AUG translation initiation in humans.
These findings suggest that FBLN5 may interfere with choroidal neovascularization by downregulating VEGF, CXCR4, and TGFB1 expression and inhibiting choroidl endothelial cell proliferation.
Apelin may play a role in the development of central retinal vein occlusion (CRVO). Apelin has a unique upstream signaling pathway, independent of the VEGF pathway.
Dll4 play an important role in choroidal neovascularization (CNV) angiogenesis, which appears to be regulated by HIF-1alpha and VEGF during the progression of CNV under hypoxic conditions.
A functional network involving VEGF, IGF2, and MMP9 in early placental trophoblast cells and maternal endometrium appears to be important for normal placentation.
This gene is a member of the PDGF/VEGF growth factor family and encodes a protein that is often found as a disulfide linked homodimer. This protein is a glycosylated mitogen that specifically acts on endothelial cells and has various effects, including mediating increased vascular permeability, inducing angiogenesis, vasculogenesis and endothelial cell growth, promoting cell migration, and inhibiting apoptosis. Elevated levels of this protein is linked to POEMS syndrome, also known as Crow-Fukase syndrome. Mutations in this gene have been associated with proliferative and nonproliferative diabetic retinopathy. Alternatively spliced transcript variants, encoding either freely secreted or cell-associated isoforms, have been characterized. There is also evidence for the use of non-AUG (CUG) translation initiation sites upstream of, and in-frame with the first AUG, leading to additional isoforms.
, vascular endothelial growth factor A
, vascular endothelial growth factor A-A
, vascular endothelial growth factor A-a
, vascular endothelial growth factor 164
, vascular permeability factor
, vascular endothelial growth factor 188
, angiogenic factor
, Vascular permeability factor
, endothelial growth factor-164
, vascular endothelial growth factor VEGF