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Vascular endothelial growth factor A

About: Vascular endothelial growth factor A is a research topic. Over the lifetime, 15203 publications have been published within this topic receiving 1271498 citations. The topic is also known as: vascular endothelial growth factor A & vascular endothelial growth factor A165.


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Journal ArticleDOI
TL;DR: A novel mechanism by which the cooperative activity of the oncogenes, ras and myc, leads directly to angiogenesis and tumor formation is described.

340 citations

Journal ArticleDOI
TL;DR: Osteoclastic function and angiogenesis are up‐regulated by a common mediator such as VEGF, which caused a dose‐ and time‐dependent increase in the area of bone resorption pits excavated by the isolated osteoclasts.

339 citations

Journal ArticleDOI
TL;DR: It is demonstrated that ET-1 induces angiogenic responses in cultured endothelial cells through ET(B)R and that stimulates neovascularization in vivo in concert with VEGF and its receptors acting asAngiogenic regulators might represent new targets for anti-angiogenic therapy.
Abstract: The endothelial cell-derived endothelin-1 (ET-1) is a potent mitogen for endothelial cells, vascular smooth muscle cells, and tumor cells. In this study, we analyzed the role of ET-1 on human umbilical vein endothelial cell (HUVEC) phenotype related to different stages of angiogenesis. ET-1 promoted HUVEC proliferation, migration, and invasion in a dose-dependent manner. The ET B receptor (ET B R. antagonist, BQ 788, blocked the angiogenic effects induced by ET-1, whereas the ET A R antagonist was less effective. ET-1 stimulated matrix metalloproteinase-2 mRNA expression and metalloproteinase-2 production, as determined by reverse transcriptase-polymerase chain reaction and gelatin zymography. Furthermore ET-1 was able to enhance HUVEC differentiation into cord vascular-like structures on Matrigel. When tested in combination with vascular endothelial growth factor (VEGF), ET-1 enhanced VEGF-induced angiogenic-related effects on endothelial cells in vitro . Finally, using the Matrigel plug neovascularization assay in vivo , ET-1 in combination with VEGF stimulated an angiogenic response comparable to that elicited by basic fibroblast growth factor. These findings demonstrated that ET-1 induces angiogenic responses in cultured endothelial cells through ET B R and that stimulates neovascularization in vivo in concert with VEGF. ET-1 and its receptors acting as angiogenic regulators might represent new targets for anti-angiogenic therapy.

339 citations

Journal ArticleDOI
TL;DR: Research is described demonstrating that VEGF is not only important for tumor vascularization, but is also a key factor produced by solid tumors to inhibit recognition and destruction of tumor cells by the immune system.
Abstract: Decreased immune function in cancer patients is well-characterized (I), and tumor cells have developed a variety of mechanisms, to avoid anti-tumor immune responses (2–8). One mechanism for inhibition of immune cell function by tumors in the production of soluble factors, such as IL-10, TNF, TGF-β, and Vascular Endothelial Growth Factor (VEGF). The effects of these factors appear, to be twofold: To inhibit effect or function and to impair the development of immune cells by acting on earlier stages of immunopoiesis. Immune suppression by tumors is accomplished by a variety of cellular and molecular mechanisms, and virtually all branches of the immune system can be affected. VEGF and its receptors have profound effects on the early development and differentiation of both vascular endothelial and hematopoetic progenitors (9). It induces proliferation of mature endothelial cells and is an important component in the formation of tumor neovasculature (10). VEGF is abundantly expressed by a large percentage of solid tumors and this over-expression is closely associated with a poor prognosis (11, 12). Some of the earliest hematopoetic progenitors express receptors for VEGF (13), and we have demonstrated that VEGF causes a defect in the functional maturation of dendritic cells (DC) from progenitors. This developmental defect is associated with impaired activation of NF-κB (14–17). This review describes research demonstrating that VEGF is not only important for tumor vascularization, but is also a key factor produced by solid tumors to inhibit recognition and destruction of tumor cells by the immune system.

339 citations

Journal ArticleDOI
TL;DR: It is suggested that TSP-1 is a useful antagonist to tumor angiogenesis and that it may have therapeutic value when used in conjunction with inhibitors of VEGF.
Abstract: Hepatocyte growth factor/scatter factor (HGF/SF), acting through the Met receptor, plays an important role in most human solid tumors, and inappropriate expression of this ligand–receptor pair is often associated with poor prognosis. The molecular basis for the malignant potential of the HGF/SF–Met signal in cancer cells has mostly been attributed to its mitogenic and invasive properties. However, HGF/SF also induces angiogenesis, but the signaling mechanism has not been fully explained, nor has this activity been directly associated with HGF/SF–Met-mediated tumorigenesis. It is known that HGF/SF induces in vitro expression of vascular endothelial growth factor (VEGF), a key agonist of tumor angiogenesis; by contrast, thrombospondin 1 (TSP-1) is a negative regulator of angiogenesis. Here, we show that, in the very same tumor cells, in addition to inducing VEGF expression, HGF/SF dramatically down-regulates TSP-1 expression. We show that TSP-1 shut-off plays an important, extrinsic role in HGF/SF-mediated tumor development, because ectopic expression of TSP-1 markedly inhibits tumor formation through the suppression of angiogenesis. Interestingly, although VEGF-induced expression is sensitive to inhibitors of several pathways, including mitogen-activated protein kinase, phosphoinositide 3-kinase, and signal transducer and activator of transcription 3, TSP-1 shut-off by HGF/SF is prevented solely by inhibiting mitogen-activated protein kinase activation. These studies identify HGF/SF as a key switch for turning on angiogenesis. They suggest that TSP-1 is a useful antagonist to tumor angiogenesis and that it may have therapeutic value when used in conjunction with inhibitors of VEGF.

339 citations


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Performance
Metrics
No. of papers in the topic in previous years
YearPapers
202394
2022189
2021293
2020347
2019306
2018333