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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: It is demonstrated that hypoxia and TGF-β cooperate in the induction of the promoter activity of vascular endothelial growth factor (VEGF), which is a major stimulus in the promotion of angiogenesis and can synergize in the regulation of VEGF gene expression at the transcriptional level.

391 citations

Journal ArticleDOI
13 Jun 1997-Science
TL;DR: Investigation of the role of growth hormone in ischemia-associated retinal neovascularization in transgenic mice and normal mice suggests systemic inhibition of GH or IGF-I, or both, may have therapeutic potential in preventing some forms of retinopathy.
Abstract: Retinal neovascularization is the major cause of untreatable blindness. The role of growth hormone (GH) in ischemia-associated retinal neovascularization was studied in transgenic mice expressing a GH antagonist gene and in normal mice given an inhibitor of GH secretion (MK678). Retinal neovascularization was inhibited in these mice in inverse proportion to serum levels of GH and a downstream effector, insulin-like growth factor-I (IGF-I). Inhibition was reversed with exogenous IGF-I administration. GH inhibition did not diminish hypoxia-stimulated retinal vascular endothelial growth factor (VEGF) or VEGF receptor expression. These data suggest that systemic inhibition of GH or IGF-I, or both, may have therapeutic potential in preventing some forms of retinopathy.

391 citations

Journal ArticleDOI
TL;DR: In this paper, the authors explored the potential of autologous mesenchymal stem cells transplantation to enhance angiogenesis and cardiac function of ischemic heart disease and found that myocardial infarction induced by occlusion of left anterior descending artery.

391 citations

Journal ArticleDOI
TL;DR: That 16K hPRL is a potent antiangiogenic factor in in vitro and an in vivo assay raises the exciting potential of this peptide being capable of inhibiting tumor growth.
Abstract: The formation of a new blood supply, angiogenesis, is an essential component of carcinogenesis and unrestricted tumor growth. A substance capable of inhibiting angiogenesis would be of considerable therapeutic potential in the treatment of cancer. We previously reported that the 16-kilodalton N-terminal fragment of rat PRL (16K rPRL) was a potent inhibitor of capillary endothelial cell proliferation via a novel receptor. We now report that the nanomolar concentrations of recombinant human 16K PRL inhibit basal and basic fibroblast growth factor- or vascular endothelial growth factor-stimulated growth of bovine brain capillary endothelial cells. 16K human (h) PRL also inhibits stimulation of human umbilical vein endothelial cell proliferation by basic fibroblast growth factor. The organization of endothelial cells into capillary-like structures in type I collagen gels is also prevented by 16K hPRL. Furthermore, in an in vivo assay, the chick embryo chorioallantoic membrane assay, 16K hPRL as well as 16K rP...

389 citations

Journal ArticleDOI
TL;DR: The expression of various genes that regulates angiogenesis in human ovarian carcinomas is associated with the pattern of the disease and its progression, and targeting specific genes that regulateAngiogenesis could offer new approaches to the treatment of ovarian cancer.
Abstract: Background: By the time patients are diagnosed with ovarian carcinoma peritoneal dissemination of the tumor often has occurred. The progressive growth and spread of ovarian carcinoma depend, in part, on the formation of an adequate blood supply. We determined whether the expression of genes that regulate distinct steps in angiogenesis (i.e., the formation of new blood vessels) was associated with the pattern and progressive growth of human ovarian carcinomas implanted in the peritoneal cavity of nude mice. Methods: Five different human ovarian carcinomas were injected individually into the peritoneal cavity of female NCr-nu/nu nude mice. The expression of basic fibroblast growth factor, vascular endothelial growth factor/vascular permeability factor (VEGF/VPF), interleukin 8 (IL-8), and collagenase type IV (MMP-2 [matrix metalloproteinase-2] and MMP-9) was determined by northern blot analysis, in situ hybridization of messenger RNA, and immunohistochemical analysis. Blood vessel distribution and density, macrophage infiltration pattern, and stromal reaction were determined by immunohistochemical analysis with specific antibodies. Results: Three of the carcinomas produced both solid lesions and ascitic tumors, whereas the remaining two produced only solid lesions. Two of the carcinomas produced rapidly progressive disease, two produced slow disease, and one produced intermediate disease. The formation of ascites was directly associated with expression of VEGF/ VPF, and survival was inversely associated with expression of IL-8. In rapidly growing tumors, the number of blood vessels was high throughout the lesion; in contrast, in slow-growing tumors, most vessels (and infiltrating macrophages) were located at the periphery. Conclusions: The expression of various genes that regulate angiogene-sis in human ovarian carcinomas is associated with the pattern of the disease and its progression. Therefore, targeting specific genes that regulate angiogenesis could offer new approaches to the treatment of ovarian cancer.

389 citations


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