Topic
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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TL;DR: Endocrine-gland-derived vascular endothelial growth factor (EG-VEGF), induced proliferation, migration and fenestration in capillary endothelial cells derived from endocrine glands, but had little or no effect on a variety of other endothelial and non-endothelial cell types tested.
Abstract: The known endothelial mitogens stimulate growth of vascular endothelial cells without regard to their tissue of origin. Here we report a growth factor that is expressed largely in one type of tissue and acts selectively on one type of endothelium. This molecule, called endocrine-gland-derived vascular endothelial growth factor (EG-VEGF), induced proliferation, migration and fenestration (the formation of membrane discontinuities) in capillary endothelial cells derived from endocrine glands. However, EG-VEGF had little or no effect on a variety of other endothelial and non-endothelial cell types tested. Similar to VEGF, EG-VEGF possesses a HIF-1 binding site, and its expression is induced by hypoxia. Both EG-VEGF and VEGF resulted in extensive angiogenesis and cyst formation when delivered in the ovary. However, unlike VEGF, EG-VEGF failed to promote angiogenesis in the cornea or skeletal muscle. Expression of human EG-VEGF messenger RNA is restricted to the steroidogenic glands, ovary, testis, adrenal and placenta and is often complementary to the expression of VEGF, suggesting that these molecules function in a coordinated manner. EG-VEGF is an example of a class of highly specific mitogens that act to regulate proliferation and differentiation of the vascular endothelium in a tissue-specific manner.
567 citations
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TL;DR: Hypoxia increases V EGF expression in retinal cells, which promotes retinal endothelial cell proliferation, suggesting that VEGF plays a major role in mediating intraocular neovascularization resulting from ischemic retinal diseases.
Abstract: Background: Vascular endothelial growth factor (VEGF) is an angiogenic protein and vasopermeability factor whose intraocular concentrations are closely correlated with active neovascularization in patients with diabetes mellitus, central retinal vein occlusion, retinopathy of prematurity, and rubeosis iridis. Objective: To determine whether hypoxia could induce expression of VEGF in retinal cells, which then promotes retinal endothelial cell proliferation. Methods: Retinal pigment epithelial cells, pericytes, and microvascular endothelial cells were exposed to hypoxic conditions in vitro, and RNA expression of VEGF was evaluated by Northern blot analysis. The VEGF-specific proliferative potential of the medium was measured by means of retinal endothelial cell growth assays and VEGF-neutralizing VEGF receptor IgG chimeric protein. Results: The VEGF RNA levels increased within 4 hours and reached elevations of threefold to 30-fold after 18 hours of hypoxia (0% to 5% oxygen, 5% carbon dioxide, 90% to 95% nitrogen) in all cell types (.01 Conclusion: Hypoxia increases VEGF expression in retinal cells, which promotes retinal endothelial cell proliferation, suggesting that VEGF plays a major role in mediating intraocular neovascularization resulting from ischemic retinal diseases.
567 citations
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TL;DR: This work has defined a “shear stress response element” (SSRE) in the promoter of the human platelet‐ derived growth factor (PDGF)‐B chain gene that interacts with DNA binding proteins in the nuclei of shears stressed endothelial cells to up‐regulate transcriptional activity.
Abstract: Vascular endothelial cells, by virtue of their unique anatomical position, are constantly exposed to the fluid mechanical forces generated by flowing blood. In vitro studies with model flow systems have demonstrated that wall shear stresses can modulate various aspects of endothelial structure and function. Certain of these effects appear to result from the regulation of expression of endothelial genes at the transcriptional level. Recent molecular biological studies have defined a "shear stress response element" (SSRE) in the promoter of the human platelet-derived growth factor (PDGF)-B chain gene that interacts with DNA binding proteins in the nuclei of shear-stressed endothelial cells to up-regulate transcriptional activity. Insertion of this element into reporter genes also renders them shear-inducible. Further characterization of this and other positive (and negative) shear-responsive genetic regulatory elements, as well as their transactivating factors, should enhance our understanding of vascular e...
567 citations
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TL;DR: The identification of VEGF set the stage for a rapid expansion in the understanding of what now appears to be one of the most important mediators of physiologic and pathologic angiogenesis yet discovered.
567 citations
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TL;DR: Angiogenesis is implicated in the pathogenesis of a variety of disorders: proliferative retinopathies, age-related macular degeneration, tumors, rheumatoid arthritis and psoriasis.
Abstract: The development of a vascular supply is a fundamental requirement for organ development and differentiation during embryogenesis as well as for wound healing and reproductive functions in the adult (Folkman 1995) Angiogenesis is also implicated in the pathogenesis of a variety of disorders: proliferative retinopathies, age-related macular degeneration, tumors, rheumatoid arthritis and psoriasis (Folkman 1995; Garner 1994)
566 citations