Vascular endothelial growth factor induced by hypoxia may mediate hypoxia-initiated angiogenesis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1992-10

AUTHORS

D Shweiki, A Itin, D Soffer, E Keshet

ABSTRACT

Inefficient vascular supply and the resultant reduction in tissue oxygen tension often lead to neovascularization in order to satisfy the needs of the tissue. Examples include the compensatory development of collateral blood vessels in ischaemic tissues that are otherwise quiescent for angiogenesis and angiogenesis associated with the healing of hypoxic wounds. But the presumptive hypoxia-induced angiogenic factors that mediate this feedback response have not been identified. Here we show that vascular endothelial growth factor (VEGF; also known as vascular permeability factor) probably functions as a hypoxia-inducible angiogenic factor. VEGF messenger RNA levels are dramatically increased within a few hours of exposing different cell cultures to hypoxia and return to background when normal oxygen supply is resumed. In situ analysis of tumour specimens undergoing neovascularization show that the production of VEGF is specifically induced in a subset of glioblastoma cells distinguished by their immediate proximity to necrotic foci (presumably hypoxic regions) and the clustering of capillaries alongside VEGF-producing cells. More... »

PAGES

843-845

Journal

TITLE

Nature

ISSUE

6398

VOLUME

359

Author Affiliations

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/359843a0

    DOI

    http://dx.doi.org/10.1038/359843a0

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1028884048

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/1279431


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