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• W2014232946 abstract "The role of hypoxia on endothelial cell function and response to growth factors is unknown. Here, we tested the hypothesis that hypoxia re-programs endothelial function by modulating vascular endothelial growth factor receptor levels which in turn alter intracellular signaling and cell function. Hypoxia stimulated VEGF-A and VEGFR1 expression but decreased VEGFR2 levels in endothelial cells. During hypoxia, plasma membrane VEGFR1 levels were elevated whereas VEGFR2 levels were depleted. One functional consequence of hypoxia is a reduction in VEGF-A-stimulated and VEGFR2-regulated intracellular signaling including lowered endothelial nitric oxide synthase activation. Venous, arterial and capillary endothelial cells subjected to hypoxia all exhibited reduced cell migration in response to VEGF-A. A mechanistic explanation is that VEGFR1:VEGFR2 ratio is substantially increased during hypoxia to block VEGF-A-stimulated and VEGFR2-regulated endothelial responses to maximize cell viability and recovery." @default.
• W2014232946 created "2016-06-24" @default.
• W2014232946 creator A5019577580 @default.
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• W2014232946 date "2011-01-01" @default.
• W2014232946 modified "2023-10-18" @default.
• W2014232946 title "Hypoxia differentially regulates VEGFR1 and VEGFR2 levels and alters intracellular signaling and cell migration in endothelial cells" @default.
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• W2014232946 doi "https://doi.org/10.1016/j.bbrc.2010.12.057" @default.
• W2014232946 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/21168388" @default.
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