Abstract
Adult human vascular endothelial cells (ECs) change their phenotype in response to changes in vascular tumor microenvironments, oxygen concentration and during wound healing. During angiogenesis, the physiological process of creating new blood vessels, hundreds of genes are activated with one of the most important being VEGF (vascular endothelial growth factor). VEGF, the signaling protein, stimulates EC migration, proliferation, and vascularization. During angiogenesis, ECs undergo an ‘angiogenic switch’; they change from a resting (quiescent) phenotype to a more elongated and mobile (tip cells) or proliferative and mobile (stalk cells) phenotype.
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