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Vascular Endothelial Cell Growth Factor A Acts via Platelet-Derived Growth Factor Receptor ? To Promote Viability of Cells Enduring Hypoxia.

ABSTRACT: Vascular endothelial cell growth factor A (VEGF) is a biologically and therapeutically important growth factor because it promotes angiogenesis in response to hypoxia, which underlies a wide variety of both physiological and pathological settings. We report here that both VEGF receptor 2 (VEGFR2)-positive and -negative cells depended on VEGF to endure hypoxia. VEGF enhanced the viability of platelet-derived growth factor receptor ? (PDGFR?)-positive and VEGFR2-negative cells by enabling indirect activation of PDGFR?, thereby reducing the level of p53. We conclude that the breadth of VEGF's influence extends beyond VEGFR-positive cells and propose a plausible mechanistic explanation of this phenomenon.

SUBMITTER: Pennock S

PROVIDER: S-EPMC5007796 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature

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Vascular Endothelial Cell Growth Factor A Acts via Platelet-Derived Growth Factor Receptor α To Promote Viability of Cells Enduring Hypoxia.

Pennock Steven S Kim Leo A LA Kazlauskas Andrius A

Molecular and cellular biology 20160826 18

Vascular endothelial cell growth factor A (VEGF) is a biologically and therapeutically important growth factor because it promotes angiogenesis in response to hypoxia, which underlies a wide variety of both physiological and pathological settings. We report here that both VEGF receptor 2 (VEGFR2)-positive and -negative cells depended on VEGF to endure hypoxia. VEGF enhanced the viability of platelet-derived growth factor receptor α (PDGFRα)-positive and VEGFR2-negative cells by enabling indirect ...[more]

PMID: 27325673

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