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Vascular endothelial growth factor receptor 2 (VEGFR2, Flk‐1/KDR) protects HEK293 cells against CoCl 2 ‐induced hypoxic toxicity
Author(s) -
Ge Xiaowen,
Zhao Le,
He Langchong,
Chen Wei,
Li Xu
Publication year - 2012
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.1829
Subject(s) - kinase insert domain receptor , angiogenesis , vascular endothelial growth factor , vascular endothelial growth factor a , chemistry , cancer research , receptor tyrosine kinase , protein kinase b , microbiology and biotechnology , pi3k/akt/mtor pathway , receptor , biology , kinase , endocrinology , signal transduction , biochemistry , vegf receptors
Vascular endothelial growth factor (VEGF) is an endothelium‐specific mitogen and a promising inducer of angiogenesis and lymphangiogenesis. The VEGF receptors on endothelial cell membrane include the tyrosine kinases VEGFR‐1 (Flt‐1), VEGFR‐2 (Flk‐1/KDR) and VEGFR‐3 (Flt‐4). KDR is a major mediator of mitogenic, angiogenic and permeability‐enhancing effects of VEGF. KDR is upregulated in response to hypoxia, a major inducer of VEGF gene transcription. A HEK293 cell line overexpressing KDR was established under cell hypoxic stress to explore the function of KDR. A hypoxia‐inducing agent, cobalt chloride (CoCl 2 ) was applied to detect whether KDR was able to prevent against chemical hypoxic toxicity. The results indicate that KDR attenuated CoCl 2 ‐induced cell injury in HEK293 cells. Furthermore, the underlying mechanisms may be explained by the increased expression of Bcl‐2, AKT1 and phosphorylated AKT, key members of cell survival pathway, and decreased expression of pro‐apoptosis protein Bax. Copyright © 2011 John Wiley & Sons, Ltd.