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Intracellular Ca 2+ can compensate for the lack of NADPH oxidase‐derived ROS in endothelial cells
Author(s) -
Lee Monica,
Spokes Katherine C.,
Aird William C.,
Abid Md. Ruhul
Publication year - 2010
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2010.05.053
Subject(s) - intracellular , nadph oxidase , protein kinase b , microbiology and biotechnology , pi3k/akt/mtor pathway , chemistry , endoplasmic reticulum , bapta , cell growth , endothelial stem cell , signal transduction , reactive oxygen species , biochemistry , biology , in vitro
The aim of the present study is to determine the role of intracellular Ca 2+ in VEGF signaling. We demonstrate that reduction in Ca 2+ by chelating compound BAPTA‐AM or by IP 3 ‐endoplasmic reticulum blocker 2‐APB selectively inhibited VEGF‐induced activation of c‐Src‐PI3K‐Akt but not ERK1/2 in human coronary artery endothelial cells (HCAEC). We also show that the selective inhibitory effects of NADPH oxidase knockdown on VEGF‐mediated activation of c‐Src‐PI3K‐Akt signaling and cell proliferation in HCAEC can be reversed by increase in intracellular Ca 2+ . These results suggest an essential role for Ca 2+ in redox‐dependent selective activation of c‐Src‐PI3K‐Akt and endothelial cell proliferation.