Intracellular Ca2+ can compensate for the lack of NADPH oxidase-derived ROS in endothelial cells.

Abstract:

: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.

journal_name

FEBS Lett

journal_title

FEBS letters

authors

Lee M,Spokes KC,Aird WC,Abid MR

doi

10.1016/j.febslet.2010.05.053

subject

Has Abstract

pub_date

2010-07-16 00:00:00

pages

3131-6

issue

14

eissn

0014-5793

issn

1873-3468

pii

S0014-5793(10)00457-6

journal_volume

584

pub_type

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