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

FEBS Letters
Monica LeeMd Ruhul Abid

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.

References

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Citations

Jan 7, 2014·Antioxidants & Redox Signaling·Francisco R M LaurindoThalita B Abrahão
Jun 28, 2016·Cell Biology and Toxicology·Georgios DivolisPanagiota Papazafiri
Nov 8, 2016·Biochimica Et Biophysica Acta. Molecular Cell Research·Estefanía Anguita, Antonio Villalobo
Apr 27, 2012·American Journal of Physiology. Endocrinology and Metabolism·Kishorchandra Gohil, George A Brooks
Aug 17, 2019·International Journal of Molecular Sciences·Francesco MocciaGermano Guerra
Dec 18, 2020·Frontiers in Chemistry·Raid AlhayazaM Ruhul Abid

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