Biomol Ther.  2016 Jul;24(4):371-379. 10.4062/biomolther.2015.130.

Inhibition of Store-Operated Calcium Entry Protects Endothelial Progenitor Cells from Hâ‚‚Oâ‚‚-Induced Apoptosis

• Wang YW
• Zhang JH
• Yu Y
• Yu J
• Huang L

• KMID: 2351685
• DOI: http://doi.org/10.4062/biomolther.2015.130

Abstract

Store-operated calcium entry (SOCE), a major mode of extracellular calcium entry, plays roles in a variety of cell activities. Accumulating evidence indicates that the intracellular calcium ion concentration and calcium signaling are critical for the responses induced by oxidative stress. The present study was designed to investigate the potential effect of SOCE inhibition on Hâ‚‚Oâ‚‚-induced apoptosis in endothelial progenitor cells (EPCs), which are the predominant cells involved in endothelial repair. The results showed that Hâ‚‚Oâ‚‚-induced EPC apoptosis was reversed by SOCE inhibition induced either using the SOCE antagonist ML-9 or via silencing of stromal interaction molecule 1 (STIM1), a component of SOCE. Furthermore, SOCE inhibition repressed the increases in intracellular reactive oxygen species (ROS) levels and endoplasmic reticulum (ER) stress and ameliorated the mitochondrial dysfunction caused by Hâ‚‚Oâ‚‚. Our findings provide evidence that SOCE inhibition exerts a protective effect on EPCs in response to oxidative stress induced by Hâ‚‚Oâ‚‚ and may serve as a potential therapeutic strategy against vascular endothelial injury.

Keyword

Endothelial progenitor cells; Oxidative stress; SOCE; STIM 1; ML-9

MeSH Terms

Apoptosis*
Calcium Signaling
Calcium*
Endoplasmic Reticulum
Endothelial Progenitor Cells*
Oxidative Stress
Reactive Oxygen Species
Calcium
Reactive Oxygen Species