Inhibition of Store-Operated Calcium Entry Protects Endothelial Progenitor Cells from H₂O₂-Induced Apoptosis.
10.4062/biomolther.2015.130
- Author:
Yan Wei WANG
1
;
Ji Hang ZHANG
;
Yang YU
;
Jie YU
;
Lan HUANG
Author Information
1. Institute of Cardiovascular Diseases of PLA, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, People's Republic of China. huanglan260@126.com
- Publication Type:Original Article
- Keywords:
Endothelial progenitor cells;
Oxidative stress;
SOCE;
STIM 1;
ML-9
- MeSH:
Apoptosis*;
Calcium Signaling;
Calcium*;
Endoplasmic Reticulum;
Endothelial Progenitor Cells*;
Oxidative Stress;
Reactive Oxygen Species
- From:Biomolecules & Therapeutics
2016;24(4):371-379
- CountryRepublic of Korea
- Language:English
-
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 H₂O₂-induced apoptosis in endothelial progenitor cells (EPCs), which are the predominant cells involved in endothelial repair. The results showed that H₂O₂-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 H₂O₂. Our findings provide evidence that SOCE inhibition exerts a protective effect on EPCs in response to oxidative stress induced by H₂O₂ and may serve as a potential therapeutic strategy against vascular endothelial injury.
