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Inhibition of Store-Operated Calcium Entry Protects Endothelial Progenitor Cells from H2O2-Induced Apoptosis.

Wang YW, Zhang JH, Yu Y, Yu J, Huang L - Biomol Ther (Seoul) (2016)

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Cardiovascular Diseases of PLA, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, People's Republic of China.

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.

No MeSH data available.


Related in: MedlinePlus

Inhibition of SOCE prevents intracellular ROS accumulation. EPCs that had been cultured for 7 days were pretreated with ML-9 for 20 min or with STIM1 shRNA before exposure to H2O2 for 6 h, and intracellular ROS levels were evaluated using a fluorescence probe (DCFHDA). *p<0.05; #p<0.05.
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f4-bt-24-371: Inhibition of SOCE prevents intracellular ROS accumulation. EPCs that had been cultured for 7 days were pretreated with ML-9 for 20 min or with STIM1 shRNA before exposure to H2O2 for 6 h, and intracellular ROS levels were evaluated using a fluorescence probe (DCFHDA). *p<0.05; #p<0.05.

Mentions: To investigate the role of ROS in the protective effects of SOCE inhibition, we used the fluorescent probe DCFH-DA to detect intracellular ROS production. Compared with the control group, the H2O2 treatment group exhibited significantly increased ROS accumulation, and the inhibition of SOCE markedly blunted this effect (Fig. 4).


Inhibition of Store-Operated Calcium Entry Protects Endothelial Progenitor Cells from H2O2-Induced Apoptosis.

Wang YW, Zhang JH, Yu Y, Yu J, Huang L - Biomol Ther (Seoul) (2016)

Inhibition of SOCE prevents intracellular ROS accumulation. EPCs that had been cultured for 7 days were pretreated with ML-9 for 20 min or with STIM1 shRNA before exposure to H2O2 for 6 h, and intracellular ROS levels were evaluated using a fluorescence probe (DCFHDA). *p<0.05; #p<0.05.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4930280&req=5

f4-bt-24-371: Inhibition of SOCE prevents intracellular ROS accumulation. EPCs that had been cultured for 7 days were pretreated with ML-9 for 20 min or with STIM1 shRNA before exposure to H2O2 for 6 h, and intracellular ROS levels were evaluated using a fluorescence probe (DCFHDA). *p<0.05; #p<0.05.
Mentions: To investigate the role of ROS in the protective effects of SOCE inhibition, we used the fluorescent probe DCFH-DA to detect intracellular ROS production. Compared with the control group, the H2O2 treatment group exhibited significantly increased ROS accumulation, and the inhibition of SOCE markedly blunted this effect (Fig. 4).

Bottom Line: 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.

View Article: PubMed Central - PubMed

Affiliation: Institute of Cardiovascular Diseases of PLA, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, People's Republic of China.

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.

No MeSH data available.


Related in: MedlinePlus