Mesenchymal stem cells (MSCs) have the potential to facilitate cardiac repair following acute myocardial infarction. However, MSC therapy is limited by apoptosis of the stem cells following transplantation. Hydrogen sulfide (H2S) has recently been proposed as an endogenous mediator
of cell apoptosis in various systems. The aim of the present study was to investigate the mechanism underlying the antiapoptotic effect of the endogenous cystathionine γlyase (CSE)/H2S system in MSCs cultivated in conditions of hypoxia and serum deprivation (H/SD). Western blotting was
performed in order to determine the expression of proteins associated with the mitochondrial injury pathway, endoplasmic reticulum stress and the phosphatidylinositol 3kinase (PI3K)/Akt signaling pathway. It was demonstrated that H/SD is able to significantly induce apoptosis in MSCs. CSE
overexpression, which enhances the endogenous H2S level, protects MSCs from H/SDinduced apoptosis via attenuation of the mitochondrial injury pathway, inhibition of endoplasmic reticulum stress and activation of the PI3K/Akt signaling pathway. In conclusion, the present findings suggest that
modulation of the CSE/H2S system may a therapeutic approach with which to promote the viability of transplanted MSCs.
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Document Type: Research Article
Department of ICU, Anhui No. 2 Provincial People's Hospital, Hefei, Anhui 230041, P.R. China
Department of Cardiology, The First Affiliated Hospital of Anhui Medical University, Hefei, Anhui 230022, P.R. China
Publication date: August 1, 2015
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Molecular Medicine Reports is a monthly, peer-reviewed journal available in print and online, that includes studies devoted to molecular medicine, underscoring aspects including pharmacology, pathology, genetics, neurosciences, infectious diseases, molecular cardiology and molecular surgery. In vitro and in vivo studies of experimental model systems pertaining to the mechanisms of a variety of diseases offer researchers the necessary tools and knowledge with which to aid the diagnosis and treatment of human diseases.
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