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ypoxia and Serum Deprivation-induced Apoptosis in Bone Marrow Stromal Cells is Inhibited by SDF-1a through PI3K/Akt and ERK1/2 Signaling Pathways
Qi Yin#, Pei-Feng Jin#, Ling-Ling Li1, Xiao-Ming Lin, Chuang Chi, Yu Liu, Cheng-Chao Sun*
Department of Thoracic and Cardiovascular Surgery, the First Affiliated Hospital of Wenzhou Mendical College, Wenzhou 325000, China; 1Department of Microbiology & Immunology, Wenzhou Medical College, Wenzhou 325000, China
Abstract: Bone marrow stromal cells (BMSCs) have been demonstrated to be one of the most promising cell sources to regenerate infarcted myocardium and restore impaired cardiac function. However， poor viability of BMSCs in infarcted myocardium apparently attenuated its clinical application potential. It has been reported that stromal cell derived factor-1a (SDF-1a) protected several cell types such as endothelial progenitor cells and embryonic stem cells from apoptosis. But whether SDF-1a protein has the same protective effects on BMSCs under conditions of hypoxia and serum deprivation (hypoxia/SD) in vitro and its mechanism is still unknown. In our study， we verified that SDF-1a (0.50-2.0 mg/ml) conspicuously inhibited the apoptosis of BMSCs， which was induced by hypoxia/SD， through mitochondrial pathway. The loss of mitochondrial membrane potential and cytochrome c release from mitochondria to cytosol were significantly inhibited， and caspase-3 activity also detected to be declined by SDF-1a. Furthermore， we found that the effect of SDF-1a on mitochondrial pathway was evidently neutralized by using PI3K inhibitor Wortmannin and ERK1/2 inhibitor U0126. Our observations suggest that SDF-1a inhibits apoptosis induced with hypoxia/SD in BMSCs through PI3K/Akt and ERK1/2 signaling pathways. And these data also imply that the anti-apoptotic effect mediated by SDF-1a may enhance cell survival in cell transplantation.
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