【摘 要】
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Principal limitation of cell therapy is cell loss following transplantation because of the interplay between ischemia, inflammation, and apoptosis.We investigated the mechanism of preconditioning of m
【机 构】
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University of Montreal,McGill University (Faculty of Experimental Medicine) Canada
【出 处】
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2013百奥泰波兰重大疾病临床峰会
论文部分内容阅读
Principal limitation of cell therapy is cell loss following transplantation because of the interplay between ischemia, inflammation, and apoptosis.We investigated the mechanism of preconditioning of mesenchymal stem cells (MSC) with oxytocin (OT), which has been proposed as a novel strategy for enhancing therapeutic potential of these cells in ischemic heart.In this study, we demonstrate that rat MSC express binding sites for OT receptor (OTR) and OTR transcript and protein as detected by RT-PCR and immunofluorescence, respectively.During the treatment with OT (10-10 to 10-6M) , MSC respond with rapid calcium mobilization and upregulation of the protective phospho-Akt and phospho-ERKl/2 proteins.In OT stimulated cells, phospho-Akt accumulates intracellularly close to the mitochondrial marker COX4.Functional analyses reveal the involvement of Akt/ERK1/2 pathways in cell proliferation, migration, and protection against the cytotoxic and apoptotic effects of hypoxia and serum deprivation.In addition, OT preconditioning increases MSC glucose uptake.
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