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首页> 外文期刊>Biochemical and Biophysical Research Communications >Therapeutic effects of erythropoietin expressed in mesenchymal stem cells for dilated cardiomyopathy in rat
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Therapeutic effects of erythropoietin expressed in mesenchymal stem cells for dilated cardiomyopathy in rat

机译:促红细胞生成素表达在小鼠间充质干细胞中的促红细胞生成蛋白在大鼠中扩张心肌病

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摘要

Dilated cardiomyopathy (DCM) is considered as the final common response of myocardium to diverse genetic and environmental insults and characterized mainly by left ventricular systolic dysfunction. The current therapies for the treatment of DCM are costly high and outcomes are often unsatisfactory. To date, mesenchymal stem cells (MSCs) have been thought to be an ideal stem cell to repair damaged myocardium but was still within relatively small scales and few cases have been conducted in clinical trials. The use of erythropoietin (EPO), a growth factor produced in the kidneys have been found prevent cardiomyocyte apoptosis. This study was aimed to transplant MSCs into DCM rat bone marrow to express EPO in vivo and investigate the regulation of EPO on cell signaling pathways after transfection. The results found that transplantation of MSCs carrying EPO could significantly relief the cardiac dysfunctions of the DCM rat. This underylying mechanism involved with inhibiting p-NF-kappa B and p-P38, regulateing and promoting the anti-inflammatory balance, thereby alleviating tissue injury in DCM rats and exhibiting a protective role. Meanwhile, the MSCs + EPO treatment in DCM rat also activated the p-Akt pathway and thus protecting the myocardium from apoptosis in DCM rats. The study revealed an potential therapeutic effect of MSCs and EPO in clinical and provided a molecular mechanism of action for treating DCM. (C) 2019 The Authors. Published by Elsevier Inc.
机译:扩张的心肌病(DCM)被认为是心肌的最终共同应对,以不同的遗传和环境侮辱,并以左心室收缩功能障碍为特征。对DCM治疗的当前疗法成本高,结果往往不令人满意。迄今为止,被认为是修复受损心肌的理想干细胞的间充质干细胞(MSCs),但在临床试验中仍然存在较少的尺度内。已经发现使用促红细胞生成素(EPO),在肾脏中产生的生长因子预防心肌细胞凋亡。该研究旨在将MSC移植到DCM大鼠骨髓中,以在体内表达EPO,并调查转染后对细胞信号传导途径的调节。结果发现,携带EPO的MSCs的移植可以显着缓解DCM大鼠的心脏功能障碍。这种低于抑制P-NF-κB和P-P38的下行机制,调节和促进抗炎平衡,从而减轻了DCM大鼠的组织损伤并表现出保护作用。同时,DCM大鼠中的MSCs + EPO治疗也活化了P-AKT途径,从而保护心肌免受DCM大鼠的凋亡。该研究揭示了MSC和EPO在临床中的潜在治疗作用,并提供了治疗DCM的分子机制。 (c)2019年作者。 elsevier公司发布

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