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作 者:张勇[1] 邹仲敏[2] 郭朝华[2] 周进明[2] 王劲[3] 罗成基[2] 程天民[2]
机构地区:[1]第三军医大学西南医院血液病中心,重庆400038 [2]第三军医大学复合伤研究所 [3]第三军医大学大坪医院血液科
出 处:《解放军医学杂志》2008年第11期1307-1310,共4页Medical Journal of Chinese People's Liberation Army
基 金:国家973项目资助课题(G1999054205)
摘 要:目的观察间充质干细胞(MSCs)被MyoD转染诱导为成肌细胞后对肌损伤的修复作用并探讨其机制。方法160只SCID小鼠随机分为正常组、致伤对照组、MSCs组和成肌细胞组,每组40只。将真核表达双顺反子质粒载体pIRES2-EGFP-MyoD转染MSCs,使MSCs分化诱导为成肌细胞,将MSCs和成肌细胞分别植入Cardiotoxin造成的小鼠损伤肌组织中,1、2、4、6周后观察肌损伤修复效果。结果成功制作了肌损伤模型,MSCs和成肌细胞对肌损伤均有促进修复作用,以成肌细胞效果显著,成肌细胞组肌肉组织抗牵引力强于MSCs组。Western blotting结果表明,修复过程中成肌细胞组MyoD表达显著高于MSCs组、损伤对照组和正常组,成肌细胞组1周时JNK1、ERK2表达显著增加,p38表达显著减少,但6周时与正常组比较均无显著差异。结论MSCs被MyoD转染诱导后形成的成肌细胞能有效修复肌损伤,JNK1、p38及ERK2在修复中起重要作用。Objective To observe the repairing effects of myoblasts from mesenchymal stem cells induced by MyoD transfection on muscle injury, and to explore its mechanism. Methods One hundred and sixty male SCID mice were randomly assigned into 4 groups [normal group, control group with injury, implantation with mesenchymal stem cells (MSCs) group, and implantation with myoblasts group]. MSCs were transfected by pIRES2-EGFP-MyoD and differentiated into myoblasts. Myoblasts and MSCs were injected respectively into the muscular tissue injuried by cardiotoxin. The repairing effect in injuried muscles, which were injected with myoblasts and MSCs, was observed 1, 2, 4 and 6 weeks after the injection. Results The muscular tissue injury model was successfully reproduced. Both MSCs and myoblasts showed obvious repairing effects on the injured muscular tissue, and the strength of muscular tissue in myoblasts group was stronger than that in MSCs group. Western blot assay showed that MyoD expression in myoblasts group was much higher than that in both MSCs and control groups, the expressions of JNK1 and ERK2 were up-regulated in myoblasts group, and the p38 expression was down regulated significantly in the 1st week, but no significant difference was found when compared with those of the normal group at the 6th week. Conclusion Myoblasts transdifferentiated from MSCs induced by MyoD can repair the injuried muscular tissue effectively. JNK1, p38 and ERK2 play important roles in the repairing process.
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