microRNA-133a拮抗苯肾上腺素诱导的小鼠心肌肥大
目的 利用心肌细胞肥大体外模型研究miR-133a抗心肌肥大的作用机制。方法 构建miR-133a腺病毒表达载体，导入293细胞并收获高表达miR-133a的病毒；取12只出生1~3 d内的小鼠心脏，采用酶消化及梯度离心法获得心肌细胞，分为对照组和模型组，模型组加入苯肾上腺素（PE）诱导；将高表达miR-133a的腺病毒感染模型组的心肌细胞，观察细胞面积的变化，RT-PCR检测Acta1、Actc1、Actb、Myh6、Myh7、BNP基因的表达。结果 模型组心肌细胞加入PE培养后，较对照组面积增大3倍以上，Acta1等基因表达显著增高；肥大后模型组的心肌细胞采用miR-133a病毒感染后较未加入miR-133a病毒的模型组的心肌细胞的面积缩小，Acta1等基因表达显著降低。结论 miR-133a是心肌肥大的重要调节因子，有拮抗心肌肥大的作用。
Objective To investigate the mechanism of miR-133a in reversing neonatal rat cardiomyocyte hypertrophy induced by phenylephrine. Methods A miR-133a precursor cDNA was used to construct an adenovirus vector, which was transfected into 293 cells to harvest miR-133a-containing virus. Neonatal rat cardiac myocytes treated by phenylephrine were exposed to miR-133a adenovirus, and the changes in cell area was measured; the expression levels of miR-133a and Acta1, Actc1, Actb, Myh6, Myh7, and BNP mRNAs were detected by quantitative RT-PCR. Results Phenylephrine treatment increased the area of cardiomyocytes by more than 3 folds and significantly enhanced the expression levels of Acta1, Actc1, Actb, Myh6, Myh7 and BNP mRNAs. All these changes were obviously reverse by miR-133a treatment. Conclusion miR-133a is an important regulator of phenylephrine-induced cardiomyocyte hypertrophy and negatively regulates this process.
周晓华、林曦、余艳红、张风波、杨祥胜、李崎、肖露、马燕琳、李玲丽
基础医学生理学分子生物学
microRNA-133a心肌肥大苯肾上腺素
周晓华,林曦,余艳红,张风波,杨祥胜,李崎,肖露,马燕琳,李玲丽.microRNA-133a拮抗苯肾上腺素诱导的小鼠心肌肥大[EB/OL].(2017-12-07)[2025-08-23].https://chinaxiv.org/abs/201712.00793.点此复制
评论