南方医科大学学报

南方医科大学学报 ›› 2015, Vol. 35 ›› Issue (09): 1283-.

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microRNA-133a拮抗苯肾上腺素诱导的小鼠心肌肥大

李崎，杨祥胜，周晓华，肖露，林曦，张风波，李玲丽，余艳红，马燕琳   

  • 出版日期:2015-09-20 发布日期:2015-09-20

MicroRNA-133a antagonizes phenylephrine-induced hypertrophy of neonatal rat
cardiomyocytes in vitro

  • Online:2015-09-20 Published:2015-09-20

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摘要： 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。

Abstract: 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