microRNA-133a拮抗苯肾上腺素诱导的小鼠心肌肥大

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

目的利用心肌细胞肥大体外模型研究mi R-133a抗心肌肥大的作用机制。方法构建mi R-133a腺病毒表达载体,导入293细胞并收获高表达mi R-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mi R-133a的腺病毒感染模型组的心肌细胞,观察细胞面积的变化,RTPCR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mi R-133a病毒感染后较未加入mi R-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 mi R-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 mi R-133 a in reversing neonatal rat cardiomyocyte hypertrophy induced by phenylephrine. Methods A mi R-133 a precursor c DNA was used to construct an adenovirus vector, which was transfected into 293 cells to harvest mi R-133a-containing virus. Neonatal rat cardiac myocytes treated by phenylephrine were exposed to mi R- 133 a adenovirus, and the changes in cell area was measured; the expression levels of mi R- 133 a and Acta1, Actc1, Actb,Myh6, Myh7, and BNP m RNAs 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 m RNAs. All these changes were obviously reverse by mi R- 133 a treatment. Conclusion mi R- 133 a is an important regulator of phenylephrine-induced cardiomyocyte hypertrophy and negatively regulates this process