CAJ | 학술논문

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。
목적：이용심기세포비대체외모형연구miR-133a항심기비대적작용궤제。방법구건miR-133a선병독표체재체，도입293세포병수획고표체miR-133a적병독；취12지출생1~3 d내적소서심장，채용매소화급제도리심법획득심기세포，분위대조조화모형조，모형조가입분신상선소（PE）유도；장고표체miR-133a적선병독감염모형조적심기세포，관찰세포면적적변화，RT-PCR검측Acta1、Actc1、Actb、Myh6、Myh7、BNP기인적표체。결과모형조심기세포가입PE배양후，교대조조면적증대3배이상，Acta1등기인표체현저증고；비대후모형조적심기세포채용miR-133a병독감염후교미가입miR-133a병독적모형조적심기세포적면적축소，Acta1등기인표체현저강저。결론 miR-133a시심기비대적중요조절인자，유길항심기비대적작용。
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