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

作　　者：李崎[1] 杨祥胜 周晓华[3] 肖露[3] 林曦 张风波[1] 李玲丽[1] 余艳红[3] 马燕琳[1,3] 

机构地区：[1]海南医学院附属医院海南省人类生殖与遗传重点实验室,海南海口570102 [2]美国德州A&M大学生命科学院,美国德州休斯顿77030 [3]南方医科大学南方医院妇产科,广东广州510515

出　　处：《南方医科大学学报》2015年第9期1283-1286,共4页Journal of Southern Medical University

基　　金：国家国际科技合作专项(2014DFA30180);国家科技部973项目(2012CB966502);国家自然科学基金(81060175;30860103;81460034;81260032;81060016;31140021);海南省重大科技计划项目(ZDZX2013003);海南省国际科技合作专项(GJXM20100004;GJXM201106;KJHZ2014-11);广州市科技计划项目(2011Y2-00019)~~

摘　　要：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

关 键 词：micro RNA-133a 心肌肥大 苯肾上腺素 

分 类 号：R542.2[医药卫生—心血管疾病]