miR-150通过靶基因c-Myb改善心肌梗死后心肌纤维化  

MiR-150 improves cardiac fibrosis after myocardial infarction by targeting c-Myb

作　　者：周小翠 汪涛[1] 李恩[2] 

机构地区：[1]郑州大学第二附属医院老年病科,450014 [2]郑州大学第二附属医院心内科,450014

出　　处：《实用医学杂志》2017年第7期1078-1082,共5页The Journal of Practical Medicine

基　　金：河南省科技厅攻关计划资助项目(编号:142102310109)

摘　　要：目的:研究miR-150在心肌梗死后心肌纤维化中的作用及机制。方法:在心梗大鼠,通过过表达miR-150的慢病毒上调miR-150,用RT-PCR及Western bloting检测梗死边缘区col1ɑ1与α-SMA的表达及Masson染色检测纤维化,研究miR-150在心梗纤维化模型中的作用。分离及培养心肌成纤维细胞,用荧光素酶报告载体、慢病毒及c-Myb的si RNA验证miR-150与c-Myb的关系。结果:体内实验表明miR-150在心梗后第2周及第4周心肌表达下调(P<0.001,P<0.05),而上调miR-150明显改善心肌纤维化(P<0.001),抑制col1ɑ1及ɑ-SMA的表达(P<0.01,P<0.05)。体外实验表明c-Myb是miR-150的靶基因且miR-150可通过c-Myb抑制col1ɑ1及ɑ-SMA的表达。结论:miR-150在心肌梗死边缘区表达下降,且可通过靶基因c-Myb改善心肌纤维化。Objective To evaluate the role and mechanism of miR-150 in cardiac fibrosis after MI. Methods A rat model of MI was established by up-regulating miR-150 through overexpressing miR-150 lentivirus. Real-time PCR and Western blot were applied in detecting the expression of collagenl α1 and α-SMA protein in infarction area border. Masson coloration was applied in measuring fibrosis. Cardiac fibroblasts were isolated and cultured. UTR was used to report the carrier and lentivirus. And e-Myb siRNA was used to verify the relationship between e-Myb and microRNA-150. Results In vivo, MiR-150 was down-regulated in myocardium border zone in 14 day and 28 day after infarction （P 〈 0.001 , P 〈 0.05 ） , and overexpressing miR-150 promoted myocardial fibrosis （P 〈 0.001 ）, and inhibited the expression of collageul ~ 1 and ct-SMA （P 〈 0.01 , P 〈 0.05 ）. In vitro, c-Myb was the direct target gene of miR-150, and inhibited the expression of c-Myb resulting in the down- regulation of collagenlal and α-SMA, suggesting that the role of miR-150 was achieved by regulating c-Myb. Conclusions MiR-150 was down-regulated in myocardimn border zone, and myocardial fibrosis can be improved by targeting c-Myb.

关 键 词：心肌梗死 纤维化 microRNA.150 c—Myb 

分 类 号：R542.22[医药卫生—心血管疾病]