MiR-150 improves cardiac fibrosis after myocardial infarction by targeting c-Myb
10.3969/j.issn.1006-5725.2017.07.016
- VernacularTitle:miR-150通过靶基因c-Myb改善心肌梗死后心肌纤维化
- Author:
Xiaocui ZHOU
;
Tao WANG
;
En LI
- Keywords:
Post-infarction myocardial fibrosis;
MicroRNA-150;
c-Myb
- From:
The Journal of Practical Medicine
2017;33(7):1078-1082
- CountryChina
- Language:Chinese
-
Abstract:
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 collagen 1 α 1 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 c-Myb siRNA was used to verify the relationship between c-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 collagen1α 1 and α-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 collagen1α 1 and α-SMA,suggesting that the role of miR-150 was achieved by regulating c-Myb.Conclusions MiR-150 was down-regulated in myocardium border zone,and myocardial fibrosis can be improved by targeting c-Myb.
