Role and mechanism of microRNA-548c-3p/c-Myb in myocardial infarction fibrosis in rats.

OBJECTIVE

To investigate the role of micro ribonucleic acid (miR)-548c-3p in myocardial fibrosis after myocardial infarction (MI), and to explore the possible underlying.

MATERIALS AND

METHODS

The rat model of MI was successfully established in-vivo. MiR-548c-3p was upregulated via lentivirus transfection with miR-548c-3p mimics. Cardiac function of rats was detected via echocardiography. Meanwhile, Sirius red and Masson staining were used to detect the level of fibrosis index in MI model. Subsequently, myocardial fibroblasts were isolated and cultured in vitro. An oxygen-glucose deprivation (OGD) model was established to mimicking the ischemic condition. Furthermore, the relationship between miR-548c-3p and c-Myb was verified, and the levels of fibrosis-related factors (including α-SMA and COL1A1) were measured.

RESULTS

In-vivo experiments showed that miR-548c-3p expression in rats was significantly down-regulated at 2 and 4 weeks after MI. Up-regulation of miR-548c-3p significantly improved cardiac function, reduced myocardial fibrosis and inhibited the protein expression of proto-oncogene c-Myb (c-Myb). In vitro experiments revealed that c-Myb was a target gene of miR-548c-3p. In addition, miR-548c-3p could inhibit the expressions of α-SMA and COL1A1 through targeting c-Myb.

CONCLUSIONS

MiR-548c-3p could improve myocardial fibrosis by targeting c-Myb.