Role and mechanism of miR-148b involved in cardiac fibrosis after myocardial infarction

AIM To explore the role and mechanisms of miR-148b involved in cardiac fibrosis after myocardial infarction. METHODS The myocardial infarction model was induced by ligation of the left anterior descending coronary artery of rats. The target of miR-148b was predicted using bioinformatic methods. The expression level of miR-148b in rat heart tissue was evaluated using real-time PCR. The expression level of PTEN and α-SMA protein in rat heart tissue was evaluated using Western blot. Cardiac fibroblast proliferative ability was assessed using MTT assay and cardiac fibrosis was analyzed using Sirius red staining. RESULTS After myocardial infarction, fibrosis tissue increased and expression of miR-148b was up-regulated significantly in the border zone (P<0.01). The binding sites between miR-148b and PTEN mRNA were found. After myocardial infarction, the expression of PTEN was significantly down-regulated in the border zone (P<0.01). In the cardiac fibroblasts, miR-148b was overexpressed, PTEN protein expression level was significantly down-regulated (P<0.01), α-SMA protein expression level was significantly up-regulated (P<0.01) and the proliferation of cardiac fibroblasts significantly increased (P<0.05). In the cardiac fibroblasts stimulated by AngII, miR-148b was inhibited, PTEN protein expression level was significantly up-regulated (P<0.05), α-SMA protein expression level was significantly down-regulated (P<0.01) and the proliferation of cardiac fibroblasts was significantly decreased (P<0.01). CONCLUSION miR-148b is involved in cardiac fibrosis via PTEN after myocardial infarction.