MiR-154 promotes myocardial fibrosis through β-catenin signaling pathway

OBJECTIVE: To discover the mechanisms of miR-154 affecting myocardial fibrosis. PATIENTS AND METHODS: Human cardiac fibroblasts (CFs) were cultured in medium containing 10% serum for 48 h. The expression of miRNA-154 in human CFs was detected by Real-time quantitative polymerase chain reaction (qRT-PCR). The miRNA-154 mimics and inhibitors were synthesized and transfected into fibroblasts, respectively. Cell proliferation rate was determined by cell counting kit-8 (CCK8). Collagen I and collagen III, myofibroblast marker (a-SMA) and beta-catenin were detected by Western blotting. Transwell migration assay was used to detect the changes of invasiveness of CFs. After the overexpression vector or siRNA of glycogen synthase kinase-3 beta (GSK-3 beta) was transfected into fibroblasts, we performed Western blot to detect a-SMA and beta-catenin expression. RESULTS: MiR-154 was overexpressed in cardiomyocytes, and when miR-154 was inhibited, the expression of collagen I, collagen III, a-SMA, beta-catenin, and the invasiveness of CFs decreased. Therefore, we considered that miR-154 could promote myocardial fibrosis by inhibiting the expression of GSK-3 beta. CONCLUSIONS: MiR-154 can inhibit GSK-3 beta expression by activating Wnt/beta-catenin signaling pathway, which promotes myocardial fibrosis.