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

P. Dong, W.-J. Liu, Z.-H. Wang

Department of Cardiovascular Medicine, Beijing Aviation General Hospital, Beijing, China. kate-wzh@163.com

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• Cardiology

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 β-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-3β (GSK-3β) was transfected into fibroblasts, we performed Western blot to detect a-SMA and β-catenin expression.

RESULTS: MiR-154 was overexpressed in cardiomyocytes, and when miR-154 was inhibited, the expression of collagen I, collagen III, a-SMA, β-catenin, and the invasiveness of CFs decreased. Therefore, we considered that miR-154 could promote myocardial fibrosis by inhibiting the expression of GSK-3β.

CONCLUSIONS: MiR-154 can inhibit GSK-3β expression by activating Wnt/β-catenin signaling pathway, which promotes myocardial fibrosis.

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