Effect of miR-203 expression on myocardial fibrosis

Q. He, C.-M. Wang, J.-Y. Qin, Y.-J. Zhang, D.-S. Xia, X. Chen, S.-Z. Guo, X.-D. Zhao, Q.-Y. Guo, C.-Z. Lu

Department of Cardiology, Tianjin First Center Hospital, Tianjin, China. chengzhiluasd@sina.com

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• Cardiology

OBJECTIVE: Cardiovascular disease is one of the diseases threatening human health. Myocardial fibrosis is a major cause of cardiovascular diseases. Studies have shown that over expression of miR-203 can inhibit the fibrosis. Therefore, in this study, the effect of differential expression of miR-203 on fibrosis of cultured mouse cardiomyocytes was investigated.

MATERIALS AND METHODS: Activators and inhibitors of miR-203 were designed according to the sequence of miR-203, synthesized, and transfected into mouse cardiomyocytes to establish activator group, inhibitor group, and control group. The expression levels of fibrosis-related factors including FN, CTGF, and TGF-β1 were measured by Western blot and RT-PCR 24 h and 36 h after transfection.

RESULTS: Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN in a time-dependent manner, compared with that in the control group (p <0.05). Inhibition of miR-203 expression in mouse cardiomyocytes significantly increased the expression levels of TGF-β1, CTGF, and FN 36 h after transfection, compared with that in the control group (p < 0.05). No significant differences were seen in the expression levels of TGF-β1, CTGF, and FN 24 h after transfection, compared with that in the control group (p >0.05).

CONCLUSIONS: Over-expression of miR-203 in mouse cardiomyocytes significantly decreased the expression levels of TGF-β1, CTGF, and FN, which might be used as a detection index for prediction of fibrosis.

 

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