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MicroRNA-663 participates in myocardial fibrosis through interaction with TGF-β1.

Experimental and therapeutic medicine (2019-10-02)
Xiangyang Wu, Jie Zhu, Yalin Wei, Xinqiang Guan, Yanchun Zhang, Wensheng Chen, Bingren Gao
RESUMEN

MicroRNA-663 (miRNA-663) regulates the expression of transforming growth factor β1 (TGF-β1), which participates in the pathogenesis of myocardial fibrosis. Therefore, microRNA-663 may also serve a role in myocardial fibrosis. The present study aimed to determine whether miRNA-663 participates in myocardial fibrosis via interaction with TGF-β1. In the present study, the expression of miRNA-663 was significantly downregulated, whereas that of TGF-β1 was significantly upregulated in the endomyocardial biopsies of patients with myocardial fibrosis compared with those in control necropsies. Pearson's correlation analysis revealed that the expression levels of miRNA-663 were negatively correlated with those of TGF-β1 in patients with myocardial fibrosis, but not in the controls. Receiver operating characteristic curve analysis demonstrated that the downregulation of miRNA-663 distinguished patients with myocardial fibrosis from controls. In the AC16 human cardiomyocyte cell line, miRNA-663 overexpression resulted in downregulated TGF-β1 expression, whereas exogenous TGF-β1 treatment exhibited no significant effects on miRNA-663 expression. These results indicate that miRNA-663 may participate in myocardial fibrosis, possibly through interaction with TGF-β1.

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AC16 Human Cardiomyocyte Cell Line, AC16 Human Cardiomyocytes can be serially passaged and can differentiate when cultured in mitogen-free medium. The cells may be used to study developmental regulation of cardiomyocytes.