MicroRNA‑663 participates in myocardial fibrosis through interaction with TGF‑β1

Wu,Xiangyang; Zhu,Jie; Wei,Yalin; Guan,Xinqiang; Zhang,Yanchun; Chen,Wensheng; Gao,Bingren

doi:10.3892/etm.2019.7902

MicroRNA‑663 participates in myocardial fibrosis through interaction with TGF‑β1

Authors:
- Xiangyang Wu
- Jie Zhu
- Yalin Wei
- Xinqiang Guan
- Yanchun Zhang
- Wensheng Chen
- Bingren Gao
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Affiliations: Department of Cardiac Surgery, The Second Hospital of Lanzhou University, Lanzhou, Gansu 730030, P.R. China
Published online on: August 16, 2019 https://doi.org/10.3892/etm.2019.7902
Pages: 3172-3176

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Abstract

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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