miRNA-1183-targeted regulation of bcl-2 contributes to the pathogenesis of rheumatic heart disease

Ni Li, Linwen Zhu, Hua Zhou, Dawei Zheng, Guodong Xu, Lebo Sun, Jianqing Gao, Guofeng Shao
Bioscience Reports 2020 October 19
To determine whether up-regulation of miR-1183 targeting the gene for anti-apoptotic factor, B cell lymphoma-2 (BCL-2) contributes to apoptosis in patients with rheumatic heart disease (RHD). Peripheral blood samples were isolated for miR-1183 characterization. The function of miRNA-1183 in RHD using miRNA mimic on PBMCs and THP-1 cell models. The binding of miR-1183 and Bcl-2 gene was confirmed by luciferase activity test.We also measured expression levels of BCL-2 in heart valve tissue from patients with RHD using ELISA and immunohistochemistry. In silico analysis and reporter gene assays indicated that miR-1183 directly targets the mRNA encoding BCL-2. It is found that miR-1183 binds directly to the 3' UTR of the BCL-2 mRNA and downregulates the mRNA and protein levels of BCL-2.Overexpression of miR-1183 in RHD patients and cell lines downregulated BCL-2 expression and induced apoptosis. With the progression of the disease, the expression of BCL-2 in the heart valve tissue of patients with RHD decreased. MiRNA-1183 is upregulated in RHD and induces cardiac myocyte apoptosis through direct targeting and suppression of BCL-2, both of which might play important roles in RHD pathogenesis. During the compensatory period of RHD, up-regulated miR-1183 destroyed the balance of apoptosis proteins (Bax、BAK) in bcl-2 family, enhance the apoptosis cascade reaction and reduce the anti apoptosis effect.The significantly higher expression levels of miR-1183 appear to play distinct roles in RHD pathogenesis by regulation BCL-2, possibly affecting myocardial apoptosis and remodeling in the context of RHD.

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