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MicroRNA-29a inhibits cardiac fibrosis in SD rats by downregulating the expression of DNMT3A [Anatol J Cardiol]
Anatol J Cardiol. Ahead of Print: AJC-98511 | DOI: 10.14744/AnatolJCardiol.2018.98511  

MicroRNA-29a inhibits cardiac fibrosis in SD rats by downregulating the expression of DNMT3A

Kai hu Shi, Run-He Qin, Hui Tao, Shi-Hao Ni, Peng Shi, Chen Dai
Department of Cardiothoracic Surgery, The Second Hospital of Anhui Medical University

Objective This study aims to explore the effect of miR-29a targeting regulation of DNMT3A on the development of cardiac fibrosis in rat SD rats. Methods In vivo experiment: SD rats were randomly divided into model group and control group. The cardiac index and left ventricular index in each group was calculated. The pathological changes of myocardium were observed. The expression levels of miR-29a, CollA1, α-SMA and DNMT3A in the myocardium of each group were detected. In vitro experiment: The cardiac fibroblasts of SD rats were isolated from the myocardial tissue of SD rats and cultured. The miR-29a mimics, inhibitors, DNMT3A-siRNA and control-siRNA were transfected into CFs respectively. The expression levels of miR-29a, DNMT3A, CollA1 and α-SMA were detected, the proliferation of CFs after transfection was observed. Results The heart weight index of the rats in the model group increased significantly compared with the control group. The obvious collagen deposition appeared in the myocardial tissue of the model group. The expression levels of CollA1, α-SMA and DNMT3A in the model group were significantly higher than those in the control group (P<0.05). Conclusions The miR-29a reduced the activation and proliferation of CFs to improve Cardiac fibrosis maybe by down regulation of DNMT3A.

Keywords: miR-29a, DNMT3A, cardiac fibroblasts (CFs), Cardiac fibrosis




Corresponding Author: Kai hu Shi, China


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