Key result
miR-29a reduces cardiac fibroblast proliferation by ~33%, suppressing cardiac fibrosis via DNMT3A downregulation.
Why the study?
The role of miR-29a targeting DNMT3A in the development of cardiac fibrosis in Sprague-Dawley rats was not fully understood.
Absolute Event Rate: 1.644% vs 2.438%
p-value: p=<0.05
Hypothesis-generating for miR-29a in cardiac fibrosis models; should not yet change clinical practice.
OBJECTIVE: This study aims to investigate the effect of miR-29a targeting the regulation of DNMT3A on the development of cardiac fibrosis in Sprague-Dawley (SD) rats. METHODS: In vivo experiment: SD rats were randomly divided into model and control groups. The cardiac and left ventricular indices in each group were calculated. The pathological changes of the 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 (CFs) 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. The expression levels of miR-29a, DNMT3A, CollA1, and α-SMA were detected, and the proliferation of CFs after transfection was observed. RESULTS: The heart weight index of the rats in the model group increased significantly compared with that in the control group. Obvious collagen deposition was observed 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). CONCLUSION: miR-29a reduced the activation and proliferation of CFs to improve cardiac fibrosis probably by the downregulation of DNMT3A.
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Kai‐Hu Shi (2018) studied Cardiac fibrosis (n=60). miR-29a vs. Control-siRNA was evaluated on Cardiac fibroblast proliferation (MTT assay OD at 48 hours) (p=<0.05). Transfection with miR-29a significantly inhibited the proliferation of activated cardiac fibroblasts (OD 1.644 vs 2.438) and suppressed cardiac fibrosis by downregulating DNMT3A expression.
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