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MicroRNA-30c 通过靶向 TGFβRII 抑制 TGF-β1 诱导的心肌成纤维细胞的促纤维化作用，预防心房纤维化。

MicroRNA-30c suppresses the pro-fibrogenic effects of cardiac fibroblasts induced by TGF-β1 and prevents atrial fibrosis by targeting TGFβRII.

机构信息

Department of Cardiology, Shanghai General Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai, China.

Department of Cardiology, Shanghai Institute of Cardiovascular Disease, Zhongshan Hospital, Fudan University, Shanghai, China.

出版信息

J Cell Mol Med. 2018 Jun;22(6):3045-3057. doi: 10.1111/jcmm.13548. Epub 2018 Mar 13.

DOI:10.1111/jcmm.13548
PMID:29532993
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5980214/
Abstract

Atrial fibrosis serves as an important contributor to atrial fibrillation (AF). Recent data have suggested that microRNA-30c (miR-30c) is involved in fibrotic remodelling and cancer development, but the specific role of miR-30c in atrial fibrosis remains unclear. The purpose of this study was to investigate the role of miR-30c in atrial fibrosis and its underlying mechanisms through in vivo and in vitro experiments. Our results indicate that miR-30c is significantly down-regulated in the rat abdominal aortic constriction (AAC) model and in the cellular model of fibrosis induced by transforming growth factor-β1 (TGF-β1). Overexpression of miR-30c in cardiac fibroblasts (CFs) markedly inhibits CF proliferation, differentiation, migration and collagen production, whereas decrease in miR-30c leads to the opposite results. Moreover, we identified TGFβRII as a target of miR-30c. Finally, transferring adeno-associated virus 9 (AAV9)-miR-30c into the inferior vena cava of rats attenuated fibrosis in the left atrium following AAC. These data indicate that miR-30c attenuates atrial fibrosis via inhibition of CF proliferation, differentiation, migration and collagen production by targeting TGFβRII, suggesting that miR-30c might be a novel potential therapeutic target for preventing atrial fibrosis.

摘要

心房纤维化是心房颤动（AF）的重要原因。最近的数据表明，microRNA-30c（miR-30c）参与纤维化重塑和癌症发展，但 miR-30c 在心房纤维化中的具体作用尚不清楚。本研究通过体内和体外实验，旨在探讨 miR-30c 在心房纤维化中的作用及其潜在机制。我们的结果表明，miR-30c 在大鼠腹主动脉缩窄（AAC）模型和转化生长因子-β1（TGF-β1）诱导的纤维化细胞模型中显著下调。心肌成纤维细胞（CFs）中 miR-30c 的过表达显著抑制 CF 增殖、分化、迁移和胶原产生，而 miR-30c 的减少则导致相反的结果。此外，我们鉴定出 TGFβRII 是 miR-30c 的靶标。最后，将腺相关病毒 9（AAV9）-miR-30c 转染到大鼠下腔静脉中，可减轻 AAC 后左心房纤维化。这些数据表明，miR-30c 通过靶向 TGFβRII 抑制 CF 增殖、分化、迁移和胶原产生，从而减轻心房纤维化，提示 miR-30c 可能是预防心房纤维化的一种新的潜在治疗靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/079cd38fb8c7/JCMM-22-3045-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/100eab098b2f/JCMM-22-3045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/f9a2da7cf5f6/JCMM-22-3045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/b01de2312018/JCMM-22-3045-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/5d72b8a6d49e/JCMM-22-3045-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/d0f7c4beaf55/JCMM-22-3045-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/079cd38fb8c7/JCMM-22-3045-g006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/100eab098b2f/JCMM-22-3045-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/f9a2da7cf5f6/JCMM-22-3045-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/b01de2312018/JCMM-22-3045-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/5d72b8a6d49e/JCMM-22-3045-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/d0f7c4beaf55/JCMM-22-3045-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1227/5980214/079cd38fb8c7/JCMM-22-3045-g006.jpg

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