Micro RNA ‐30c suppresses the pro‐fibrogenic effects of cardiac fibroblasts induced by TGF ‐β1 and prevents atrial fibrosis by targeting TGF β RII
Autor: | Songwen Chen, Haiqing Wu, Juan Xu, Genqing Zhou, Yong Wei, Li-qun Zhao, Shaowen Liu, Baozhen Qi, Lidong Cai |
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Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
TGFβRII 030204 cardiovascular system & hematology Inferior vena cava Transforming Growth Factor beta1 03 medical and health sciences 0302 clinical medicine Cell Movement In vivo Fibrosis Atrial Fibrillation microRNA medicine Animals Humans Heart Atria Myofibroblasts Cell Proliferation business.industry Myocardium Receptor Transforming Growth Factor-beta Type II Cell Differentiation Atrial fibrillation Original Articles Cell Biology medicine.disease In vitro Rats MicroRNAs HEK293 Cells 030104 developmental biology medicine.vein atrial fibrosis cardiovascular system Cancer research Molecular Medicine Original Article Cellular model business miR‐30c Transforming growth factor |
Zdroj: | Journal of Cellular and Molecular Medicine |
ISSN: | 1582-4934 1582-1838 |
DOI: | 10.1111/jcmm.13548 |
Popis: | 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. |
Databáze: | OpenAIRE |
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