...
首页> 外文期刊>Journal of cellular and molecular medicine. >MicroRNA‐30c suppresses the pro‐fibrogenic effects of cardiac fibroblasts induced by TGF‐β1 and prevents atrial fibrosis by targeting TGFβRII
【24h】

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

机译:MicroRNA-30C抑制TGF-β1诱导的心肌成纤维细胞的促纤纤效果,并通过靶向TGFβRII来防止心房纤维化

获取原文
   

获取外文期刊封面封底 >>

       

摘要

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.
机译:心房纤维化是心房颤动的重要因素(AF)。最近的数据表明,MicroRNA-30C(miR-30c)参与纤维化重塑和癌症发育,但MiR-30c在心房纤维化中的具体作用仍然不清楚。本研究的目的是探讨miR-30c在心房纤维化中的作用及其在体内和体外实验中的潜在机制。我们的结果表明,在大鼠腹主动脉抑制(AAC)模型中和通过转化生长因子-β1(TGF-β1)诱导的纤维化细胞模型中的miR-30c显着下调。 miR-30c在心肌成纤维细胞(CFS)的过度表达显着抑制CF的增殖,分化,迁移和胶原蛋白,而MiR-30C的降低导致相反的结果。此外,我们将TGFβRII识别为MIR-30C的目标。最后,将腺相关病毒9(AAV9) - MIR-30C转移到AAC之后左心房的大鼠衰减纤维化的下腔静脉中。这些数据表明MiR-30C通过靶向TGFβRII抑制CF增殖,分化,迁移和胶原蛋白产生的衰减心房纤维化,表明miR-30c可能是预防心房纤维化的新潜在治疗靶标。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号