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首页> 外文期刊>Life sciences >MiR-142-3p blocks TGF-β-induced activation of hepatic stellate cells through targeting TGFβRI
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MiR-142-3p blocks TGF-β-induced activation of hepatic stellate cells through targeting TGFβRI

机译：MiR-142-3P通过靶向TGFβRI阻断TGF-β诱导的肝星状细胞的激活

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Abstract Aim To understand the contribution of miR-142-3p in the activation of hepatic stellate cells (HSCs) and liver fibrosis, and the underlying mechanism. Materials and methods We detected microRNAs expression profiles in quiescent and activated HSCs by microRNA-array, and performed qRT-PCR to validate these data in HSCs and plasma of cirrhosis patients. In vitro, the 3rd–5th passage HSCs was transfected with mir-142-3p mimics or stimulated with TGF β. The markers of HSCs activation (i.e. FN and α-SMA) were examined by qRT-PCR and western blotting, and cell viability was detected by MTT, colony formation assays respectively. Key finding In our study, we identified miR-142-3p as a novel regulator of HSCs activation and indicator of hepatic cirrhosis. We found that miR-142-3p was significantly reduced in activated HSCs, while TGFβRI was distinctly up-regulated in activated HSCs. Ectopic expression of miR-142-3p in activated HSCs inhibited cell viability as well as cell growth, and blocked HSCs activation, concomitant with decreased transdifferentiation markers (i.e. FN and α-SMA). Further, we confirmed that miR-142-3p was reduced upon TGF-β exposure, while diminishing TGF-β-Smad signaling pathway in turn by reducing TGFβRI expression in HSCs. Besides, the plasma level of miR-142-3p declined significantly in patients with hepatic cirrhosis. Significance In conclusion, we demonstrated that miR-142-3p repressed TGF-β-Smad signaling pathway to prevent HSCs activation through directly targeting TGFβRI in HSCs.
机译：摘要目的理解的miR-142-3p的在肝星状细胞（HSC）和肝纤维化，其机制的激活作用。材料和方法我们检测在静态微RNA表达谱和激活的HSCs由微小RNA阵列，和进行的qRT-PCR来验证在HSC中这些数据和肝硬化患者血浆。在体外，第3-5通道的HSC用的mir-142-3p的模拟物转染或与TGFβ刺激。造血干细胞的活化通过qRT-PCR和免疫印迹，和细胞活力进行了检查标记物（即FN和α-SMA）通过MTT，分别集落形成测定来检测。主要发现在我们的研究中，我们确定的miR-142-3p的造血干细胞作为激活和肝硬化指标的新的调节。我们发现的miR-142-3p的在激活的HSCs被显著减少，而TGFβRI是明显在激活的HSCs上调。在激活的HSCs抑制细胞存活力的miR-142-3p的异位表达以及细胞生长，并且阻止肝星状细胞的活化，同时具有降低的转分化标记物（即FN和α-SMA）。进一步，我们证实了miR-142-3p的是在TGF-β曝光减少，同时减少TGF-β-Smad信号反过来通路通过降低造血干细胞表达TGFβRI。此外，的miR-142-3p的血浆水平在肝硬化患者显著下跌。意义总之，我们证明了的miR-142-3p的抑制TGF-β-Smad蛋白通过造血干细胞直接针对TGFβRI信号传导通路预防肝星状细胞的活化。

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  • 来源
    《Life sciences》 |2017年第2017期|共9页
  • 作者

    Xiaoxue Yang; Xuelian Dan; Ruoting Men; Liping Ma; Maoyao Wen; Yong Peng; Li Yang;

  • 作者单位

    Department of Gastroenterology and Hepatology West China Hospital West China School of Clinical;

    Department of Biomedical Sciences City University of Hong Kong;

    Department of Gastroenterology and Hepatology West China Hospital West China School of Clinical;

    Department of Thoracic Surgery West China Hospital Sichuan University;

    Department of Gastroenterology and Hepatology West China Hospital West China School of Clinical;

    Department of Thoracic Surgery West China Hospital Sichuan University;

    Department of Gastroenterology and Hepatology West China Hospital West China School of Clinical;

  • 收录信息
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类 医药、卫生;
  • 关键词

    miR-142-3p; TGF-β-Smad signaling pathway; TGFβRI; Hepatic stellate cells; Liver fibrosis;

    机译：miR-142-3p;tgf-β-smad信号通路;tgfβri;肝星状细胞;肝纤维化;

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