微小RNA-877-3p靶向Smad7，并与肌成纤维细胞分化及博来霉素诱导的肺纤维化相关。
miR-877-3p targets Smad7 and is associated with myofibroblast differentiation and bleomycin-induced lung fibrosis.
作者信息
Wang Cong, Gu Shen, Cao Honghui, Li Zutong, Xiang Zou, Hu Kebin, Han Xiaodong
机构信息
Immunology and Reproduction Biology Laboratory &State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing, Jiangsu 210093, China.
Jiangsu Key Laboratory of Molecular Medicine, Nanjing University, Nanjing, Jiangsu 210093, China.
出版信息
Sci Rep. 2016 Jul 22;6:30122. doi: 10.1038/srep30122.
Myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSC) plays an important role in idiopathic pulmonary fibrosis. By comparing the expression profiles of miRNAs before and after myofibroblast differentiation of LR-MSC, we identified miR-877-3p as a fibrosis-related miRNA. We found that miR-877-3p sequestration inhibited the myofibroblast differentiation of LR-MSC and attenuates bleomycin-induced lung fibrosis by targeting Smad7. Smad7, as an inhibitory smad in the TGF-β1 signaling pathway, was decreased in the myofibroblast differentiation of LR-MSC and up-regulation of Smad7 could inhibit the differentiation process. Our data implicates a potential application of miR-877-3p as a fibrosis suppressor for pulmonary fibrosis therapy and also as a fibrosis marker for predicting prognosis.
肺驻留间充质干细胞（LR-MSC）向肌成纤维细胞的分化在特发性肺纤维化中起重要作用。通过比较LR-MSC向肌成纤维细胞分化前后miRNA的表达谱，我们鉴定出miR-877-3p为一种与纤维化相关的miRNA。我们发现，抑制miR-877-3p可通过靶向Smad7抑制LR-MSC向肌成纤维细胞的分化，并减轻博来霉素诱导的肺纤维化。Smad7作为TGF-β1信号通路中的抑制性Smad，在LR-MSC向肌成纤维细胞的分化过程中表达降低，上调Smad7可抑制分化过程。我们的数据表明，miR-877-3p作为一种纤维化抑制剂在肺纤维化治疗中具有潜在应用价值，同时也可作为预测预后的纤维化标志物。
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