Upregulated miR-29c suppresses silica-induced lung fibrosis through the Wnt/β-catenin pathway in mice.

摘要: Silicosis is an irreversible lung disease resulting from long-term inhalation of occupational dust containing silicon dioxide. However, the pathogenesis silicosis has not been clearly understood yet. Accumulating evidence suggests that miR-29 may have a significant anti-fibrotic capacity, meanwhile it relate to Wnt/β-catenin pathway. The purpose this study was discuss role in progression silicosis. A lentiviral vector constructed, named Lv-miR-29c, which overexpressing miR-29c. In vivo, intratracheal treatment with Lv-miR-29c significantly increased expression miR-29c, and reduced β-catenin, matrix metalloproteinase (MMP)-2, MMP-9 levels transforming growth factor-beta 1 (TGF-β1) interleukin-6 (IL-6) bronchoalveolar lavage fluid, notably attenuated pulmonary fibrosis as evidenced by hydroxyproline content silica-administered mice. These results indicated miR-29c inhibited development silica-induced fibrosis. Thus, be candidate target for via its regulation