Lei, Guang-ShengKline, Hannah L.Lee, Chao-HungWilkes, David S.Zhang, Chen2018-03-062018-03-062016-09Lei, G.-S., Kline, H. L., Lee, C.-H., Wilkes, D. S., & Zhang, C. (2016). Regulation of Collagen V Expression and Epithelial-Mesenchymal Transition by miR-185 and miR-186 during Idiopathic Pulmonary Fibrosis. The American Journal of Pathology, 186(9), 2310–2316. https://doi.org/10.1016/j.ajpath.2016.04.0150002-9440https://hdl.handle.net/1805/15369Idiopathic pulmonary fibrosis is a devastating disease, with no good diagnostic biomarker and limited treatment options. Previous studies suggest that collagen V overexpression and collagen V–mediated immune response play roles in the pathogenesis of idiopathic pulmonary fibrosis. This study aimed to identify dysregulated miRNA-related collagen V overexpression during idiopathic pulmonary fibrosis. We found that the expression levels of miR-185 and miR-186 were decreased in the lungs of idiopathic pulmonary fibrosis patients. The levels of miR-185 and miR-186 were not correlated with disease severity of idiopathic pulmonary fibrosis. The direct regulation of COL5A1 by miR-185 and miR-186 was confirmed by a luciferase reporter assay. Furthermore, mimics of miR-185 and miR-186 blocked transforming growth factor-β–induced collagen V overexpression and alleviated transforming growth factor-β–induced epithelial-mesenchymal transition in A549 cells and HCC827 cells. Our findings suggest that attenuated expression of miR-185 and miR-186 may be responsible for collagen V overexpression during idiopathic pulmonary fibrosis, and these miRNAs may serve as pathogenesis-related biomarkers and treatment targets.en-USPublisher PolicyCollagenmiR-185miR-186Pulmonary FibrosisArticle