• Guang-Sheng Lei, Hannah L Kline, Chao-Hung Lee, David S Wilkes, and Chen Zhang.
• Department of Pathology and Laboratory Medicine, Indiana University School of Medicine, Indianapolis, Indiana.
• Am. J. Pathol. 2016 Sep 1; 186 (9): 2310-6.

AbstractIdiopathic 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.Copyright © 2016 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.

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