Regulation of Collagen V Expression and Epithelial-Mesenchymal Transition by miR-185 and miR-186 during Idiopathic Pulmonary Fibrosis

Guang Sheng Lei, Hannah L. Kline, Chao Hung Lee, David S. Wilkes, Chen Zhang

Research output: Contribution to journalArticle

11 Citations (Scopus)

Abstract

Idiopathic 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.

Original languageEnglish (US)
Pages (from-to)2310-2316
Number of pages7
JournalAmerican Journal of Pathology
Volume186
Issue number9
DOIs
StatePublished - Sep 1 2016

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Idiopathic Pulmonary Fibrosis
Epithelial-Mesenchymal Transition
Collagen
Transforming Growth Factors
MicroRNAs
Biomarkers
Luciferases
Lung
Therapeutics

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

Cite this

Regulation of Collagen V Expression and Epithelial-Mesenchymal Transition by miR-185 and miR-186 during Idiopathic Pulmonary Fibrosis. / Lei, Guang Sheng; Kline, Hannah L.; Lee, Chao Hung; Wilkes, David S.; Zhang, Chen.

In: American Journal of Pathology, Vol. 186, No. 9, 01.09.2016, p. 2310-2316.

Research output: Contribution to journalArticle

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AB - Idiopathic 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.

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