The role of miR-497-5p in myofibroblast differentiation of LR-MSCs and pulmonary fibrogenesis

Xiang Chen, Chaowen Shi, Cong Wang, Weilin Liu, Yanhong Chu, Xiang Zou, Kebin Hu, Ping Dong, Xiaodong Han

Research output: Journal article publicationJournal articleAcademic researchpeer-review

40 Citations (Scopus)


Idiopathic pulmonary fibrosis (IPF) is a chronic, progressive and fatal fibrotic lung disease characterized by profound changes in stem cell differentiation, epithelial cell phenotypes and fibroblast proliferation. In our study, we found that miR-497-5p was significantly upregulated both during myofibroblast differentiation of lung resident mesenchymal stem cells (LR-MSCs) and in the lung tissues of a pulmonary fibrosis model. In addition, as determined by luciferase assays and Western blot analysis, reversion-inducing cysteine-rich protein with kazal motifs (Reck) was identified to be one of the target genes of miR-497-5p, and Reck could suppress the expression of matrix metalloproteinase-2 (Mmp2) and Mmp9, which could activate latent transforming growth factor-β1 (TGF-β1). To test the potential therapeutic significance of this miRNA, we modulated the expression of miR-497-5p in LR-MSCs and relevant animal models. The results demonstrated that upregulation of miR-497-5p could induce LR-MSCs to differentiate into myofibroblasts and promote pulmonary fibrogenesis, while inhibition of its expression could effectively retard these processes. In conclusion, our work supports that controlling pulmonary fibrogenesis via inhibition of miR-497-5p expression may provide a potential therapeutic strategy for IPF.
Original languageEnglish
Article number40958
JournalScientific Reports
Publication statusPublished - 18 Jan 2017

ASJC Scopus subject areas

  • General


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