MiR-27b inhibits fibroblast activation via targeting TGFβ signaling pathway. Issue 1 (December 2017)

• Record Type: Journal Article
• Authors: Zeng, Xiangming; Huang, Chaoqun; Senavirathna, Lakmini; Wang, Pengcheng; Liu, Lin
• Is Part Of: BMC cell biology. Volume 18:Issue 1(2017)
• Page Start: 1
• Page End: 7
• Publication Date: 2017-12
• Subjects: miR-27b -- Fibroblast activation -- TGFβ -- Idiopathic pulmonary fibrosis; Cytology -- Periodicals; 571.605
• DOI: 10.1186/s12860-016-0123-7
• Languages: English
• ISSNs: 1471-2121

Abstract

Abstract Background MicroRNAs are a group of small RNAs that regulate gene expression at the posttranscriptional level. They regulate almost every aspect of cellular processes. In this study, we investigated whether miR-27b regulates pulmonary fibroblast activation. Results We found that miR-27b was down-regulated in fibrotic lungs and fibroblasts from an experimental mouse model of pulmonary fibrosis. The overexpression of miR-27b with a lentiviral vector inhibited TGFβ1-stimulated mRNA expression of collagens (COL1A1, COL3A1, and COL4A1) and alpha-smooth muscle actin, and protein expression of Col3A1 and alpha-smooth muscle actin in LL29 human pulmonary fibroblasts. miR-27b also reduced contractile activity of LL29. TGFβ receptor 1 and SMAD2 were identified as the targets of miR-27b by 3'-untranslated region luciferase reporter and western blotting assays. Conclusions Our results suggest that miR-27b is an anti-fibrotic microRNA that inhibits fibroblast activation by targeting TGFβ receptor 1 and SMAD2. This discovery may provide new targets for therapeutic interventions of idiopathic pulmonary fibrosis.