MiR-23b controls TGF-β1 induced airway smooth muscle cell proliferation via direct targeting of Smad3. (February 2017)

• Record Type: Journal Article
• Authors: Chen, Ming; Shi, Jianting; Zhang, Wei; Huang, Linjie; Lin, Xiaoling; Lv, Zhiqiang; Zhang, Wei; Liang, Ruiyun; Jiang, Shanping
• Is Part Of: Pulmonary pharmacology & therapeutics. Volume 42(2017:Feb.)
• Page Start: 33
• Page End: 42
• Publication Date: 2017-02
• Subjects: MiR-23b -- TGF-β1/Smad3 -- Asthma -- Airway smooth muscle cells; ASMCs airway smooth muscle cells -- BSA bovine serum albumin -- DMEM Dulbecco's modified Eagle's medium -- Smad drosophila mothers against decapentaplegic protein -- FBS fetal bovine serum -- HBSS Hanks' balanced salt solution -- LCM Laser capture microdissection -- NC negative control -- OCT optimal cutting temperature -- PBS phosphate-buffered saline -- PVDF polyvinylidene difluoride -- TGF-β1 transforming growth factor-β1; Respiratory organs -- Diseases -- Chemotherapy -- Periodicals; 615.7205
• DOI: 10.1016/j.pupt.2017.01.001
• Languages: English
• ISSNs: 1094-5539

Abstract

Abstract: Background: MicroRNAs are small yet versatile gene tuners that regulate a variety of cellular processes, including cell growth and proliferation. Here we report that miR-23b inhibited airway smooth muscle cells (ASMCs) proliferation through directly targeting of Smad3. Methods: We obtained ASMCs by laser capture microdissection of normal and asthmatic mice lung tissues. Mice ASMCs were cultured and induced by TGF-β1. The implication between TGF-β1 and miR-23b in ASMCs were detected by RT-PCR. The effects of miR-23b on ASMCs proliferation and apoptosis were assessed by transient transfection of miR-23b mimics and inhibitor. The expression of Smad3 in ASMCs were detected by RT-PCR and Western blotting analysis. Dual-Luciferase Reporter Assay System will be applied to identify whether Smad3 is a target gene of miR-23b. Results: TGF-β1 and miR-23b mRNA expression of in-situ bronchial ASMCs collected by laser capture microdissection were increased in asthmatic mice compared to non-asthma controls. This is accompanied by an increase in miR-23b mRNA expression in TGF-β1 induced ASMCs. miR-23b up-regulation significantly inhibited TGF-β1-induced ASMCs proliferation and promoted apoptosis. MiR-23b negatively regulates the expression of Smad3 in ASMCs. Dual-Luciferase Reporter Assay System demonstrated that Smad3 was a direct target of miR-23b. Conclusions: MiR-23b may function as an inhibitor of asthma airway remodeling by suppressing ASMCs proliferation via direct targeting of Smad3.