MiR-23b controls TGF-β1 induced airway smooth muscle cell proliferation via TGFβR2/p-Smad3 signals. (February 2016)

• Record Type: Journal Article
• Authors: Chen, Ming; Huang, Linjie; Zhang, Wei; Shi, Jianting; Lin, Xiaoling; Lv, Zhiqiang; Zhang, Wei; Liang, Ruiyun; Jiang, Shanping
• Is Part Of: Molecular immunology. Volume 70(2016:Feb.)
• Page Start: 84
• Page End: 93
• Publication Date: 2016-02
• Subjects: 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 -- NC negative control -- PBS phosphate-buffered saline -- PVDF polyvinylidene difluoride -- TGF-β1 transforming growth factor-β1 -- TGFβR2 transforming growth factor-β1 receptor II; miR-23b -- TGFβR2/p-Smad3 -- Airway smooth muscle cells; Immunochemistry -- Periodicals; Molecular biology -- Periodicals; Immunochemistry -- Periodicals; Allergy and Immunology -- Periodicals; Molecular Biology -- Periodicals; Immunochimie -- Périodiques; Biologie moléculaire -- Périodiques; Immunochemistry; Molecular biology; Periodicals; Electronic journals; 571.96
• DOI: 10.1016/j.molimm.2015.12.012
• Languages: English
• ISSNs: 0161-5890

Abstract

Highlights: Overexpression of miR-23b significantly inhibited TGF-β1-induced ASMCs proliferation and promoted apoptosis. MiR-23b negatively regulates the expression of TGFβR2 and p-Smad3 in ASMCs. MiR-23b may function as an inhibitor of asthma airway remodeling by suppressing ASMCs proliferation through inactivation of TGFβR2/p-Smad3 pathway. Abstract: Background: Abnormal proliferation of ASM (airway smooth muscle) directly contributes to the airway remodeling during development of lung diseases such as asthma. Here we report that a specific microRNA (miR-23b) controls ASMCs proliferation through directly inhibiting TGFβR2/p-Smad3 pathway. Methods: The expression of miR-23b in ASMCs was detected by quantitative real-time polymerase chain reaction (RT-PCR). The effects of miR-23b on cell proliferation and apoptosis of ASMCs were assessed by transient transfection of miR-23b mimics and inhibitor. The target gene of miR-23b and the downstream pathway were further investigated. Results: Overexpression of miR-23b significantly inhibited TGF-β1-induced ASMCs proliferation and promoted apoptosis. RT-PCR and Western blotting analysis showed miR-23b negatively regulates the expression of TGFβR2 and p-Smad3 in ASMCs. Subsequent analyses demonstrated that TGFβR2 was a direct and functional target of miR-23b, which was validated by the dual luciferase reporter assay. Conclusions: MiR-23b may function as an inhibitor of airway smooth muscle cells proliferation through inactivation of TGFβR2/p-Smad3 pathway.