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MiR-23b controls TGF-ß1 induced airway smooth muscle cell proliferation via direct targeting of Smad3.

Chen, Ming; Shi, Jianting; Zhang, Wei; Huang, Linjie; Lin, Xiaoling; Lv, Zhiqiang; Zhang, Wei; Liang, Ruiyun; Jiang, Shanping.
Pulm Pharmacol Ther; 42: 33-42, 2017 02.
Artículo en Inglés | MEDLINE | ID: mdl-28062322


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.


We obtained ASMCs by laser capture microdissection of normal and asthmatic mice lung tissues. Mice ASMCs were cultured and induced by TGF-ß1. The implication between TGF-ß1 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.


TGF-ß1 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-ß1 induced ASMCs. miR-23b up-regulation significantly inhibited TGF-ß1-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.


MiR-23b may function as an inhibitor of asthma airway remodeling by suppressing ASMCs proliferation via direct targeting of Smad3.