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MiR-23b controls TGF-ß1 induced airway smooth muscle cell proliferation via TGFßR2/p-Smad3 signals.

Chen, Ming; Huang, Linjie; Zhang, Wei; Shi, Jianting; Lin, Xiaoling; Lv, Zhiqiang; Zhang, Wei; Liang, Ruiyun; Jiang, Shanping.
Mol Immunol; 70: 84-93, 2016 Feb.
Artículo en Inglés | MEDLINE | ID: mdl-26748386

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 TGFßR2/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-ß1-induced ASMCs proliferation and promoted apoptosis. RT-PCR and Western blotting analysis showed miR-23b negatively regulates the expression of TGFßR2 and p-Smad3 in ASMCs. Subsequent analyses demonstrated that TGFßR2 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 TGFßR2/p-Smad3 pathway.