Ming Chen1, Linjie Huang1, Wei Zhang1, Jianting Shi1, Xiaoling Lin1, Zhiqiang Lv1, Wei Zhang1, Ruiyun Liang1, Shanping Jiang3. 1. Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China. 2. Department of Geratology, The Second People's Hospital of Shenzhen, Shenzhen 518000, China. 3. Department of Respiratory Medicine, Sun Yat-Sen Memorial Hospital, Sun Yat-sen University, Guangzhou, Guangdong Province 510120, China. Electronic address: shanpingjiang@126.com.
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.
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.
Authors: Tanwir Hashem; Ananth K Kammala; Kanedra Thaxton; Ryan M Griffin; Kellie Mullany; Reynold A Panettieri; Hariharan Subramanian; Rupali Das Journal: Front Immunol Date: 2020-05-12 Impact factor: 7.561