Ming Chen1, Jianting Shi1, Wei Zhang1, Linjie Huang1, 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: 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.
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. MiceASMCs 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.
Authors: Madhur D Shastri; Wai Chin Chong; Kamal Dua; Gregory M Peterson; Rahul P Patel; Malik Q Mahmood; Murtaza Tambuwala; Dinesh K Chellappan; Nicole G Hansbro; Shakti D Shukla; Philip M Hansbro Journal: Inflammopharmacology Date: 2020-11-05 Impact factor: 4.473
Authors: Eugenel B Espiritu; Amanda E Crunk; Abha Bais; Daniel Hochbaum; Ailen S Cervino; Yu Leng Phua; Michael B Butterworth; Toshiyasu Goto; Jacqueline Ho; Neil A Hukriede; M Cecilia Cirio Journal: Sci Rep Date: 2018-10-30 Impact factor: 4.379