MiR-149 attenuates the proliferation and migration of TGF-β1-induced airway smooth muscle cells by targeting TRPM7 and affecting downstream MAPK signal pathway

Zhengyu  Zhu; Liya  Zhang; Ting  Jiang; Yan  Qian; Yun  Sun; Qian Zhang

doi:10.18388/abp.2020_5417

Zhengyu Zhu Department of Pediatrics, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou City, Jiangsu Province, 213000, China
Liya Zhang Department of Emergency, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou City, Jiangsu Province, 213000, China
Ting Jiang Department of Respiratory and Critical Care Medicine, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou City, Jiangsu Province, 213000, China
Yan Qian
Yun Sun Department of Respiratory and Critical Care Medicine, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou City, Jiangsu Province, 213000, China
Qian Zhang Department of Respiratory and Critical Care Medicine, The Affiliated Changzhou No.2 People’s Hospital of Nanjing Medical University, Changzhou City, Jiangsu Province, 213000, China https://orcid.org/0000-0001-6372-1938

DOI: https://doi.org/10.18388/abp.2020_5417

Abstract

Asthma is considered as a general term for various chronic inflammatory diseases of the respiratory tract. Growing evidences have supported that microRNAs were involved in mediating cell proliferation, migration, and other cellular functions. MiR-149 has been found to take part in the development of various cancers. However, whether miR-149 participated in the proliferation and migration of transforming growth factor beta 1 (TGF-β1)-induced airway smooth muscle cells was still unknown. In this study, the expression level of miR-149 in human airway smooth muscle cells (ASMCs) was decreased after TGF-β1 treatment in vitro. Additionally, the over-expression of miR-149 obviously suppressed proliferation and migration in human ASMCs. Besides, we found that overexpression of miR-149 could inhibit the expression of transient receptor potential melastatin 7 (TRPM7) both in protein and gene levels. Furthermore, we demonstrated that miR-149 could inhibit the cell proliferation and migration in human ASMCs by targeting TRPM7 through modulating mitogen-activated protein kinases (MAPKs) signaling pathway. Taken together, we strongly supported that miR-149 might be a key inhibitor of asthma by targeting TRMP7. Therefore, our finding suggests a promising biomarker for the development of further targeted therapies for asthma.