SHP-1 mediates cigarette smoke extract-induced epithelial–mesenchymal transformation and inflammation in 16HBE cells
He Quan,
Xu Shuanglan,
Ma Xiaomei,
Qian Yuanxia,
Lu Xuzhi,
Feng Weiqi,
Chen Zi
Affiliations
He Quan
Department of Respiratory and Critical Care Medicine, Zhenjiang Hospital of Integrated Traditional Chinese and Western Medicine, Zhenjiang, Jiangsu, 212000, China
Xu Shuanglan
Department of Respiratory and Critical Care Medicine, The Affiliated Hospital of Yunnan University, The Second People’s Hospital of Yunnan Province, Kunming, Yunnan, 650021, China
Ma Xiaomei
Department of Respiratory and Critical Care Medicine, Zhenjiang Hospital of Integrated Traditional Chinese and Western Medicine, Zhenjiang, Jiangsu, 212000, China
Qian Yuanxia
Department of Pharmacy, Zhenjiang Hospital of Integrated Traditional Chinese and Western Medicine, Zhenjiang, Jiangsu, 212000, China
Lu Xuzhi
Department of Respiratory and Critical Care Medicine, Zhenjiang Hospital of Integrated Traditional Chinese and Western Medicine, Zhenjiang, Jiangsu, 212000, China
Feng Weiqi
Department of Respiratory and Critical Care Medicine, Zhenjiang Hospital of Integrated Traditional Chinese and Western Medicine, Zhenjiang, Jiangsu, 212000, China
Chen Zi
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital, Nanjing Medical University, 300 Guangzhou Road, Nanjing, Jiangsu, 210029, China
Src-homology region 2 domain-containing phosphatase 1 (SHP-1) is considered an anti-inflammatory factor, but its role in chronic obstructive pulmonary disease (COPD) remains unknown. Herein, overexpression of SHP-1 was utilized to explore the functions of SHP-1 in COPD models established by stimulating 16HBE cells with cigarette smoke extracts (CSE) in vitro. SHP-1 was downregulated in both COPD patients and CES-treated 16HBE cells. SHP-1 overexpression reinforced cell viability and significantly prevented CSE-induced cell apoptosis in 16HBE cells. Furthermore, SHP-1 overexpression greatly reversed the CSE-induced migration, epithelial–mesenchymal transition (EMT), and pro-inflammatory factor production in 16HBE cells. In addition, CSE activated the P65 and PI3K/AKT pathways in 16HBE cells, which was also reversed by SHP-1 overexpression. Our findings indicated that SHP-1 alleviated CSE-induced EMT and inflammation in 16HBE cells, suggesting that SHP-1 regulated the development of COPD, and these functions may be linked to the inhibition of the PI3K/AKT pathway.
