CD147 Promoted Epithelial Mesenchymal Transition in Airway Epithelial Cells Induced by Cigarette Smoke via Oxidative Stress Signaling Pathway. (3rd May 2020)

• Record Type: Journal Article
• Authors: Zhou, Hongbin; Liu, Yuanshun; Wang, Zhehua; Yang, Yang; Li, Mengyu; Yuan, Dong; Zhang, Xiaoqin; Li, Yaqing
• Is Part Of: COPD. Volume 17:Number 3(2020)
• Page Start: 269
• Page End: 279
• Publication Date: 2020-05-03
• Subjects: Chronic obstructive pulmonary disease (COPD) -- cigarette smoke -- epithelial mesenchymal transition (EMT) -- CD147 -- HBE; Lungs -- Diseases, Obstructive -- Periodicals; 616.24
• DOI: 10.1080/15412555.2020.1758051
• Languages: English
• ISSNs: 1541-2555

Abstract

Abstract: Chronic obstructive pulmonary disease (COPD) is a common airway disease, and epithelial mesenchymal transition (EMT) is participated in the pathogenesis of COPD. However, the role of CD147 in COPD remains largely unknown. In order to clarify the role of CD147 in EMT induced by cigarette smoke, we established animal and cell model of EMT by mean of cigarette smoke exposure and detected the expressions of CD147 and EMT markers via PCR, WB and IF. RNA inference was applied to study the role of CD147 in CSE induced EMT in vitro . NAC and H2 O2 were used to study oxidative stress signaling pathway in this model. As a result, cigarette smoke exposure upregulated the expressions of CD147, α-SMA, and Vimentin and downregulated the expression of Ecadherin and ZO1 both in vivo and in vitro, which was accompanied by augmented level of oxidative stress. CD147 knockdown would partly inhibit CSE induced EMT, while preincubation of H2 O2 could inverse this effect. In conclusion, CD147 promoted EMT in mice and HBE cells induced by cigarette smoke via oxidative stress signaling pathway.