659
Views
6
CrossRef citations to date
0
Altmetric
Articles

CD147 Promoted Epithelial Mesenchymal Transition in Airway Epithelial Cells Induced by Cigarette Smoke via Oxidative Stress Signaling Pathway

, , , , , ORCID Icon, & ORCID Icon show all
Pages 269-279 | Received 01 Feb 2020, Accepted 07 Apr 2020, Published online: 05 May 2020
 

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 H2O2 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 H2O2 could inverse this effect. In conclusion, CD147 promoted EMT in mice and HBE cells induced by cigarette smoke via oxidative stress signaling pathway.

Author contributions

H. Zhou contributed to establishing cell model, molecular biology detection by PCR and WB, analysis and interpretation of data and drafting manuscript. Y. Liu was responsible for IHC of animal tissues and IF of cell samples. Z. Wang, Y. Yang, D. Yuan and M. Li took part in animal treating and collecting various kinds of samples. X. Zhang carried out statistical analysis and revised manuscript. Y. Li designed this study and revised manuscript. All authors reviewed the manuscript.

Disclosure Statement

No potential conflict of interest was reported by the author(s).

Additional information

Funding

This work was supported by grants from the Natural Science Foundation of Zhejiang Province (No. LQ17H010006), National Natural Science Foundation of China (Nos. 81870028, 81470241, 81700040), Medical Science and Technology Project of Zhejiang Province (No. 2016KYA012), the Foundation of Science and Technology Department of Zhejiang Province (No. 2017C33124); Sponsored by Zhejiang Provincial Program for the Cultivation of High-level Innovative Health talents (No. A-2017-CXCR02).

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.