Particulate matters increase epithelial-mesenchymal transition and lung fibrosis through the ETS-1/NF-kappa B-dependent pathway in lung epithelial cells
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Univ Arizona, Dept Basic Med Sci, Coll MedIssue Date
2020-08
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Chen, YC., Chuang, TY., Liu, CW. et al. Particulate matters increase epithelial-mesenchymal transition and lung fibrosis through the ETS-1/NF-κB-dependent pathway in lung epithelial cells. Part Fibre Toxicol 17, 41 (2020). https://doi.org/10.1186/s12989-020-00373-zJournal
PARTICLE AND FIBRE TOXICOLOGYRights
© The Author(s). 2020 Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this licence, visithttp://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.Collection Information
This item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at repository@u.library.arizona.edu.Abstract
Background Particulate matters (PMs) in ambient air pollution are closely related to the incidence of respiratory diseases and decreased lung function. Our previous report demonstrated that PMs-induced oxidative stress increased the expression of proinflammatory intracellular adhesion molecule-1 (ICAM-1) through the IL-6/AKT/STAT3/NF-kappa B pathway in A549 cells. However, the role of O-PMs in epithelial-mesenchymal transition (EMT) development and pulmonary fibrosis and the related mechanisms have not been determined. The aim of this study was to investigate the effects of O-PMs on the pathogenesis of EMT and pulmonary fibrosis as well as the expression of ETS-1 and NF-kappa B p65, in vitro and in vivo. Results O-PMs treatment induced EMT development, fibronectin expression, and cell migration. O-PMs affected the expression of the EMT-related transcription factors NF-kappa B p65 and ETS-1. Interference with NF-kappa B p65 significantly decreased O-PMs-induced fibronectin expression. In addition, O-PMs affected the expression of fibronectin, E-cadherin, and vimentin through modulating ETS-1 expression. ATN-161, an antagonist of integrin alpha 5 beta 1, decreased the expression of fibronectin and ETS-1 and EMT development. EMT development and the expression of fibronectin and ETS-1 were increased in the lung tissue of mice after exposure to PMs for 7 and 14 days. There was a significant correlation between fibronectin and ETS-1 expression in human pulmonary fibrosis tissue. Conclusion O-PMs can induce EMT and fibronectin expression through the activation of transcription factors ETS-1 and NF-kappa B in A549 cells. PMs can induce EMT development and the expression of fibronectin and ETS-1 in mouse lung tissues. These findings suggest that the ETS-1 pathway could be a novel and alternative mechanism for EMT development and pulmonary fibrosis.Note
Open access journalISSN
1743-8977PubMed ID
32799885Version
Final published versionae974a485f413a2113503eed53cd6c53
10.1186/s12989-020-00373-z
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Except where otherwise noted, this item's license is described as © The Author(s). 2020 Open Access. This article is licensed under a Creative Commons Attribution 4.0 International License. To view a copy of this licence, visithttp://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.