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Particulate matters increase epithelial-mesenchymal transition and lung fibrosis through the ETS-1/NF-κB-dependent pathway in lung epithelial cells

  • Chen, Yu-Chen1
  • Chuang, Tzu-Yi2, 3
  • Liu, Chen-Wei4
  • Liu, Chi-Wei5
  • Lee, Tzu-Lin1
  • Lai, Tsai-Chun1
  • Chen, Yuh-Lien1
  • 1 College of Medicine, National Taiwan University, No. 1, Sec 1, Jen-Ai Road, Taipei, Taiwan, Republic of China , Taipei (Taiwan)
  • 2 Min-Sheng General Hospital, No. 168 Ching-Kuo Road, Taoyuan, Taiwan, Republic of China , Taoyuan (Taiwan)
  • 3 College of Medicine and National Taiwan University Hospital, No.7, Chung-Shan South Road, Taipei, Taiwan, Republic of China , Taipei (Taiwan)
  • 4 University of Arizona College of Medicine, Phoenix, AZ, USA , Phoenix (United States)
  • 5 Taoyuan General Hospital, Ministry of Health and Welfare, Taoyuan, Taiwan, Republic of China , Taoyuan (Taiwan)
Published Article
Particle and Fibre Toxicology
BioMed Central
Publication Date
Aug 14, 2020
DOI: 10.1186/s12989-020-00373-z
Springer Nature


BackgroundParticulate 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-κB 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-κB p65, in vitro and in vivo.ResultsO-PMs treatment induced EMT development, fibronectin expression, and cell migration. O-PMs affected the expression of the EMT-related transcription factors NF-κB p65 and ETS-1. Interference with NF-κB 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 α5β1, 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.ConclusionO-PMs can induce EMT and fibronectin expression through the activation of transcription factors ETS-1 and NF-κB 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.

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