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Blocking TGF-β expression inhibits silica particle-induced epithelial-mesenchymal transition in human lung epithelial cells.

Abstract
The main characteristic of silicosis is irreversible fibrosis. Certain studies have shown that epithelial-mesenchymal transition (EMT) regulated by transforming growth factor-β (TGF-β) is involved in fibrosis. Thus, we suggest that TGF-β regulated EMT may play an important role in silicosis. In this study, we determined the expression of TGF-β-Smad2/3, EMT- and ECM-related markers in lung epithelial cells treated with silica particle by RT-PCR, western-blot and ELISA. In order to explore the role of TGF-β, we used TGF-β inhibitor in the cell model. We found that the cells lost the expression of epithelial phenotypic markers and acquired increased expression of mesenchymal cells markers with ECM deposition after treatment with silica particle. Moreover, the changes of EMT-related event was restricted in response to TGF-β inhibitor. These findings suggest that EMT is essentially involved in the pathogenesis of fibrosis induced by silica particles and down-regulating the TGF-β expression can inhibit the process of EMT.
AuthorsYi Rong, Yan Shen, Zhihong Zhang, Xiuqing Cui, Lili Xiao, Yuewei Liu, Xin Luo, Weihong Chen
JournalEnvironmental toxicology and pharmacology (Environ Toxicol Pharmacol) Vol. 40 Issue 3 Pg. 861-9 (Nov 2015) ISSN: 1872-7077 [Electronic] Netherlands
PMID26476888 (Publication Type: Journal Article)
CopyrightCopyright © 2015 Elsevier B.V. All rights reserved.
Chemical References
  • Extracellular Matrix Proteins
  • Pyrazoles
  • Quinolines
  • SMAD2 protein, human
  • SMAD3 protein, human
  • Smad2 Protein
  • Smad3 Protein
  • Transforming Growth Factor beta
  • LY-2157299
  • Silicon Dioxide
Topics
  • Cell Line
  • Cell Proliferation (drug effects)
  • Epithelial Cells (cytology, drug effects, metabolism)
  • Epithelial-Mesenchymal Transition (drug effects)
  • Extracellular Matrix Proteins (genetics, metabolism)
  • Gene Expression Regulation (drug effects)
  • Humans
  • Pyrazoles (pharmacology)
  • Quinolines (pharmacology)
  • Silicon Dioxide (toxicity)
  • Smad2 Protein (genetics, metabolism)
  • Smad3 Protein (genetics, metabolism)
  • Transforming Growth Factor beta (genetics, metabolism)

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