NDLI: Cigarette smoke extract induces the epithelial-to-mesenchymal transition via the PLTP/TGF-β1/Smad2 pathway in RLE-6TN cells

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Toxicology Research Vol - 6 Issue - 1

Toxicology Research Vol -5

Toxicology Research Vol -4

Toxicology Research Vol -3

Toxicology Research Vol -2

Toxicology Research Vol -1

Cigarette smoke extract induces the epithelial-to-mesenchymal transition via the PLTP/TGF-β1/Smad2 pathway in RLE-6TN cells

Content Provider	Royal Society of Chemistry (RSC)
Author	Zhang, Hui Zhang, Lu Wu, Feng-ping Yang, Yong-zhen Chen, Hong Yu, Xiu-ying Chen, Ya-juan
Copyright Year	2017
Abstract	Aim: The role of phospholipid transfer protein (PLTP) in the pathogenesis of the cigarette smoke extract (CSE)-induced epithelial-to-mesenchymal transition (EMT) has not been well described. In this study we investigated the effect of PLTP on the CSE-induced EMT of rat alveolar epithelial cells (RLE-6TN). Methods: The rats were exposed to air and cigarette smoke (CS) for 3 d and then the lungs were sectioned and examined using immunohistochemistry techniques. RLE-6TN cells were treated with different concentrations of CSE. PLTP siRNA was transfected into cells or SB431542 – an inhibitor of the transforming growth factor-β1 (TGF-β1) type I receptor – was administered prior to CSE exposure. The expression of EMT markers and PLTP was detected by qRT-PCR. The levels of PLTP, TGF-β1, p-Smad2, Smad2, and EMT proteins were analyzed by western blotting. Results: Lung injury and EMT were accompanied by up-regulation of PLTP and TGF-β1 in the CS-exposed rat model. EMT was induced by CSE in vitro, and the expression of PLTP, TGF-β1, and p-Smad2 was significantly increased after exposure to CSE (P < 0.05). Moreover, knockdown of PLTP and blocking of the TGF-β1/Smad2 pathway restrained the CSE-induced activation of the TGF-β1/Smad2 pathway and partly inhibited EMT by reversing E-cadherin expression and retarding the induction of N-cadherin and vimentin. In contrast, SB431542 had no effect on the expression of PLTP, while it ameliorated CSE-induced EMT. Conclusion: PLTP promotes the CSE-induced EMT process, in which the TGF-β1/Smad2 pathway is activated.
Starting Page	215
Ending Page	222
Page Count	8
File Format	HTM / HTML PDF
ISSN	2045452X
Volume Number	6
Issue Number	2
Journal	Toxicology Research
DOI	10.1039/c6tx00378h
Language	English
Publisher	Royal Society of Chemistry
Access Restriction	Open
Subject Keyword	Phospholipid transfer protein Immunohistochemistry Western blot Vimentin TGF beta 1 Small interfering RNA Enzyme inhibitor Cadherin Epithelial\u2013mesenchymal transition Mothers against decapentaplegic homolog 2 CSE CDH2 Pulmonary alveolus Real-time polymerase chain reaction
Content Type	Text
Resource Type	Article
Subject	Health, Toxicology and Mutagenesis Toxicology

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