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Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury
Persistent injury and the following improper repair in bronchial epithelial cells are involved in the pathogenesis of airway inflammation and airway remodeling of asthma. E-cadherin (ECAD) has been shown to be involved in airway epithelium injury repair, but its underlying mechanisms to this process...
Autores principales: | , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144967/ https://www.ncbi.nlm.nih.gov/pubmed/33946207 http://dx.doi.org/10.3390/biom11050669 |
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author | Han, Li Luo, Huaiqing Huang, Wenjie Zhang, Jiang Wu, Di Wang, Jinmei Pi, Jiao Liu, Chi Qu, Xiangping Liu, Huijun Qin, Xiaoqun Xiang, Yang |
author_facet | Han, Li Luo, Huaiqing Huang, Wenjie Zhang, Jiang Wu, Di Wang, Jinmei Pi, Jiao Liu, Chi Qu, Xiangping Liu, Huijun Qin, Xiaoqun Xiang, Yang |
author_sort | Han, Li |
collection | PubMed |
description | Persistent injury and the following improper repair in bronchial epithelial cells are involved in the pathogenesis of airway inflammation and airway remodeling of asthma. E-cadherin (ECAD) has been shown to be involved in airway epithelium injury repair, but its underlying mechanisms to this process is poorly understood. Here, we describe a previously undetected function of ECAD in regulating the balance of EMT and MET during injury repair. Injury in mice and human bronchial epithelial cells (HBECs) was induced by successive ozone stress for 4 days at 30 min per day. ECAD overexpression in HBECs was induced by stable transfection. EMT features, transforming growth factor beta1 (TGF-β1) secretion, transcriptional repressor Snail expression, and β-catenin expression were assayed. Ozone exposure and then removal successfully induced airway epithelium injury repair during which EMT and MET occurred. The levels of TGF-β1 secretion and Snail expression increased in EMT process and decreased in MET process. While ECAD overexpression repressed EMT features; enhanced MET features; and decreased TGF-β1 secretion, Snail mRNA level, and β-catenin protein expression. Moreover, activating β-catenin blocked the effects of ECAD on EMT, MET and TGF-β1 signaling. Our results demonstrate that ECAD regulates the balance between EMT and MET, by preventing β-catenin to inhibit TGFβ1 and its target genes, and finally facilitates airway epithelia repair. |
format | Online Article Text |
id | pubmed-8144967 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-81449672021-05-26 Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury Han, Li Luo, Huaiqing Huang, Wenjie Zhang, Jiang Wu, Di Wang, Jinmei Pi, Jiao Liu, Chi Qu, Xiangping Liu, Huijun Qin, Xiaoqun Xiang, Yang Biomolecules Article Persistent injury and the following improper repair in bronchial epithelial cells are involved in the pathogenesis of airway inflammation and airway remodeling of asthma. E-cadherin (ECAD) has been shown to be involved in airway epithelium injury repair, but its underlying mechanisms to this process is poorly understood. Here, we describe a previously undetected function of ECAD in regulating the balance of EMT and MET during injury repair. Injury in mice and human bronchial epithelial cells (HBECs) was induced by successive ozone stress for 4 days at 30 min per day. ECAD overexpression in HBECs was induced by stable transfection. EMT features, transforming growth factor beta1 (TGF-β1) secretion, transcriptional repressor Snail expression, and β-catenin expression were assayed. Ozone exposure and then removal successfully induced airway epithelium injury repair during which EMT and MET occurred. The levels of TGF-β1 secretion and Snail expression increased in EMT process and decreased in MET process. While ECAD overexpression repressed EMT features; enhanced MET features; and decreased TGF-β1 secretion, Snail mRNA level, and β-catenin protein expression. Moreover, activating β-catenin blocked the effects of ECAD on EMT, MET and TGF-β1 signaling. Our results demonstrate that ECAD regulates the balance between EMT and MET, by preventing β-catenin to inhibit TGFβ1 and its target genes, and finally facilitates airway epithelia repair. MDPI 2021-04-30 /pmc/articles/PMC8144967/ /pubmed/33946207 http://dx.doi.org/10.3390/biom11050669 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Han, Li Luo, Huaiqing Huang, Wenjie Zhang, Jiang Wu, Di Wang, Jinmei Pi, Jiao Liu, Chi Qu, Xiangping Liu, Huijun Qin, Xiaoqun Xiang, Yang Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury |
title | Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury |
title_full | Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury |
title_fullStr | Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury |
title_full_unstemmed | Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury |
title_short | Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury |
title_sort | modulation of the emt/met process by e-cadherin in airway epithelia stress injury |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8144967/ https://www.ncbi.nlm.nih.gov/pubmed/33946207 http://dx.doi.org/10.3390/biom11050669 |
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