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...
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doaj-dc94d81f3acd492a9867ceddb874d9db2021-04-30T23:01:09ZengMDPI AGBiomolecules2218-273X2021-04-011166966910.3390/biom11050669Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress InjuryLi Han0Huaiqing Luo1Wenjie Huang2Jiang Zhang3Di Wu4Jinmei Wang5Jiao Pi6Chi Liu7Xiangping Qu8Huijun Liu9Xiaoqun Qin10Yang Xiang11Department of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medicine, Changsha Medical University, Changsha 410219, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaDepartment of Physiology, School of Basic Medical Science, Central South University, Changsha 410007, ChinaPersistent 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.https://www.mdpi.com/2218-273X/11/5/669E-cadherininjury repairepithelial-mesenchymal transformationmesenchymal–epithelial transformationTGFβ1β-catenin |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Li Han Huaiqing Luo Wenjie Huang Jiang Zhang Di Wu Jinmei Wang Jiao Pi Chi Liu Xiangping Qu Huijun Liu Xiaoqun Qin Yang Xiang |
spellingShingle |
Li Han Huaiqing Luo Wenjie Huang Jiang Zhang Di Wu Jinmei Wang Jiao Pi Chi Liu Xiangping Qu Huijun Liu Xiaoqun Qin Yang Xiang Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury Biomolecules E-cadherin injury repair epithelial-mesenchymal transformation mesenchymal–epithelial transformation TGFβ1 β-catenin |
author_facet |
Li Han Huaiqing Luo Wenjie Huang Jiang Zhang Di Wu Jinmei Wang Jiao Pi Chi Liu Xiangping Qu Huijun Liu Xiaoqun Qin Yang Xiang |
author_sort |
Li Han |
title |
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_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_sort |
modulation of the emt/met process by e-cadherin in airway epithelia stress injury |
publisher |
MDPI AG |
series |
Biomolecules |
issn |
2218-273X |
publishDate |
2021-04-01 |
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. |
topic |
E-cadherin injury repair epithelial-mesenchymal transformation mesenchymal–epithelial transformation TGFβ1 β-catenin |
url |
https://www.mdpi.com/2218-273X/11/5/669 |
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