Modulation of the EMT/MET Process by E-Cadherin in Airway Epithelia Stress Injury
Li Han, Huaiqing Luo, Wenjie Huang, Jiang Zhang, Di Wu, Jinmei Wang, Jiao Pi, Chi Liu, Xiangping Qu, Huijun Liu, Xiaoqun Qin, Yang Xiang
Journal：Biomolecules
IF：4.88
DOI：10.3390/biom11050669
PMID：33946207
Published：2021-04-30
research field：分子生物学植物防御机制采后生理学信号转导植物病理学
Abstract
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.Keywords:E-cadherin;injury repair;epithelial-mesenchymal transformation;mesenchymal–epithelial transformation;TGFβ1;β-catenin
本文使用的Yeasen产品
