Soluble E‐cadherin participates in BLM‐induced pulmonary fibrosis by promoting EMT and lung fibroblast migration

Author:

Huang Chaowen1,Liang Congmin2,Tong Jinzhai1,Zhong Xueying1,Luo Lishan3,Liang Liping1,Wen Yuting1,Zhong Liandi1,Deng Jiongrui1,Peng Ming1,Wu Weiliang1,Huang Weijian1,Xie Anlun2,Huang Yanming1,Chen Jialong2ORCID

Affiliation:

1. Department of Pulmonary and Critical Care Medicine Jiangmen Institute of Respiratory Disease, Jiangmen Central Hospital Jiangmen China

2. The First Dongguan Affiliated Hospital of Guangdong Medical University Guangdong Medical University Dongguan Guangdong Province China

3. Department of Respiratory and Critical Care Medicine Huizhou Municipal Central Hospital Huizhou Guangdong Province China

Abstract

AbstractSoluble E‐cadherin (sE‐cad) is an 80 kDa fragment derived from E‐cadherin that is shed from the cell surface through proteolytic cleavage and is a biomarker in various cancers that promotes invasion and migration. Alveolar epithelial destruction, aberrant lung fibroblast migration and inflammation contribute to pulmonary fibrosis. Here, we hypothesized that E‐cadherin plays an important role in lung fibrosis. In this study, we found that E‐cadherin was markedly increased in the bronchoalveolar lavage fluid (BALF) and serum of mice with pulmonary fibrosis and that blocking sE‐cad with HECD‐1, a neutralizing antibody targeting the ectodomain of E‐cadherin, effectively inhibited myofibroblast accumulation and collagen deposition in the lungs after bleomycin (BLM) exposure. Moreover, transforming growth factor‐β (TGF‐β1) induced the shedding of sE‐cad from A549 cells, and treatment with HECD‐1 inhibited epithelial–mesenchymal transition (EMT) stimulated by TGF‐β1. Fc‐E‐cadherin (Fc‐Ecad), which is an exogenous form of sE‐cad, robustly promoted lung fibroblast migration. E‐cadherin participates in bleomycin (BLM)‐induced lung fibrosis by promoting EMT in the alveolar epithelium and fibroblast activation. E‐cadherin may be a novel therapeutic target for lung fibrosis.

Funder

Basic and Applied Basic Research Foundation of Guangdong Province

National Natural Science Foundation of China

Publisher

Wiley

Subject

Health, Toxicology and Mutagenesis,Management, Monitoring, Policy and Law,Toxicology,General Medicine

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