CTNNAL1 inhibits ozone-induced epithelial-mesenchymal transition in human bronchial epithelial cells.

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Abstract

What is the central question of this study? What is the effect of catenin alpha-like 1 (CTNNAL1), an asthma-related epithelial adhesion molecule that plays a vital role in airway epithelial wound repair, on airway epithelial-mesenchymal transition? What is the main finding and its importance? CTNNAL1 inhibits ozone-induced airway epithelial-mesenchymal transition features, mediated by repressing the expression of Twist1 mRNA and reducing TGF-β1 levels. These findings contribute to our understanding of the pathology of airway EMT and may indicate a possible therapeutic target for airway remodelling in bronchial asthma.

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Journal

Journal ID (iso-abbrev): Exp. Physiol.

Title: Experimental physiology

Publisher: Wiley

ISSN (Electronic): 1469-445X

ISSN (Print): 0958-0670

Publication date (Electronic): August 2018

Volume: 103

Issue: 8

Affiliations

[1 ] School of Basic Medicine, Central South University, Changsha, Hunan, 410078, China.

[2 ] Changzhou Key Laboratory of Respiratory Medical Engineering, Institute of Biomedical Engineering and Health Sciences, Changzhou, Jiangsu, 213164, China.

Article

DOI: 10.1113/EP086839

PubMed ID: 29791759

SO-VID: 823bce93-2b26-4fd1-9ba0-03da575a2479

History

Keywords: CTNNAL1,TGF-β1,ozone,EMT,bronchial epithelium

Data availability:

Keywords: CTNNAL1, TGF-β1, ozone, EMT, bronchial epithelium

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