Airway epithelial ITGB4 deficiency induces airway remodeling in a mouse model.

Humans Mice Animals Airway Remodeling / physiology Fibroblast Growth Factor 2 / metabolism Respiratory System / metabolism Asthma / pathology Pyroglyphidae Dermatophagoides pteronyssinus Epithelial Cells / metabolism Mice, Knockout Disease Models, Animal Integrin beta4 / genetics
Integrin β4 airway epithelium airway remodeling asthma epithelial-mesenchymal trophic unit

Journal

The Journal of allergy and clinical immunology
ISSN: 1097-6825
Titre abrégé: J Allergy Clin Immunol
Pays: United States
ID NLM: 1275002

Informations de publication

Date de publication:
02 2023
Historique:
received: 23 11 2021
revised: 25 08 2022
accepted: 16 09 2022
pubmed: 16 10 2022
medline: 8 2 2023
entrez: 15 10 2022
Statut: ppublish

Résumé

Airway epithelial cells (AECs) with impaired barrier function contribute to airway remodeling through the activation of epithelial-mesenchymal trophic units (EMTUs). Although the decreased expression of ITGB4 in AECs is implicated in the pathogenesis of asthma, how ITGB4 deficiency impacts airway remodeling remains obscure. This study aims to determine the effect of epithelial ITGB4 deficiency on the barrier function of AECs, asthma susceptibility, airway remodeling, and EMTU activation. AEC-specific ITGB4 conditional knockout mice (ITGB4 ITGB4 deficiency in AECs enhanced asthma susceptibility and airway remodeling by disrupting airway epithelial barrier function. Aggravated airway remodeling in HDM-exposed ITGB4 Airway epithelial ITGB4 deficiency induces airway remodeling in a mouse model of asthma through enhanced EMTU activation that is regulated by the SHP2/JNK/c-Jun/FGF2 pathway.

Sections du résumé

BACKGROUND
Airway epithelial cells (AECs) with impaired barrier function contribute to airway remodeling through the activation of epithelial-mesenchymal trophic units (EMTUs). Although the decreased expression of ITGB4 in AECs is implicated in the pathogenesis of asthma, how ITGB4 deficiency impacts airway remodeling remains obscure.
OBJECTIVE
This study aims to determine the effect of epithelial ITGB4 deficiency on the barrier function of AECs, asthma susceptibility, airway remodeling, and EMTU activation.
METHODS
AEC-specific ITGB4 conditional knockout mice (ITGB4
RESULTS
ITGB4 deficiency in AECs enhanced asthma susceptibility and airway remodeling by disrupting airway epithelial barrier function. Aggravated airway remodeling in HDM-exposed ITGB4
CONCLUSIONS
Airway epithelial ITGB4 deficiency induces airway remodeling in a mouse model of asthma through enhanced EMTU activation that is regulated by the SHP2/JNK/c-Jun/FGF2 pathway.

Identifiants

DOI: 10.1016/j.jaci.2022.09.032 PMID: 36243221
pubmed: 36243221
pii: S0091-6749(22)01342-2
doi: 10.1016/j.jaci.2022.09.032
pii:
doi:

Substances chimiques

Fibroblast Growth Factor 2 103107-01-3
ITGB4 protein, human 0
Integrin beta4 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

431-446.e16

Informations de copyright

Copyright © 2022 American Academy of Allergy, Asthma & Immunology. All rights reserved.

Auteurs

Lin Yuan (L)

Department of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, Xiangya Hospital, Central South University, Changsha, China; Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China; Basic and Clinical Research Laboratory of Major Respiratory Diseases, Central South University, Changsha, China.

Huijun Liu (H)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Xizi Du (X)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Ye Yao (Y)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Ling Qin (L)

Department of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, Xiangya Hospital, Central South University, Changsha, China; Basic and Clinical Research Laboratory of Major Respiratory Diseases, Central South University, Changsha, China.

Zhenkun Xia (Z)

Department of Thoracic Surgery, the Second Xiangya Hospital, Central South University, Changsha, China.

Kai Zhou (K)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Xinyu Wu (X)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Yunchang Yuan (Y)

Department of Thoracic Surgery, the Second Xiangya Hospital, Central South University, Changsha, China.

Bei Qing (B)

Department of Thoracic Surgery, the Second Xiangya Hospital, Central South University, Changsha, China.

Yang Xiang (Y)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Xiangping Qu (X)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Xiaoqun Qin (X)

Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China.

Ming Yang (M)

the Centre for Asthma and Respiratory Disease, School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle and Hunter Medical Research Institute, Callaghan, Australia.

Chi Liu (C)

Department of Respiratory Medicine, National Clinical Research Center for Respiratory Diseases, Xiangya Hospital, Central South University, Changsha, China; Department of Physiology, School of Basic Medicine Science, Central South University, Changsha, China. Electronic address: liu.chi@csu.edu.cn.

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Classifications MeSH

questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Primates › Haplorhini › Catarrhini › Hominidae › Humains › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Eucaryotes › Animaux › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Phénomènes physiologiques respiratoires et circulatoires › Phénomènes physiologiques respiratoires › Remodelage des voies aériennes › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Facteurs biologiques › Protéines et peptides de signalisation intercellulaire › Facteurs de croissance fibroblastique › Facteur de croissance fibroblastique de type 2 › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Appareil respiratoire › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Maladies du système immunitaire › Hypersensibilité › Hypersensibilité immédiate › Hypersensibilité respiratoire › Asthme › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Eucaryotes › Animaux › Invertébrés › Arthropodes › Arachnida › Acari › Mites (acariens) › Pyroglyphidae › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Eucaryotes › Animaux › Invertébrés › Arthropodes › Arachnida › Acari › Mites (acariens) › Pyroglyphidae › Dermatophagoides pteronyssinus › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Cellules › Cellules épithéliales › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Souris transgéniques › Souris knockout › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Techniques d'investigation › Modèles théoriques › Modèles biologiques › Modèles animaux de maladie humaine › Airway epithelial ITGB4 deficiency induces...
questionsmedicales.fr › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs immunologiques › Intégrines › Chaines bêta des intégrines › Intégrine bêta4 › Airway epithelial ITGB4 deficiency induces...