The receptor for advanced glycation end-products enhances lung epithelial wound repair: An in vitro study.
Cell migration
Cell proliferation
Lung epithelial injury
Receptor for advanced glycation end-products
Wound healing
Journal
Experimental cell research
ISSN: 1090-2422
Titre abrégé: Exp Cell Res
Pays: United States
ID NLM: 0373226
Informations de publication
Date de publication:
15 06 2020
15 06 2020
Historique:
received:
30
03
2020
revised:
17
04
2020
accepted:
19
04
2020
pubmed:
25
4
2020
medline:
1
1
2021
entrez:
25
4
2020
Statut:
ppublish
Résumé
Re-epithelialization of the alveolar surface is a key process of lung alveolar epithelial barrier repair after acute lung injury. The receptor for advanced glycation end-products (RAGE) pathway plays key roles in lung homeostasis, and its involvement in wound repair has been already reported in human bronchial epithelial cells. However, its effects on lung alveolar epithelial repair after injury remain unknown. We investigated whether RAGE stimulation with its ligands high-mobility group box 1 protein (HMGB1) or advanced glycation end-products (AGEs), alone or associated with RAGE inhibition using RAGE antagonist peptide, affects in vitro wound healing in human alveolar epithelial A549 cells. We further asked whether these effects could be associated with changes in cell proliferation and migration. We found that treatment of A549 cells with HMGB1 or AGEs promotes RAGE-dependent wound healing after a scratch assay. In addition, both RAGE ligands increased cell proliferation in a RAGE-dependent manner. Treatment with HMGB1 increased migration of alveolar epithelial cells at 12 h, independently of RAGE, whereas AGEs stimulated migration as measured 48 h after injury in a RAGE-dependent manner. Taken together, these results suggest that RAGE pathway is involved in lung alveolar epithelial wound repair, possibly through enhanced cell migration and proliferation.
Identifiants
pubmed: 32330509
pii: S0014-4827(20)30257-3
doi: 10.1016/j.yexcr.2020.112030
pii:
doi:
Substances chimiques
Glycation End Products, Advanced
0
HMGB1 Protein
0
Receptor for Advanced Glycation End Products
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
112030Informations de copyright
Copyright © 2020 Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest This work was supported by grants from the Auvergne Regional Council and the French Agence Nationale de la Recherche and the Direction Générale de l’Offre de Soins. RZ was funded by a PhD grant from the Ecole Doctorale des Sciences de la Vie, Santé, Agronomie, Environnement (ED SVSAE, ED 65, Université Clermont Auvergne). The funders had no influence in the study design, conduct, and analysis or in the preparation of this article. The authors state that they have no conflict of interest to declare in relationship with this work.