Postnatal requirement of the epithelial sodium channel for maintenance of epidermal barrier function.

Détails

ID Serval
serval:BIB_A57720F31A9F
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Postnatal requirement of the epithelial sodium channel for maintenance of epidermal barrier function.
Périodique
Journal of Biological Chemistry
Auteur(s)
Charles R.P., Guitard M., Leyvraz C., Breiden B., Haftek M., Haftek-Terreau Z., Stehle J.C., Sandhoff K., Hummler E.
ISSN
0021-9258
Statut éditorial
Publié
Date de publication
2008
Peer-reviewed
Oui
Volume
283
Numéro
5
Pages
2622-2630
Langue
anglais
Notes
Publication types: Journal Article
Résumé
In skin, the physiological consequence of an epithelial sodium channel (ENaC) deficiency is not obvious directly at birth. Nevertheless, within hours after birth, mice deficient for the alpha-subunit of the highly amiloride-sensitive epithelial sodium channel (alphaENaC/Scnn1a) suffer from a significant increased dehydration. This is characterized by a loss of body weight (by 6% in 6 h) and an increased transepidermal water loss, which is accompanied by a higher skin surface pH in 1-day-old pups. Although early and late differentiation markers, as well as tight junction protein distribution and function, seem unaffected, deficiency of alphaENaC severely disturbs the stratum corneum lipid composition with decreased ceramide and cholesterol levels, and increased pro-barrier lipids, whereas covalently bound lipids are drastically reduced. Ultrastructural analysis revealed morphological changes in the formation of intercellular lamellar lipids and the lamellar body secretion. Extracellular formation of the lamellar lipids proved to be abnormal in the knockouts. In conclusion, ENaC deficiency results in progressive dehydration and, consequently, weight loss due to severe impairment of lipid formation and secretion. Our data demonstrate that ENaC expression is required for the postnatal maintenance of the epidermal barrier function but not for its generation.
Mots-clé
Adaptation, Physiological, Animals, Animals, Newborn, Epithelial Sodium Channel/deficiency, Epithelial Sodium Channel/genetics, Lipid Metabolism, Mice, Mice, Knockout, Permeability, Skin/ultrastructure, Skin Physiological Phenomena, Tight Junctions/physiology, Tight Junctions/ultrastructure
Pubmed
Web of science
Open Access
Oui
Création de la notice
07/03/2008 23:41
Dernière modification de la notice
20/08/2019 16:10
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