The epidthelial sodium channel ENaC and its regulators in the epidermal permeability barrier function

Détails

Ressource 1Télécharger: TODJ-4-27.pdf (735.27 [Ko])
Etat: Public
Version: Final published version
ID Serval
serval:BIB_E45C10BB88B1
Type
Article: article d'un périodique ou d'un magazine.
Sous-type
Synthèse (review): revue aussi complète que possible des connaissances sur un sujet, rédigée à partir de l'analyse exhaustive des travaux publiés.
Collection
Publications
Titre
The epidthelial sodium channel ENaC and its regulators in the epidermal permeability barrier function
Périodique
The Open Dermatology Journal
Auteur(s)
Frateschi S., Charles R-P., Hummler E.
ISSN
1874-3722
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
4
Pages
27-35
Langue
anglais
Résumé
The highly amiloride-sensitive epithelial sodium channel ENaC is well known to be involved in controlling whole body sodium homeostasis and lung liquid clearance. ENaC expression has also been detected in the skin of amphibians and mammals. Mice lacking ENaC expression lose rapidly weight associated with an epidermal barrier defect that develops following birth. This dehydration is accompanied with a highly abnormal lipid matrix composition and an impaired skin surface acidification. This strongly suggests a role of ENaC in the maturation of barrier function rather than in the prenatal generation of the barrier, and may be as such an important modulator for skin hydration. In parallel, gene targeting experiments of regulators of ENaC activity, membrane serine proteases, also termed channel activating proteases, like CAP1/Prss8 and matriptase/MT-SP1 by themselves have been shown to be crucial for the epidermal barrier function. In our review, we mainly focus on the role of ENaC and its regulators in the skin and discuss their importance in the epidermal permeability barrier function.
Mots-clé
Sodium channel, transmembrane ion flux, regulators of ENaC, serine protease, barrier dysfunction
Open Access
Oui
Création de la notice
18/11/2010 18:11
Dernière modification de la notice
20/08/2019 17:07
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