RESEARCH ARTICLE
The Epithelial Sodium Channel ENaC and its Regulators in the Epidermal Permeability Barrier Function
Simona Frateschi1, Roch-Philippe Charles1, #, Edith Hummler*, 1
Article Information
Identifiers and Pagination:
Year: 2010Volume: 4
First Page: 27
Last Page: 35
Publisher ID: TODJ-4-27
DOI: 10.2174/1874372201004010027
Article History:
Received Date: 15/09/2009Revision Received Date: 19/11/2009
Acceptance Date: 10/12/2009
Electronic publication date: 23/4/2010
Collection year: 2010
open-access license: This is an open access article distributed under the terms of the Creative Commons Attribution 4.0 International Public License (CC-BY 4.0), a copy of which is available at: https://creativecommons.org/licenses/by/4.0/legalcode. This license permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Abstract
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.
