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Mice deficient in involucrin, envoplakin and periplakin have a defective epidermal barrier

Sevilla, L.M. and Nachat, R. and Groot, K.R. and Klement, J.F. and Uitto, J. and Djian, P. and Määttä, A. and Watt, F.M. (2007) 'Mice deficient in involucrin, envoplakin and periplakin have a defective epidermal barrier.', Journal of cell biology., 179 (7). pp. 1599-1612.

Abstract

The cornified envelope is assembled from transglutaminase cross-linked proteins and lipids in the outermost epidermal layers and is essential for skin barrier function. Involucrin, envoplakin, and periplakin form the protein scaffold on which the envelope assembles. To examine their combined function, we generated mice deficient in all three genes. The triple knockouts have delayed embryonic barrier formation and postnatal hyperkeratosis (abnormal accumulation of cornified cells) resulting from impaired desquamation. Cornified envelopes form but are ultrastructurally abnormal, with reduced lipid content and decreased mechanical integrity. Expression of proteases is reduced and the protease inhibitor, serpina1b, is highly upregulated, resulting in defective filaggrin processing and delayed degradation of desmoglein 1 and corneodesmosin. There is infiltration of CD4+ T cells and a reduction in resident γδ+ T cells, reminiscent of atopic dermatitis. Thus, combined loss of the cornified envelope proteins not only impairs the epidermal barrier, but also changes the composition of T cell subpopulations in the skin.

Item Type:Article
Additional Information:Supplemental Material can be found at: http://jcb.rupress.org/content/suppl/2008/02/01/jcb.200706187.DC1.html
Full text:PDF - Published Version (5289Kb)
Status:Peer-reviewed
Publisher Web site:http://dx.doi.org/10.1083/jcb.200706187
Publisher statement:This article is published under the Creative Commons Attribution (CC-BY) license.
Record Created:06 Jun 2012 09:35
Last Modified:12 Jun 2012 11:17

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