Involucrin-claudin-6 tail deletion mutant (CDelta206) transgenic mice: a model of delayed epidermal permeability barrier formation and repair

Disease Models & Mechanisms
Adebola EnikanolaiyeKursad Turksen

Abstract

Preterm birth is a major global health problem that results in a large number of infant deaths, many of which are attributable to the complications of an immature epidermal permeability barrier (EPB), for which there is currently no effective therapeutic option. The mammalian EPB is formed during development and is essential for survival as it maintains thermoregulation and hydration, and provides a defense against infection. Using transgenic mouse technology, we have demonstrated the importance of claudin (Cldn)-containing tight junctions (TJs) in epidermal differentiation and, in particular, that epidermal suprabasal overexpression of Cldn6 results in an EPB-deficient phenotype that phenocopies the dysfunctional EPB of premature human infants. In this study, we used the same approach to target a Cldn6 tail deletion mutant to the epidermis of mice [involucrin (Inv)-Cldn6-CDelta206 transgenic mice]. The Inv-Cldn6-CDelta206 transgenic mice displayed a developmental delay in EPB formation, as shown by the expression of keratins and Cldns, and by X-Gal penetration assays. Trans-epidermal water loss measurements and immunolocalization studies indicated that the epidermal differentiation program was also perturbed in postnatal Inv-C...Continue Reading

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Citations

Nov 18, 2016·Pflügers Archiv : European journal of physiology·Katja Bäsler, Johanna M Brandner
Apr 27, 2018·Environmental Science and Pollution Research International·Joshua B LewisPaul R Reynolds

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