Gruber, R., Börnchen, C., Rose, K., Daubmann, A., Volksdorf, T., Wladykowski, E., Vidal, Y.Sy S., Peters, E.M., Danso, M., Bouwstra, J.A., Hennies, Hans C., Moll, I., Schmuth, M. and Brandner, J.M. (2015) Diverse regulation of claudin-1 and claudin-4 in atopic dermatitis. American Journal of Physical Anthropology, 185 (10). pp. 2777-2789. ISSN 0002-9483Metadata only available from this repository.
Tight junctions are important for skin barrier function. The tight junction protein claudin 1 (Cldn-1) has been reported to be down-regulated in nonlesional skin of atopic dermatitis (AD) patients. In contrast, we did not observe a significant down-regulation of Cldn-1 in nonlesional skin of the AD cohort used in this study. However, for the first time, a significant down-regulation of Cldn-1 in the upper and lower epidermal layers of lesional skin was detected. In addition, there was a significant up-regulation of Cldn-4 in nonlesional, but not lesional, AD skin. For occludin, no significant alterations were observed. In an AD-like allergic dermatitis mouse model, Cldn-1 down-regulation in eczema was significantly influenced by dermal inflammation, and significantly correlated with hallmarks of eczema (ie, increased keratinocyte proliferation, altered keratinocyte differentiation, increased epidermal thickness, and impaired barrier function). In human epidermal equivalents, the addition of IL-4, IL-13, and IL-31 resulted in a down-regulation of Cldn-1, and Cldn1 knockdown in keratinocytes resulted in abnormal differentiation. In summary, we provide the first evidence that Cldn-1 and Cldn-4 are differentially involved in AD pathogenesis. Our data suggest a role of Cldn-1 in AD eczema formation triggered by inflammation.
|Additional Information:||Unmapped bibliographic data: ST - Diverse regulation of claudin-1 and claudin-4 in atopic dermatitis [Field not mapped to EPrints] AD - Department of Dermatology, Venerology, and Allergology, Medical University of Innsbruck, Innsbruck, Austria; Division of Human Genetics, Medical University of Innsbruck, Innsbruck, Austria. Electronic address: email@example.com. [Field not mapped to EPrints] AN - 26319240 [Field not mapped to EPrints]|
|Subjects:||Q Science > QH Natural history > QH301 Biology
Q Science > QH Natural history > QH426 Genetics
|Schools:||School of Applied Sciences|
|Depositing User:||Hans Hennies|
|Date Deposited:||06 Jul 2016 14:33|
|Last Modified:||29 Jul 2016 12:55|
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