E-cadherin and p120ctn protein expression are lost in hidradenitis suppurativa lesions.
Authors of this article are:
Nelson AM, Cong Z, Gettle SL, Longenecker AL, Kidacki M, Kirby JS, Adams DR, Stairs DB, Danby FW.
A summary of the article is shown below:
Hidradenitis suppurativa (HS) is a chronic, inflammatory skin disease affecting the pilosebaceous units in the axilla, groin and buttocks. While the pathogenesis of HS is not clear, mechanical stress exacerbates HS. In this study, we aimed to determine whether intracellular adhesive junctions may be aberrant in HS patient skin. Strikingly, we observed loss of E-cadherin and p120ctn protein expression, two key adherens junction proteins, in ~85% of HS severe skin lesions. Moreover, loss of protein expression was apparent in non-lesional skin from HS patients and the degree of loss positively correlated with HS Hurley Stage of disease. E-cadherin expression was unaltered in other inflammatory skin conditions including chronic wound epithelium, atopic dermatitis, and acne vulgaris compared to healthy skin suggesting that its loss may be uniquely relevant to HS pathogenesis. A complete loss of α-catenin, β-catenin and ZO-1 was not observed; however some cytoplasmic staining of the catenins was noted in HS epithelium. We also demonstrated diminished desmosome size in HS lesional skin. Overall, our data suggested that loss of adherens junction proteins and diminished desmosome size in HS skin contributes to the skin’s inability to withstand mechanical stress, and provides rationale as to why mechanical stress exacerbates HS symptoms. This article is protected by copyright. All rights reserved.This article is protected by copyright. All rights reserved.
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