E‐cadherin and p120ctn protein expression are lost in hidradenitis suppurativa lesions. Issue 7 (20th June 2019)

• Record Type: Journal Article
• Authors: Nelson, Amanda M.; Cong, Zhaoyuan; Gettle, Samantha L.; Longenecker, Amy L.; Kidacki, Michal; Kirby, Joslyn S.; Adams, David R.; Stairs, Douglas B.; Danby, Frederick W.
• Is Part Of: Experimental dermatology. Volume 28:Issue 7(2019)
• Page Start: 867
• Page End: 871
• Publication Date: 2019-06-20
• Subjects: adhesion junction -- Hidradenitis suppurativa -- skin; Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.13973
• Languages: English
• ISSNs: 0906-6705

Abstract

Abstract: 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 with 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.