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  • 1.
    Persson, Gabriella
    et al.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Johansson-Jänkänpää, Emma
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Ganceviciene, Ruta
    Karadag, Ayse Serap
    Bilgili, Serap Gunes
    Omer, Hélène
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    Alexeyev, Oleg A.
    Umeå University, Faculty of Medicine, Department of Medical Biosciences, Pathology.
    No evidence for follicular keratinocyte hyperproliferation in acne lesions as compared to autologous healthy hair follicles2018In: Experimental dermatology, ISSN 0906-6705, E-ISSN 1600-0625, Vol. 27, no 6, p. 668-671Article in journal (Refereed)
    Abstract [en]

    Abnormal hyperkeratinization in sebaceous hair follicles has long been believed to play an important role in acne pathogenesis. Several early reports purported to provide histological evidence for hyperproliferation of keratinocytes in acne lesions by showing a higher expression of the Ki67 as well as certain keratins. The evidence is, however, not robust, and a number of methodological and technical limitations can be identified in these studies. In this study, we looked at the expression of proliferation, mitosis and apoptosis markers directly at acne skin lesions in 66 patients with acne vulgaris. Ki67 was assessed using immunohistochemistry and -tubulin, phospho-histone H3 and cleaved-PARP with immunofluorescence microscopy. Allogenic unaffected hair follicles from the same acne patients were used as an internal control. In both acne and control hair follicles, the -tubulin staining was universal, approaching 100% cells and showed no signs of changed assembly. Expression of cleaved-PARPthe apoptosis markerwas a rare event. Cell proliferation rate measured by the expression of Ki67 and phospho-histone H3 was virtually identical between acne and the two control groups. Our findings show the absence of increased keratinocyte proliferation in acne vulgaris. Alternative mechanisms are likely responsible for infundibular hyperkeratinization in acne pathogenesis.

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