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Increased in situ expression of melanocortin‐1 receptor in sebaceous glands of lesional skin of patients with acne vulgaris
Author(s) -
Ganceviciene Ruta,
Graziene Vida,
Böhm Markus,
Zouboulis Christos C.
Publication year - 2007
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2007.00565.x
Subject(s) - acne , melanocortin , melanocortin 1 receptor , melanocortin receptor , receptor , sebaceous gland , human skin , melanocortins , endocrinology , medicine , immunohistochemistry , inflammation , melanocyte stimulating hormone , dermatology , biology , phenotype , gene , biochemistry , genetics
Central or peripheral stress may induce the development of clinical inflammation in the pilosebaceous unit, leading to the development of acne lesions or to exacerbation of pre‐existing acne. Melanocortin peptides such as α ‐melanocyte‐stimulating hormone and its receptors do not only regulate melanogenesis but can also affect non‐pigmentary processes, such as inflammation, apoptosis and sebogenesis. The purpose of the study was to investigate by immunohistochemistry if changes of melanocortin‐1 receptor expression exist in acne lesions versus normal skin. In all, 33 patients with acne vulgaris and seven age‐matched volunteers without acne participated in the study. Skin biopsies were taken from acne‐involved faces, the non‐involved thigh skin of the same patients and from normal human skin. Melanocortin‐1 receptor immunoreactivity was most prominently detectable in adnexal structures. Sebocytes and keratinocytes of the ductus seboglandularis of acne‐involved and non‐involved skin showed very intense melanocortin‐1 receptor expression in contrast to less intense scattered immunoreactivity in normal skin samples. These data suggest that melanocortin‐1 receptor is involved in the pathogenesis of acne.