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Involvement of the corticotropin‐releasing hormone system in the pathogenesis of acne vulgaris
Author(s) -
Ganceviciene R.,
Graziene V.,
Fimmel S.,
Zouboulis C.C.
Publication year - 2009
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1111/j.1365-2133.2008.08959.x
Subject(s) - acne , pathogenesis , medicine , hormone , corticotropin releasing hormone , dermatology , endocrinology
Summary Background  The sebaceous gland exhibits an independent peripheral endocrine function and expresses receptors for neuropeptides. Previous reports have confirmed the presence of a complete corticotropin‐releasing hormone (CRH) system in human sebocytes in vitro . The capability of hypothalamic CRH to induce lipid synthesis, induce steroidogenesis and interact with testosterone and growth hormone implicates a possibility of its involvement in the clinical development of acne. Objectives  The purpose of the study was to detect expression changes of CRH/CRH binding protein (CRHBP)/CRH receptors (CRHRs) in acne‐involved skin, especially in the sebaceous glands. Methods  Expression of CRH/CRHBP/CRHRs was analysed by immunohistochemistry in biopsies from facial skin of 33 patients with acne, noninvolved thigh skin of the same patients and normal skin of eight age‐matched healthy volunteers. Results  Very strong positive reaction for CRH was observed in acne‐involved skin in all types of sebaceous gland cells, irrespective of their differentiation stage, whereas in noninvolved and normal skin sebaceous glands exhibited a weaker CRH staining depending upon the differentiation stage of sebocytes. The strongest reaction for CRHBP in acne‐involved sebaceous glands was in differentiating sebocytes. CRHR‐1 and CRHR‐2 exhibited the strongest expression in sweat glands and sebaceous glands, respectively. Conclusions  Expression of the complete CRH system is abundant in acne‐involved skin, especially in the sebaceous glands, possibly activating pathways which affect immune and inflammatory processes leading to the development and stress‐induced exacerbation of acne.

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