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Sebocytes differentially express and secrete adipokines.

Exp Dermatol. 2015 Oct 17;

Authors: Kovács D, Lovászi M, Póliska S, Oláh A, Bíró T, Veres I, Zouboulis CC, Ståhle M, Rühl R, Remenyik É, Törőcsik D

Abstract
In addition to producing sebum, sebocytes link lipid metabolism with inflammation at a cellular level and hence, greatly resemble adipocytes. However, so far no analysis was performed to identify and characterize the adipocyte-associated inflammatory proteins, the members of the adipokine family in sebocytes. Therefore, we determined the expression profile of adipokines (adiponectin, interleukin [IL] 6, resistin, leptin, serpin E1, visfatin, apelin, chemerin, retinol-binding protein 4 [RBP4] and monocyte chemoattractant protein 1 [MCP1]) in sebaceous glands of healthy and various disease-affected (acne, rosacea, melanoma and psoriasis) skin samples. Sebaceous glands in all examined samples expressed adiponectin, IL6, resistin, leptin, serpin E1 and visfatin, but not apelin, chemerin, RBP4 and MCP1. Confirming the presence of the detected adipokines in the human SZ95 sebaceous gland cell line we further characterized their expression and secretion patterns under different stimuli mimicking bacterial invasion (by using Toll-like receptor [TLR] 2 and 4 activators), or by 13-cis retinoic acid (13CRA; also known as isotretinoin), a key anti-acne agent. With the exception of resistin, the expression of all of the detected adipokines (adiponectin, IL6, leptin, serpin E1 and visfatin) could be further regulated at the level of gene expression, showing a close correlation with the secreted protein levels. Besides providing further evidence on similarities between adipocytes and sebocytes, our results strongly suggest that sebocytes are not simply targets of inflammation but may exhibit initiatory and modulatory roles in the inflammatory processes of the skin through the expression and secretion of adipokines. This article is protected by copyright. All rights reserved.

PMID: 26476096 [PubMed - as supplied by publisher]

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