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Keratinocyte-derived IL-36 gamma plays a role in hydroquinone-induced chemical leukoderma through inhibition of melanogenesis in human epidermal melanocytes

Authors
Pyo, Jeong JooAhn, SungjinJin, Sun HeeAn, SeungchanLee, EunyoungChoi, JungminShin, Jeayoung C.Choi, HyunjungKim, Hyoung-JuneChoi, DalwoongNoh, Minsoo
Issue Date
8월-2019
Publisher
SPRINGER HEIDELBERG
Keywords
Chemical leukoderma; Hydroquinone; Human epidermal keratinocytes (HEKs); IL-36 gamma; Anti-melanogenic activity
Citation
ARCHIVES OF TOXICOLOGY, v.93, no.8, pp.2307 - 2320
Indexed
SCIE
SCOPUS
Journal Title
ARCHIVES OF TOXICOLOGY
Volume
93
Number
8
Start Page
2307
End Page
2320
URI
https://scholar.korea.ac.kr/handle/2021.sw.korea/63685
DOI
10.1007/s00204-019-02506-6
ISSN
0340-5761
Abstract
Chemical leukoderma is an acquired type of vitiligo that can be initiated by various exogenous chemicals such as hydroquinone (HQ), rhododendrol (RD), or 4-tertiary butyl phenol (4-TBP). Despite the importance of epidermal keratinocytes in diverse dermatological conditions, their toxicological role in chemical leukoderma is poorly understood. To elucidate their role in the pathogenesis of chemical leukoderma, genome-scale transcriptional analysis was performed in human epidermal keratinocytes (HEKs) treated with a sub-cytotoxic HQ concentration (10 mu M). The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway-based functional enrichment analysis of HQ-induced differentially expressed genes (DEGs) revealed that HQ significantly upregulated DEGs related to the IL-17 signaling pathway and significantly downregulated DEGs associated with melanogenesis in HEKs. The meta-analysis between the HQ-induced and cytokine-induced transcriptional data (GSE53751) showed that 58 DEGs were commonly upregulated between HQ- and IL-17A-treated HEKs. Notably, the expression of IL36G was significantly increased in HEKs in response to both HQ and IL-17A. IL-36 gamma (2 mu g/ml) directly inhibits melanin biosynthesis in cultured human epidermal melanocytes (HEMs) and downregulates the gene transcription of key enzymes in the melanogenesis pathway including TYR, DCT, and TYRP1. Moreover, IL-36 gamma autocrinally regulated keratinocyte function to produce the proinflammatory cytokines IL-36 gamma, IL-6, and CXCL8/IL-8 in a concentration-dependent manner, suggesting that IL-36 gamma may stimulate the amplification cycle of cutaneous inflammation. In this regard, hydroquinone-induced IL-36 gamma from human keratinocytes plays a pivotal role in the development of chemical leukoderma by autocrinally or paracrinally modulating the crosstalk between keratinocytes and melanocytes.
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