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학술저널
저자정보
김정은 (순천향대학교) 김혜란 (한림대학교 강남성심병원 피부과) 강석영 (한림대학교 강남 세브란스 병원 피부과) 정민재 (한림대학교 의과대학 강남성심병원 피부과학교실) 허남훈 (순천향대학교 천안병원 임상시험센터) 이현주 (순천향대학교) 류애리 (순천향대학교) 김혜원 (한림대학교) 박천욱 (한림대학교) 정보영 (한림대학교)
저널정보
대한피부과학회 Annals of Dermatology Annals of Dermatology 제33권 제2호
발행연도
2021.1
수록면
138 - 146 (9page)

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Background: The aryl hydrocarbon receptor (AHR) and autophagy are both important to maintain skin homeostasis. However, they are also involved in skin disorders. So far, their roles in psoriasis pathogenesis are unknown. Objective: We studied the immunohistochemical and gene expression of AHR, CYP1A1, and microtubule-associated protein light chain 3 (LC3) in lesional skin of psoriasis patients to determine correlations among them. Methods: We included 24 psoriasis patients and ten healthy volunteers. Skin biopsies were collected. AHR, CYP1A1, and LC3 protein expression was examined by immunohistochemistry, immunofluorescence, and western blotting. AHR, CYP1A1, LC3, ATG5, BECN1 and Nrf2 mRNA levels were measured by quantitative polymerase chain reaction. Results: AHR and CYP1A1 protein expression were higher in psoriasis lesional skin than in normal skin. LC3 protein expression was lower in psoriasis lesions than in normal controls. AHR and CYP1A1 protein expression in psoriasis lesions showed significant positive correlations with mean epidermal thickness and inflammatory cell density. Significant negative correlations were noted between LC3 protein expression in psoriasis lesions and the mean epidermal thickness or inflammatory cell density. A significant negative correlation was found between AHR and LC3 expression in psoriatic skin. AHR, CYP1A1 and Nrf2 mRNA expression were upregulated while LC3, ATG5, and BECN1 mRNA were down-regulated, in psoriatic lesional skin compared with normal controls. Conclusion: AHR and autophagy could play a role in psoriasis pathogenesis by modifying epidermal hyperproliferation and inflammation. AHR and autophagy regulation are potential therapeutic targets in chronic inflammatory skin diseases.

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