Bombesin receptor-activated protein homolog deficiency altered the pattern of pathological changes of psoriasis - like skin lesion in mice.

Autor:	Zheng J; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.; Department of pathology, The Second Xiangya Hospital, Central South University, China., Wang H; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Wang J; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Peng Z; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Yao X; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.; Functional Center, School of Basic Medical Sciences, Xinjiang Medical University, China., Weber HC; Boston University School of Medicine, Section of Gastroenterology, and Department of Pathology and Laboratory Medicine, Boston, MA 02118, USA., Qin X; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Xiang Y; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Liu C; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Ji M; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Liu H; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China., Qu X; Department of physiology, School of Basic Medical Science, Central South University, Changsha 410008, Hunan, China.
Jazyk:	angličtina
Zdroj:	International journal of medical sciences [Int J Med Sci] 2024 Jan 01; Vol. 21 (2), pp. 357-368. Date of Electronic Publication: 2024 Jan 01 (Print Publication: 2024).
DOI:	10.7150/ijms.89492
Abstrakt:	This study investigated the potential role of the mouse homolog of bombesin receptor-activated protein (BRAP) in imiquimod (IMQ) induced psoriasis - like skin inflammation. The expression of both human BRAP, encoded by C6orf89 , and its mouse homolog, encoded by BC004004 , has been found to be expressed abundantly in the keratinocytes. BC004004 knockout mice ( BC004004 -/- ) were topically treated with IMQ daily for 7 days to test whether they were more vulnerable to psoriasis - like inflammation. We found that those mice exhibited an altered pattern of inflammation process compared to isogenic wild type control mice ( BC004004 +/+ ). BC004004 -/- mice developed skin lesions with earlier and more acute onset, as well as a quicker remission. The cytokines related to pathogenesis of psoriasis also exhibited different expression patterns in IMQ treated BC004004 -/- mice. On day 4 of IMQ treatment, BC004004 -/- mice exhibited a higher expression level of IL-17A compared to BC004004 +/+ mice, suggesting a more robust activation of Th17 cells in the knockout mice. The serum level of thymic stromal lymphopoietin (TSLP), one of the keratinocyte derived cytokines, was also increased in BC004004 -/- mice and reached its peak on day 4. Knockdown of BRAP in cultured human keratinocyte-derived HaCaT cells by siRNA silencing led to increased release of TSLP. Our data suggest that the elevated of level of TSLP released from keratinocytes due to BRAP deficiency might mediate the crosstalk between the epidermal cells and immune cells and thereby contributing to the altered pathological changes observed in psoriasis - like skin lesion in knockout mice. Competing Interests: Competing Interests: The authors have declared that no competing interest exists. (© The author(s).)
Databáze:	MEDLINE
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