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机制研究 WW0X 在 NF-kB 诱导的银屑病皮肤炎症中的作用。

Mechanistic Investigation of WWOX Function in NF-kB-Induced Skin Inflammation in Psoriasis.

机构信息

Department of Dermatology, College of Medicine, Soonchunhyang University Cheonan Hospital, Cheonan 31151, Republic of Korea.

Department of Dermatology, Soonchunhyang University Graduate School of Medicine, Asan 31538, Republic of Korea.

出版信息

Int J Mol Sci. 2023 Dec 21;25(1):167. doi: 10.3390/ijms25010167.

DOI:10.3390/ijms25010167
PMID:38203337
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC10779412/
Abstract

Psoriasis is a chronic inflammatory skin disease characterized by epidermal hyperproliferation, aberrant differentiation of keratinocytes, and dysregulated immune responses. WW domain-containing oxidoreductase (WWOX) is a non-classical tumor suppressor gene that regulates multiple cellular processes, including proliferation, apoptosis, and migration. This study aimed to explore the possible role of WWOX in the pathogenesis of psoriasis. Immunohistochemical analysis showed that the expression of WWOX was increased in epidermal keratinocytes of both human psoriatic lesions and imiquimod-induced mice psoriatic model. Immortalized human epidermal keratinocytes were transduced with a recombinant adenovirus expressing microRNA specific for WWOX to downregulate its expression. Inflammatory responses were detected using Western blotting, real-time quantitative reverse transcription polymerase chain reaction (PCR), and enzyme-linked immunosorbent assay. In human epidermal keratinocytes, WWOX knockdown reduced nuclear factor-kappa B signaling and levels of proinflammatory cytokines induced by polyinosinic: polycytidylic acid [(poly(I:C)] in vitro. Furthermore, calcium chelator and protein kinase C (PKC) inhibitors significantly reduced poly(I:C)-induced inflammatory reactions. WWOX plays a role in the inflammatory reaction of epidermal keratinocytes by regulating calcium and PKC signaling. Targeting WWOX could be a novel therapeutic approach for psoriasis in the future.

摘要

银屑病是一种慢性炎症性皮肤病，其特征为表皮过度增殖、角质形成细胞分化异常以及免疫反应失调。WW 结构域包含氧化还原酶（WWOX）是一种非经典的肿瘤抑制基因，调节多种细胞过程，包括增殖、凋亡和迁移。本研究旨在探讨 WWOX 在银屑病发病机制中的可能作用。免疫组织化学分析显示，人银屑病皮损和咪喹莫特诱导的小鼠银屑病模型的表皮角质形成细胞中 WWOX 的表达增加。用表达 WWOX 特异性 microRNA 的重组腺病毒转导永生化人表皮角质形成细胞以下调其表达。使用 Western blot、实时定量逆转录聚合酶链反应（PCR）和酶联免疫吸附试验检测炎症反应。在人表皮角质形成细胞中，WWOX 敲低减少了核因子-κB 信号和多聚肌苷酸：多聚胞苷酸[（poly（I：C）]体外诱导的促炎细胞因子的水平。此外，钙螯合剂和蛋白激酶 C（PKC）抑制剂显著降低了 poly（I：C）诱导的炎症反应。WWOX 通过调节钙和 PKC 信号在表皮角质形成细胞的炎症反应中发挥作用。靶向 WWOX 可能是未来银屑病的一种新的治疗方法。

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