Imiquimod‐induced skin inflammation is relieved by knockdown of sodium channel Nax. Issue 5 (14th May 2019)

• Record Type: Journal Article
• Authors: Zhao, Jingling; Xie, Ping; Galiano, Robert D.; Qi, Shaohai; Mao, Renxiang; Mustoe, Thomas A.; Hong, Seok Jong
• Is Part Of: Experimental dermatology. Volume 28:Issue 5(2019)
• Page Start: 576
• Page End: 584
• Publication Date: 2019-05-14
• Subjects: Nax -- psoriasis -- RNAi -- S100A9 -- skin inflammation; Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.13917
• Languages: English
• ISSNs: 0906-6705

Abstract

Abstract: Nax is an atypical sodium channel that mediates inflammatory pathways in pathological conditions of the skin. In this study, we developed a skin inflammation model in the rabbit ear through application of imiquimod (IMQ). Knockdown of Nax using RNAi attenuated IMQ‐induced skin inflammation, including skin erythema, scaling and papule formation. Histologic analysis showed that thickening and insufficient differentiation of the epidermis found in psoriasis‐like skin were normalized by administration of Nax ‐RNAi. Excessive infiltration of inflammatory cells found in inflammatory lesions, such as mast cells, eosinophils, neutrophils, T cells and macrophages, was reduced by Nax ‐RNAi. Expression of S100A9, which is a downstream gene of Nax and a mediator of inflammation, was decreased by Nax ‐RNAi. Our results demonstrated that knockdown of Nax ameliorated IMQ‐induced psoriasis‐like skin inflammation in vivo. Thus, targeting of Nax may represent a potential therapeutic option for the treatment of psoriasis.