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Imiquimod‐induced skin inflammation is relieved by knockdown of sodium channel Na x
Author(s) -
Zhao Jingling,
Xie Ping,
Galiano Robert D.,
Qi Shaohai,
Mao Renxiang,
Mustoe Thomas A.,
Hong Seok Jong
Publication year - 2019
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.13917
Subject(s) - imiquimod , inflammation , gene knockdown , dermatology , medicine , chemistry , pharmacology , biochemistry , apoptosis
Na x 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 Na x using RNA i 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 Na x ‐ RNA i. Excessive infiltration of inflammatory cells found in inflammatory lesions, such as mast cells, eosinophils, neutrophils, T cells and macrophages, was reduced by Na x ‐ RNA i. Expression of S100A9, which is a downstream gene of Na x and a mediator of inflammation, was decreased by Na x ‐ RNA i. Our results demonstrated that knockdown of Na x ameliorated IMQ ‐induced psoriasis‐like skin inflammation in vivo. Thus, targeting of Na x may represent a potential therapeutic option for the treatment of psoriasis.