Imiquimod-induced skin inflammation is relieved by knockdown of sodium channel Nax

Jingling Zhao, Ping Xie, Robert D. Galiano, Shaohai Qi, Renxiang Mao, Thomas A. Mustoe*, Seok Jong Hong

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

6 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)576-584
Number of pages9
JournalExperimental Dermatology
Issue number5
StatePublished - May 2019


  • Na
  • RNAi
  • S100A9
  • psoriasis
  • skin inflammation

ASJC Scopus subject areas

  • Dermatology
  • Molecular Biology
  • Biochemistry


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