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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 576-584 |
| Number of pages | 9 |
| Journal | Experimental Dermatology |
| Volume | 28 |
| Issue number | 5 |
| DOIs | |
| State | Published - May 2019 |
Funding
This study was supported by internal funding from the Division of Plastic and Reconstructive Surgery, Northwestern University, Feinberg School of Medicine. We thank Dr. Mimi Wu Young and Dr. David Dolivo for their critical review of the manuscript.
Keywords
- Na
- RNAi
- S100A9
- psoriasis
- skin inflammation
ASJC Scopus subject areas
- Dermatology
- Molecular Biology
- Biochemistry