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- W4285992564 abstract "One of the most common skin diseases is atopic dermatitis (AD), a chronic inflammation featuring skin barrier dysfunction and immune dysregulation. Previously, we reported that the nuclear orphan nuclear receptor RORα was highly expressed in the epidermis of human skin and positively regulated the expression of skin barrier-related genes, including filaggrin, in human keratinocytes. In contrast, RORα was downregulated in AD lesions. We then aimed to evaluate the in vivo function of RORα in regulating AD pathogenesis, using the newly generated mice with epidermis-specific Rora knockout (RoraΔepi) and an AD mouse model induced by MC903. We observed that the MC903-triggered ear thickening was greatly accelerated and enhanced in RoraΔepi mice compared to their wild-type littermates. On day 11, RoraΔepi mice displayed severe AD symptoms, including scaling, excoriation, and the histological features of epidermal hyperplasia and heavy dermal infiltrations (of eosinophils, neutrophils, and macrophages). In addition, we found the earlier AD onset in RoraΔepi mice to be associated with a marked reduction of keratin 10 and filaggrin expression in the epidermis and not a higher production of TSLP, the key cytokine for AD initiation in this model. These results substantiate the importance of epidermal RORα in suppressing AD development and that it functions at least in part through regulating keratinocyte differentiation and skin barrier function. Further mechanistic studies should help uncover the potential of RORα as a novel therapeutic target for AD and other diseases related to skin barrier dysfunction." @default.
- W4285992564 created "2022-07-21" @default.
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- W4285992564 date "2022-08-01" @default.
- W4285992564 modified "2023-09-25" @default.
- W4285992564 title "042 Epidermal loss of RORα accelerates skin inflammation in a mouse model of atopic dermatitis" @default.
- W4285992564 doi "https://doi.org/10.1016/j.jid.2022.05.096" @default.
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