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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Alleviation of imiquimod-induced psoriasis-like symptoms in Rorメ-deficient mouse skin
Koog Chan Park1,2 (Research Professor), Jiwon Kim2 (Graduate student), Aram Lee1,2 (Post-doc), Jong-Seok Lim1,2 (Professor), Keun Il Kim 1,2,* (Professor)
1Research Institute of Women’s Health and 2Department of Biological Sciences, Sookmyung Women's University
Retinoic acid receptor-related orphan receptor メ (RORメ) plays a vital role in various physiological processes, including metabolism, cancer, circadian rhythm, cerebellar development, and inflammation. Although RORメ is expressed in the skin, its role in skin physiology remains poorly elucidated. Herein, Rorメ was expressed in the basal and suprabasal layers of the epidermis; however, keratinocyte-specific Rorメ deletion did not impact normal epidermal formation. Under pathophysiological conditions, Rorメ-deficient mice exhibited alleviated psoriasis-like symptoms, including relatively intact epidermal stratification, reduced keratinocyte hyperproliferation, and low-level expression of inflammatory cytokines in keratinocytes. Unexpectedly, the splenic population of Th17 cells was significantly lower in keratinocyte-specific RORメ deficient mice than in the control. Additionally, Rorメ-deficiency reduced imiquimod-induced activation of nuclear factor-リB and STAT3 in keratinocytes. Therefore, we expect that RORメ inhibitors act on immune cells and keratinocytes to suppress the onset and progression of psoriasis.
Abstract, Accepted Manuscript(in press) [Submitted on October 24, 2022, Accepted on January 25, 2023]
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