Transcriptional regulation of nerve repulsion factors in normal epidermal keratinocytes: implication of application to intractable itch in atopic dermatitis
| Project/Area Number |
26860387
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Pain science
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| Research Institution | Juntendo University |
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Principal Investigator |
Negi Osamu 順天堂大学, 医学部, 准教授 (40648531)
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| Research Collaborator |
KAMATA Yayoi 順天堂大学, 大学院医学研究科, 非常勤助教 (00410035)
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| Project Period (FY) |
2014-04-01 – 2016-03-31
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| Project Status |
Completed (Fiscal Year 2015)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | 神経反発因子 / かゆみ / 表皮角化細胞 / 遺伝子発現調節 / ケラチノサイト / 皮膚バリア機能 / アトピー性皮膚炎 / 発現調節 |
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| Outline of Final Research Achievements |
In this study, we evaluated the ability of RORα to induce endogenous Sema3A in normal human epidermal keratinocytes (NHEKs). This study found that the endogenous RORα agonist cholesterol sulfate and RORα/γ agonist SR1078 dose-dependently upregulated Sema3A expression. However, RORα/γ inverse agonist SR1001 dose-dependently inhibited Sema3A expression in cultured NHEKs. In contrast, the RORα inverse agonist ursolic acid had no effect on Sema3A expression in the NHEKs. Taken together, these findings suggest that an RORα agonist may be useful as a topical antipruritic treatment of skin diseases with peripheral itch sensitization involving epidermal hyperinnervation, such as AD, by inducing endogenous Sema3A expression.
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Report
(3 results)
Research Products
(5 results)
