Cathelicidin LL-37 induces semaphorin 3A expression in human epidermal keratinocytes: implications for possible application to pruritus
| Project/Area Number |
26860898
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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 |
Dermatology
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| Research Institution | Juntendo University |
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Principal Investigator |
Kamata Yayoi 順天堂大学, 医学(系)研究科(研究院), 非常勤助教 (00410035)
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| Research Collaborator |
UMEHARA Yoshie 順天堂大学, 大学院医学研究科, 博士研究員 (40707072)
NIYONSABA Francois 順天堂大学, 国際教養学部, 先任准教授 (60365640)
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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 |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 神経反発因子 / 抗菌ペプチド / アトピー性皮膚炎 / かゆみ |
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| Outline of Final Research Achievements |
In this study, we investigated the effects of antimicrobial peptide LL-37 on nerve repulsion factor semaphorin 3A (Sema3A) expression in cultured normal human epidermal keratinocytes (NHEKs), as well as the signaling pathways involved in LL-37-induced Sema3A expression. We found that Sema3A expression in cultured NHEK was increased by stimulation with LL-37. LL-37-induced Sema3A expression was completely inhibited by pertussis toxin and PD98059. These results suggested that Gi-coupled GTP-binding protein coupled receptor and extracellular signal-regulated kinase (ERK) 1/2 signaling may be required for Sema3A induction.
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Report
(3 results)
Research Products
(20 results)
