Cathelicidin LL-37 induces semaphorin 3A expression in human epidermal keratinocytes: implications for possible application to pruritus

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860898
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Dermatology
• Research Institution: Juntendo University
• Principal Investigator: Kamata Yayoi 順天堂大学, 医学(系)研究科(研究院), 非常勤助教 (00410035)
• 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)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 神経反発因子 / 抗菌ペプチド / アトピー性皮膚炎

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.

Free Research Field

皮膚科学