Regulatory mechanism of hair follicle stem cell quiescence by cell polariry protein aPKC

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K09755
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Dermatology
• Research Institution: Akita University
• Principal Investigator: OSADA Shin-Ichi 秋田大学, 医学(系)研究科(研究院), 准教授 (00244484)
• Co-Investigator(Kenkyū-buntansha): 能登 舞 秋田大学, 医学部, 助教 (10738462)
• Co-Investigator(Renkei-kenkyūsha): HIROSE Tomonori 横浜市立大学, 大学院医学系研究科, 講師 (10142027)
• Research Collaborator: SUZUKI Tomoko ; KAGAYA Masami
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 細胞極性 / プロテインキナーゼC / aPKC / 創傷治癒 / 毛包幹細胞 / 毛包新生 / 細胞移動 / Wnt経路

Outline of Final Research Achievements

The isoforms of atypical protein kinase C (aPKC), aPKCζ and aPKCλ, regulate cell polarity and are expressed in the epidermis. Here, we addressed whether aPKCs are implicated in two major processes for maintaining epidermal homeostasis: cutaneous wound healing and wound-induced hair follicle neogenesis (WIHN). In epidermis-specific aPKCλ-knockout mice, wound healing was significantly retarded and WIHN was upregulated concomitantly with an increase in Wnt signaling. Conversely, wound healing and WIHN in aPKCζ-null mice were comparable to those in control littermates. These results represent the first evidence that aPKCλ, but not aPKCζ, is a key molecule linking cutaneous wound healing and WIHN.

Free Research Field

皮膚科学