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
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2017: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
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 / 休眠機構 / 脱毛 |
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.
|