Skin regeneration -Signal transduction in hair follicles-
Project/Area Number |
20591345
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Osaka University |
Principal Investigator |
ITAMI Satoshi Osaka University, 大学院・医学系研究科, 寄附講座教授 (30136791)
|
Co-Investigator(Kenkyū-buntansha) |
INUI Shigeki 大阪大学, 大学院・医学系研究科, 寄附講座准教授 (30324750)
|
Project Period (FY) |
2008 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | 毛包 / 幹細胞 / LRIG1 / 再生 / ARA55 / hic-5 / ケロイド / 線維芽細胞 / TGF-β-Smad / ARA55/hic-5 / 男性ホルモン |
Research Abstract |
Lrig1 expressing keratinocytes localize the hair follicle junctional zone. Loss of Lrig1 causes a selective increase in β-catenin-induced ectopic hair follicle formation in the interfollicular epidermis. Lrig1 expressing keratinocytes constitutively shed LRIG1 ectodomains in vitro by ADAM17, and the ectodomains regulate cell proliferation and EGF signaling in a paracrine manner. ARA55/hic-5 was strongly expressed in keloid tissues and fibroblasts. ARA55/hic-5 overexpression stimulated the collagen production through TGF-β-Smad pathway.
|
Report
(4 results)
Research Products
(41 results)