Project/Area Number |
18591245
|
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, Graduate School of Medicine, Endowed Chair Professor (30136791)
|
Co-Investigator(Kenkyū-buntansha) |
INUI Shigeki Osaka Univetsty, Graduate School of Medicine, Endowed Chair Associate Professor (30324750)
|
Project Period (FY) |
2006 – 2007
|
Project Status |
Completed (Fiscal Year 2007)
|
Budget Amount *help |
¥3,950,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2007: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2006: ¥2,000,000 (Direct Cost: ¥2,000,000)
|
Keywords | leptin / STAT3 / keratinocvte / dermal papilla cell / Hair cycle / androgen / Hic-5 / ARA55 |
Research Abstract |
One of the typical examples of the signal transduction in the human hair cycle progression is androgen-androgen receptor system. We developed an in vitro coculture system using DPC and follicular epithelial cells. Androgen-inducible TGF-β1 derived from DPCs plays a central role for the growth suppression. Ketoconazol inhibited androgen induced androgen receptor transactivity, and showed clinical improvement of androgenetic alopecia. We also found that androgen receptor co-activator Hic5/ARA55 regulate the androgen sensitivity in dermal papilla cells. Stat3 plays a crucial role in transducing a signal for the anagen initiation and wound healing. The anagen initiation represents vertical wound healing. Leptin strongly activates stat3 in the keratinocytes and promoted growth of keratinocytes. Db/Db mice showed the retardation of second anagen initiation, and leptin injection promoted anagen entry in Ob/Ob and normal mice. Leptin would be a potential therapeutic approach for the treatment of alopecia.
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