1999 Fiscal Year Final Research Report Summary
Mechanism of action of androgen in human hair follicles
| Project/Area Number |
10670787
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Dermatology
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| Research Institution | Osaka University |
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Principal Investigator |
ITAMI Satoshi Osaka University Graduate School of Medicine, Associate professor, 医学系研究科, 助教授 (30136791)
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| Co-Investigator(Kenkyū-buntansha) |
TADOKORO Taketsugu Osaka University Graduatel School of Medicine, Assistant Professor, 医学系研究科, 助手 (60264339)
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| Project Period (FY) |
1998 – 1999
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| Keywords | Hair cycle / Dermal papilla cells / Androgen / 5α-reductase / Androgen receptor / 17β-HSD / Growth factor / STAT3 |
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| Research Abstract |
One of the typical example of the signal transduction in the cell is androgen-androgen receptor system. Androgen receptor, ligand dependent transcription factor, is apparently involved in hair cycle control in hunman. Beard and axillary dermal papilla cells (DPC) strongly expressed androgen receptor mRNA. While the expression of type I 5α-reductase is ubiquitous property of DPC, type II 5α-reductase gene expression is limited to beard DPC. Type II 17β-hydroxysteroid dehydrogenas (HSD) mRNA was strongly expressed in outer root sheath cells, while DPCs except for male axillary hair expressed no type II 17β-HSD mRNA. In contrast, type III 17β-HSD mRNA was strongly expressed in beard DPCs and axillary DPCs from both sexes, ORSCs showed a low level of expression.
Expression of type III 17β-HSD mRNA was not regulated by androgen in DPCs. These results suggest that the sensitivity of hairs to androgen is partially controlled by the site specific expression of AR, 5α-reductase and 17β-HSD in DPCs.
EGF receptor signaling has been found to play an important role in catagen induction by the experiments of transgenic mouse models. Stat3 is a down stream signaling molecule of cytokines, growth factors including EGF and HGF. Conditional gene targeting of Stat3 in mice showed severely compromised hair cycle and wound healing processes. Growth factor-dependent in vitro migration of the Stat3-disrupted keratinocytes was impaired despite normal proliferative responses. Stat3 plays a crucial role in skin remodeling, that is, anagen induction and wound healing.
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