2005 Fiscal Year Final Research Report Summary
Analysis of pathomechanism of androgenetic alopecia by investigating TGF-β1 promoter
| Project/Area Number |
16591098
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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 |
INUI Shigeki Osaka University, Graduate School of Medicine, Assistant, 医学系研究科, 助手 (30324750)
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| Co-Investigator(Kenkyū-buntansha) |
ITAMI Satoshi Osaka University, Graduate School of Medicine, Associate Professor, 医学系研究科, 助教授 (30136791)
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| Project Period (FY) |
2004 – 2005
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| Keywords | androgen receptor / androgenetic alopecia / TGF-β1 promoter / dermal papilla cell / reporter plasmid / AP-1 |
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| Research Abstract |
We reported that TGF-β1 is up-regulated by androgen in dermal papilla cells (DPCs) from androgenetic alopecia (AGA) using our coculture system of DPCs transiently transfected with androgen receptor (AR) expression vector and keratinocytes (KCs). This finding suggested that the regulation of TGF-β1 by androgen is a key step in the pathogenesis of AGA. To examine the possible regulatory mechanism of TGF-β1 gene expression by androgen, we analysed TGF-β1 promoter activity of the pTGF-β1-Luc vector, which was constructed by connecting the 5' upstream region of the TGF-β1 gene (-1362 bp upstream from the transcription start site) to the luciferase reporter gene. When pTGF-β1-Luc and AR expression vector were cotransfected in DPCs from AGA, R1881 increased luciferase activity to around 10-fold. In contrast, this induction did not occur in CV-1 cells and transformed DPCs. Thus the regulation of promoter activity by androgen may be cell-specific. From analysis of deleted pTGF-β1-Luc vector using DPCs from AGA, there are two possible regulatory regions (-1131〜-731 and -459〜 -323) and two negative regulatory regions (-1326〜-1127 and -735〜-459). We found two AP-1 binding sites in the region at -459〜-323. Using the reporter vector containing the mutation at these two AP-1 sites, we found that these sites are involved in the suppression of TGF-β1 promoter and that AR can release this suppression.
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[Book] 脱毛症のすべて2006
Author(s)
乾 重樹
Total Pages
17-21
Publisher
全日本病院出版会
Description
「研究成果報告書概要(和文)」より
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[Book] Alopecia2006
Author(s)
Inui S
Total Pages
17-21
Publisher
MB Derma
Description
「研究成果報告書概要(欧文)」より
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