| Project/Area Number |
14370526
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
ASO Takeshi Tokyo Medical and Dental University, Graduate School, Comprehensive Reproductive Medicine, Professor, 大学院・医歯学総合研究科, 教授 (60093176)
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| Co-Investigator(Kenkyū-buntansha) |
KUBOTA Toshiro Tokyo Medical and Dental University, Associate Professor, 大学院・医歯学総合研究科, 助教授 (50126223)
HARADA Tatsuya Tokyo Medical and Dental University, Assistant Professor, 大学院・医歯学総合研究科, 助手 (80376748)
TERAUCHI Masakazu Tokyo Medical and Dental University, Assistant Professor, 大学院・医歯学総合研究科, 助手 (90361708)
己斐 秀樹 東京医科歯科大学, 大学院・医歯学総合研究科, 助手 (20280969)
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| Project Period (FY) |
2002 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥12,200,000 (Direct Cost: ¥12,200,000)
Fiscal Year 2005: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2004: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2003: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2002: ¥10,400,000 (Direct Cost: ¥10,400,000)
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| Keywords | cytotrophoblast / decidua / virus vector / fetomaternal interface / gene therapy / 子宮内膜間質細胞 / MMP-1 / androgen / testosterone / 絨毛栄養膜細胞 / polyamine pathway / arginase / eNOS / 胎盤 / EVT / prothrombinase / FGL2 / HCMV / MHC class I / VT / ナチュラルキラー細胞 |
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| Research Abstract |
The aim of this study is to elucidate the molecular biological mechanism of implantation and to acquire the comprehensive knowledge about the gene therapy on fetomaternal interface by virus vector
1. We have elucidated the biological mechanism of implantation, mainly in the control of invasion of extravillous trophoblast and decidua. We have described protease activated receptor (PAR)1, PAR2, and PAR3 protein distribution in the developing human placenta and implicated PAR1 and PAR2 activation in functions central to EVT invasion.
2. We have elucidated the mechanisms of viral infection (adenovirus, coxackievirus, herpes simplex virus, human cytomegalovirus) in fetomaternal interface. We have reported that differentiated EVT prepared from human first-trimester chorionic villi persistently express class I MHC molecules upon HCMV infection. Furthermore, we have reported that differentiation of cytotrophoblasts into syncytiotrophoblasts may be associated with the L-arginine metabolic pathway through modulation of L-arginine availability as a substrate for nitric oxide synthase and arginase
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