| Project/Area Number |
12671590
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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 |
Obstetrics and gynecology
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| Research Institution | Hamamatsu University, School of Medicine |
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Principal Investigator |
SUGIMURA Motoi associate Professor, 医学部附属病院, 助教授 (30273189)
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| Co-Investigator(Kenkyū-buntansha) |
KANAYAMA Naohiro Professor, 医学部, 教授 (70204550)
KOBAYASHI Takao associate Professor, 医学部, 助教授 (20107808)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,400,000 (Direct Cost: ¥2,400,000)
Fiscal Year 2002: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | macrophage / MIF / phosphatidylserin / antisense MIF adenovirus / protein C / intrauterine growth restriction model in mice / 胎盤内凝固 / 胎盤マクロファージ / 子宮内胎児発育遅延 / recombinant adenovirus / macrophage / IUGR |
|---|
| Research Abstract |
In this research project, in order to establish the research tool for the investigation of function of macrophage in placenta, we established phosphatidylserin (PS)-induced intrauterine growth restriction (IUGR) mice model first. Then, we developed the recombinant adenovirus vector bearing sense and antisense macrophage migration inhibitory factor cDNA.
In the PS-induced IUGR model, exogenous anticoagulants, annexin V, activated protein C and heparin inhibited significantly the growth restriction in mice model, indicating that the model is associated with the hypercoagulable state by PS.Furthermore, in the BCG-lipopolysaccharide (LPS) induced liver failure model in mice, recombinant adenovirus vector bearing antisense macrophage migration inhibitory factor (MIF) cDNA suppressed significantly the damage in liver tissue suggesting that antisense MIF adenovirus vector modulates the BCG-LPS-induced inflammatory process through cytokine network in liver tissue.
We established the system for the analysis of macrophage functions by using recombinant virus vectors bearing sense and antisense MIF in animal model.
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