| Project/Area Number |
18591803
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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 | Ehime University |
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Principal Investigator |
MATSUBARA Keiichi Ehime University, University Hospital, Associate Professor (80263937)
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| Co-Investigator(Kenkyū-buntansha) |
ABE Emiko Ehime University, Graduate School of Medicine, Assistant Professor (70363223)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥3,410,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥210,000)
Fiscal Year 2007: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2006: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | hypertension / cell-tissue / embryogenesis / preeclampsia |
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| Research Abstract |
Female NOD/SCID mice were sublethally irradiated and GFP-transgenic bone marrow-derived cells were transplanted. GFP-positive (bone marrow derived) cells were closely aggregated around the embryo in the uterine endometrial decidua early in pregnancy. In the 3rd weeks of gestation, GFP-positive cells formed capillary tubes like vessels in the placenta. Bone marrow derived cells could be involved in the placental neovascularization.
Secondly, male GFP-transgenic mice and female NOD/SCID mice were mated. In the 2nd weeks of gestation, GFP-positive (fetus origin) cells existed in the kidney. Since GFP-positive cells differentiated into renal tubular epithelium the fetal cells may be at work as stem cell in the maternal kidney. Usually, maternal renal cells express angiotensin receptor subtype 1 (AT 1) dominantly ; however, fetal cells in maternal kidney expressed subtype2 (AT2). Fetal cells in maternal blood could not only differentiate partly into maternal organ but also be involved in the maternal physiology via the crosstalk between AT1 and AT2.
Circulating EPCs in female human peripheral blood was increased from proliferative phase through luteal phase and decreased with the course of pregnancy. The number of circulating EPCs was not changed in preeclampsia ; however, EPCs' proliferation derived from preeclamptic patients was significantly increased compared with normal pregnant women after a week culture. We also demonstrated that VEGF stimulated EPCs' mobilization and sFlt-1, which is increased in the peripheral blood in preeclampsia, inhibited the effect using live imaging system. Given the above-mentioned results circulating EPCs' mobilization could be inhibited by increased some serum factors (sFlt-1, etc) in preeclampsia.
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