Investigation on cell specific mechanism in the tube-like differentiation in extra-villous trophoblast
Project/Area Number |
20591301
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Embryonic/Neonatal medicine
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Research Institution | Kyushu University |
Principal Investigator |
FUKUSHIMA Kotaro Kyushu University, 大学病院, 講師 (40304779)
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Co-Investigator(Kenkyū-buntansha) |
月森 清巳 九州大学, 大学病院, 講師 (90253450)
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Project Period (FY) |
2008 – 2010
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Project Status |
Completed (Fiscal Year 2010)
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Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2008: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
|
Keywords | 絨毛細胞 / 血管内皮様分化 / 低酸素 / 活性酸素種 / 酸化ストレス / 妊娠高血圧症候群 / 胎盤 / 絨毛細胞分化 / 分化 / アポトーシス / HIF1A |
Research Abstract |
We investigated on cell specific mechanism in the tube-like differentiation in extra-villous trophoblast. As a result, the gene expression profile in EVT during tube formation is very different from that of endothelial cells despite these cells presented morphological change. HIF1A has a crucial role in regulating EVT behavior including matrigel-induced endovascular differentiation under normoxic condition. On the contrary, ROS produced by XO in hypoxia-reperfusion induced apoptosis and affected invasion ability and differentiation in EVT. M directly injures the placental syncytiotrophoblast in PIH patients and that elevated UA in PIH patients, at least partly, indicates placental damage induced by ROS. Moreover, the role and significance of ROS injury in the placenta may differ between early-onset and late-onset type PIH.
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Report
(4 results)
Research Products
(24 results)
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[Presentation]2008
Author(s)
福嶋恒太郎, ほか
Organizer
第16回 日本胎盤学会
Place of Presentation
浜松市
Year and Date
2008-11-13
Related Report
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