| Project/Area Number |
23591596
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Kyushu University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ASANOMA Kazuo 九州大学, 大学病院, 助教 (30380413)
FUJITA Yasuyuki 九州大学, 大学病院, 助教 (20398077)
MOROKUMA Seiichi 九州大学, 学内共同利用施設等, 研究員 (50380639)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
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| Keywords | Trophoblast / 妊娠高血圧症候群 / 胎盤 / 活性酸素種 / 絨毛細胞 |
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| Research Abstract |
This study was aim to clarify the biological influence of reactive oxygen species (ROS) produced by XO on extravillous trophoblast (EVT) cell and investigate possible role of the EVT function ion the pathogenesis of preeclampsia. X/XO decreased the cell growth by H2O2 produciton, increased the urate level and the apoptotic cell ratio significantly. The Pre-HT group had a significantly lower mean birth weight and a larger negative deviation from the standard birth weight. The DBP elevation after 32 weeks of gestation was a risk factor for SGA. After 28-30 weeks, there was a statistically significant difference in the incidence of PIH. In conclusion, ROS produced by XO induced apoptosis and affected EVT function including invasion and differentiation. Our clinical data from a recent population database in Japan could strengthen epidemiologic evidence that trophoblast invasion is related to the pathogenesis of PIH.
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