| Project/Area Number |
26462483
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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 |
Obstetrics and gynecology
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| Research Institution | Hamamatsu University School of Medicine |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
鳴本 敬一郎 浜松医科大学, 医学部, 特任助教 (90647603)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | PAR-2 / sFLT1 / trophoblast / preeclampsia / 絨毛外絨毛細胞 / 胎児発育不全 / 妊娠高血圧症候群 / 炎症性サイトカイン / trophoblast cells / PAR / invasion |
|---|
| Outline of Final Research Achievements |
Fetal growth restriction (FGR) is one of the causes of cerebral palsy. Previous research on the pathophysiology of FGR has suggested that the maternal hypercoagulability- systemic inflammatory cytokinemia is one of the key players in the placentation in the early phase of pregnancy. This disturbed process of placentation could lead to the placental dysfunction in FGR. However, it has remained unclear how the hypercoagulability- systemic inflammatory cytokinemia- inflammation network modulates the early placentation. In this project, we have shown that the down-regulation of PAR (protease-activated receptor)-2 expression in both TCL-1 cells and HTR-8/SVneo cells (placenta-derived immortalized human trophoblast) is TNF-alpha dependent. The data presented in the reports may indicate that,in early phase of placentation, the suppressed expression of PAR-2 by inflammatory cytokine,plays roles in pathogenesis of dysfunctional placentation leading to preeclampsia.
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