2016 Fiscal Year Final Research Report
The injury and repair system in trophoblast cells through potease-activated receptor and signal transduction.
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 |
Section | 一般 |
Research Field |
Obstetrics and gynecology
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Research Institution | Hamamatsu University School of Medicine |
Principal Investigator |
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Project Period (FY) |
2014-04-01 – 2017-03-31
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Keywords | PAR-2 / sFLT1 / trophoblast / preeclampsia |
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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Free Research Field |
産科学
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