| Project/Area Number |
26462493
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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 | Ehime University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
松原 裕子 愛媛大学, 医学部附属病院, 講師 (60403820)
那波 明宏 名古屋大学, 医学系研究科, 特任教授 (90242859)
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| Research Collaborator |
Yamamoto Sawa
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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 |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2015: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2014: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | 妊娠高血圧症候群 / 血管内皮 / 絨毛細胞 / 高血圧 / HMGA1 / トロホブラスト / マウス |
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| Outline of Final Research Achievements |
On the third day after the implantation, trophoblastic cells were aggregated around the embryo and HMGA1 was observed in the cytoplasm as well as the nuclei derived from the preeclampsia model mouse. A part of HMGA1 was also released out of the cells by the implantation site. Furthermore, HMGA1 was transported into the cytoplasm from the nuclei in the human preeclamptic placenta. We demonstrated that DCA could stimulate the transportation of HMGA1 from nuclei to cytoplasm. In culture system, DCA decreased the proliferation and invasive capacity of extravillous trophoblast. In normal pregnancy, extravillous trophoblasts could invade into maternal decidua and uterine myometrium resulted in increased utero-maternal circulation to maintain the pregnancy. However, it is known that the effects were reduced in preeclampsia. Extra nuclear transport of HMGA1 is involved in the pathogenesis of preeclampsia through inhibiting extravillous trophoblasts invasion.
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