Regulatory mechanisms of inflammasome-mediated placental inflammation by alpha1-antitrypsin
| Project/Area Number |
15K10694
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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 | Tokyo University of Pharmacy and Life Science |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
YOSHIE Mikihiro 東京薬科大学, 薬学部, 講師 (50434014)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Project Status |
Completed (Fiscal Year 2017)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 胎盤絨毛 / インフラマソーム / α1-アンチトリプシン / HTRA1 / 栄養膜細胞 / 脱落膜 / 子宮内膜 / 合胞体栄養膜細胞 / 絨毛外栄養膜細胞 / IL-1β / ダメージ関連分子パターン / 病原体関連分子パターン |
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| Outline of Final Research Achievements |
We provide evidence that the NLRP3 inflammasome pathway contributes to IL-1beta secretion in trophoblasts and that glibenclamide partially blocks this pathway. NLRP3 may be involved in placental inflammation such as infection-associated pregnancy complication. A1AT is highly expressed in decidual tissues rather than syncytiotrophoblasts, whereas HTRA1 expression is expressed in syncytiotrophoblasts and extravillous trophoblasts (EVT). Functional interaction between decidual A1AT and trophoblastic HTRA1 may regulate trophoblast invasion. Imbalance of both molecules activities might be involved in the progression of HDP, supporting the notion the possible role of A1AT and HTRA1 at the maternal-fetal interface.
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Report
(4 results)
Research Products
(15 results)
