| Project/Area Number |
25861488
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Kyoto University |
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Principal Investigator |
MOGAMI Haruta 京都大学, 医学(系)研究科(研究院), 助教 (40378766)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
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| Keywords | 早産 / 前期破水 / 胎児フィブロネクチン / 細胞外マトリックス / マトリックスメタロプロテナーゼ / プロスタグランジン / 羊膜 / 胎児ファイブロネクチン |
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| Outline of Final Research Achievements |
Fetal fibronectin (fFN) has been used as a marker of preterm birth. We have shown that fFN increased the synthesis of matrix metalloproteinases, which degraded collagens, in primary amnion mesenchymal cells, or the production of prostaglandin E2, which leaded to the ripening of cervix or uterine contraction. These results indicate that fFN is a pathogenic factor in preterm rupture of membrane (PROM) and preterm birth.
In this study, we showed that extra domain A (EDA) is the functional exon in fFN, which activated toll-like receptor-4 (TLR4) in amnion mesenchymal cells. Moreover, intrauterine injection of EDA in pregnant mice caused preterm birth in vivo. We clarified the one of mechanisms how fFN caused PROM and preterm birth.
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