2014 Fiscal Year Final Research Report
Progesterone receptor signaling contributing to parturition and preterm labor
| Project/Area Number |
25870150
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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 |
Developmental biology
Obstetrics and gynecology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Keywords | 黄体ホルモン / プロゲステロン受容体 / 分娩 / 早産 / mTOR / マウスモデル |
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| Outline of Final Research Achievements |
More than 15 million babies are born preterm each year. A better understanding of prematurity is necessary to prevent it effectively. This study revealed that a mild inflammation induced by LPS absolutely causes preterm birth and neonatal deaths in the uterine p53-deleted mouse model, which naturally exhibits approximately 50% incidence of spontaneous preterm delivery due to cellular senescence and prostaglandin induction in the uterus, and these impairments of parturition are markedly rescued by the combination treatment with an mTOR inhibitor rapamycin and progesterone. Our findings suggest that the combined treatment with low doses of rapamycin and progesterone help to reduce the incidence of preterm birth in its high-risk women.
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| Free Research Field |
産婦人科学、周産期医学、生殖医学、生殖生物学
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