| Project/Area Number |
26670732
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Meiji University (2015-2016)
National Research Institute for Child Health and Development (2014) |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
MIYADO Kenji (国)国立成育医療研究センター, 細胞医療研究部, 室長 (60324844)
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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 |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
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: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 生殖免疫 / 子宮内殺精子因子 / 補体 / 精漿タンパク質 / 子宮内細菌 / 体内受精の免疫 / 性周期 |
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| Outline of Final Research Achievements |
At the beginning of this research, steroid hormones were expected to define the sperm survival in female uterus; however, any sperm-killing inducible steroid hormone was not detected in the uterine fluid. The shotgun analysis of the uterine fluid by using LC/MS revealed that complement C3 existed with extremely high concentration if the fluid showed spermicide. C3 was highly expressed in the uterus if the mouse was in estrus period; but C3 was neither in diestrus period nor after injection of hCG. From ovariectomized mice, the secretion of C3 in the uterus was under controlled by estradiol. Both immuno-depletion of C3 and heat inactivation (56°C for 30 min) of the uterine secretion decreased the sperm killing effect. A mass of complement C3 in the uterus was easy to detect by western blotting; but the incubation with sperm could not activate uterine C3. The sperm killing mechanism in uterus continues to be investigated.
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