| Project/Area Number |
24592490
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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 | Nippon Medical School |
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Principal Investigator |
AKIRA Shigeo 日本医科大学, 医学部, 教授 (40231849)
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| Co-Investigator(Kenkyū-buntansha) |
NEMOTO Takahiro 日本医科大学, 医学部, 准教授 (40366654)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2014: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 子宮内膜症 / ウロコルチン２ / 病態生理 / 発現調節 / 診断ツール |
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| Outline of Final Research Achievements |
To determine the physiological significance of Urocortin2 (Ucn2) in the regulatory mechanisms of endometriosis, we examined the expression of Ucn2 mRNA in rat uterus and the tissue of endometrial cyst, and measured Ucn2 concentration in plasma and peritoneal fluid from patients with and without endometriosis by EIA.
Ucn2 like immunoreactivity was detected in the endometrial gland epithelial cells of the rat uterus. The expression level of Ucn2 mRNA was reduced by estradiol. Human Ucn2 mRNA was detected in the tissue of endometrialcyst.Plasma Ucn2 levels were not statistically different between patients of stage Ⅰ, Ⅲ endometriosis and myoma uteri. By contrast, Ucn2 concentrations in the peritoneal fluid of stage Ⅲ endometriosis were significantly elevated compared to stage Ⅰendometriosis and myoma uteri.
Thus, Ucn2 may play a role in the regulatory mechanisms of proliferation of endometriosis.
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