| Project/Area Number |
11671599
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
KUBOTA Toshiro Tokyo Medical and Dental University, Associate Professor, 大学院・医歯学総合研究科, 助教授 (50126223)
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| Co-Investigator(Kenkyū-buntansha) |
ASO Takeshi Tokyo Medical and Dental University, Professor, 大学院・医歯学総合研究科, 教授 (60093176)
田口 誠 東京医科歯科大学, 大学院・医歯学総合研究科, 助手 (50251525)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2001: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2000: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1999: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | endothelin / nitric oxide / nitric oxide synthase / luteal function / granulosa cells / human endometrium / Northern blot analysis / Immunohistochemistry / ヒト妊娠初期脱落膜 / iNOS / NO合成酵素(NOS) / エストラジオール / プロゲステロン / 分子生物学的手法 |
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| Research Abstract |
The present study was undertaken to investigate the effects of endothelin (ET), that is the potent vasoconstrictive peptide, and nitric oxide (NO) that is the free radical gas believed to be endothelium-derived relaxing factor on the luteinization in granulosa cells (GC) and on the differentiation in human endometrial cells of the secretory phase in order to clarify the control mechanism of luteal function.
We have demonstrated that ET acts as a luteinization-inhibitor by attenuating key biosynthetic steps leading to progesterone production and induces the cell proliferation in GC, indicating the significant effects of luteal function as a local factor. NO/NOS suppresses the luteinization of GC in immature follicle, but the suppression decreases in the process of follicle maturation. NO also significantly suppressed the estradiol (E_2) release in basal and Gn-stimulated PGC. We also elucidate that the cooperative biological effects between the decrease in ET and the increase in endothelial NO synthase (NOS) contribute to the regulation of human uterine blood flow by causing dilatation of endometrial blood vessels, follwing to induce the differentiation in endometrial cells of secretory phase. These findings suggest that ET and NO/NOS may have a potential role in.the control of corpus luteum function.
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