| Project/Area Number |
13470348
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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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 | Kanazawa University |
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Principal Investigator |
SHOZU Makio Kanazawa University, Hospital, Center for perinatal and reproductive health, associate professor, 医学部附属病院, 助教授 (30226302)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Masaki Kanazawa University, Graduate School of Obstetrics and Gynecology, professor, 医学系研究科, 教授 (10127186)
MURAKAMI Koichi Kanazawa University, Hospital, Center for perinatal and reproductive health, assistant professor, 医学部附属病院, 助手 (20242555)
瀬川 智也 金沢大学, 医学部附属病院, 助手 (40301197)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥8,600,000 (Direct Cost: ¥8,600,000)
Fiscal Year 2003: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2002: ¥3,000,000 (Direct Cost: ¥3,000,000)
Fiscal Year 2001: ¥2,900,000 (Direct Cost: ¥2,900,000)
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| Keywords | aromatase / granulosa cells / steroidogenic factor-1 / IL-β / estrogen / ovulation / 子宮内膜症 / IL=1β |
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| Research Abstract |
Aromatization of androgens, catalyzed by aromatase P450, is essential for estrogen biosynthesis, hetero for folliculogenesis. Here we investigated the transcriptional regulation of aromatase in granulosa cells and identify both steroidogenic factor-1 and LRH-1 as important regulatory factors binding to the nuclear half site of proximal promoter PII of aromatase. Both transcriptional factors were expressed in granulosa cell of healthy growing follicles and luteal cells. COV432, a cell lines established from a human granulosa cell, express exclusively LRH-1 and granulosa cells in growing follicle expressed much LRH-1 than SF-l. Granulosa luteal cells expressed much LRH-1, while theca luteal cells almost exclusively expressed SF-1. Co-expression of SF-1 or LRH-1 stimulated the expression of promoter vectors containing various lengths of PII sequences. We also investigated mechanism of IL-lb- and GnRH agonsit- induced induction of aromatase in endometriosis-derived stromal cells. IL-lb increased aromatase expression through COX2-dependent and COX2-independent mechanisms. GnRH agonists transiently stimulated aromatase expression through the activation of PKC. IGF-1 and BMP also stimulated aromatase expression in the presence of FSH.
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