1997 Fiscal Year Final Research Report Summary
Common hormones and mechanisms of luteal regression, ovulation and follicular atresia.
| Project/Area Number |
08671909
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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 | Sapporo Medical University |
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Principal Investigator |
ENDO Toshiaki School of Medicine, Department of Obstetrics and Gynecology, assistant professor, 医学部, 講師 (90213595)
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| Project Period (FY) |
1996 – 1997
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| Keywords | Luteal regression / Ovulation / Follicular atresia / GnRH / Apoptosis / Growth hormone / Matrix metalloproteinase |
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| Research Abstract |
We investigated common hormones and mechanisms of luteal regression, ovulation and follicular atresia. We previously reported that prolactin (PRL) treatment following bromocryptine (Brom) treatment to superovulated rats caused structural luteolysis, and that this treatment stimulated matrix metalloproteinase activity in involuted corpus luteum and caused apoptosis.
We designed to investigate whether other hormones except PRL may cause structural luteolysis in rats, and also investigated about mechanisms of luteal regression in human. We got some exellent data as below.
Growth hormone treatment following Brom treatment caused structural luteolysis by MMP activation and apoptosis. Gonadotropin releasing hormone agonist (GnRHa) treatment from day 5 through day 9 after hCG injection also caused structural luteolysis in rats. Gelatin zymography, Northem blot analysis revealed that GnRHa treatment stimulated MMP-2, MT-MMP activity.
Extracts of human corpus luteum of late luteal phase had much more activities of MMP-2, MT1-MMP than those of other stages. Tissue inhibitor of metalloproteinse (TIMP)-1 expression of corpus luteum decreased at late luteal phase. However, TIMP-2 expression slightly increased at late luteal phase compared with other stages. It is possible that MT1-MMP activates pro-MMP-2 under the existence of TIMP-2 as previously reported in other kinds of cells.
It became clear that luteal regression, ovulation and follicular atresia have same kinds of mechanisms as mentioned above.
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