| Project/Area Number |
07670001
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | Yamagata University |
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Principal Investigator |
WATANABE Hiroshi Yamagata Univ.Sch.of Med., Professor, 医学部, 教授 (80004662)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 1996: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1995: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | mouse ovary / atretic follicle / apoptosis / macrophage / gap junction / gonadtrophin / hyper-ovulation / connexin / 微細構造 / 卵胞上皮細胞 / アクチン |
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| Research Abstract |
The purpose of this study was to elucidate the functional role of gap junctions (GJs) on the apoptotic cell death of follicular epithelium. Atretic mechanism was also investigated morphologically in the mouse ovarian follicles. The results obtained in this study are as follows.
1.GJs increased the number and size as the follicular maturation proceed. Then, the number and size rapidly decreased just before the ovulation. This was due to internalization of GJ membranes within the granulosa cell cytoplasm. The present study has failed to clarify the subcellular distribution and the transport process of GJ-proteins, connexin (Cxs). This may be due to low density of Cxs within cell organelles such as RER and Golgi apparatus.
2.At initial stage of apoptosis, GJs were phagocytosed by the neighboring normal cell. Consequently, these two cells were separated by each other. This may suggests that the apoptotic signal will be transmitted from the apoptotic cell to normal cell through GJs.
3.In the nuclei of apoptotic granulosa cells and neutrophils, thick bundles of actin filaments were frequently found. Such a structure is closely related with morphological alteration of nucleus and cellular configuration.
4.In the premature mice, apoptotic granulosa cells began to appear frequently at 3W old, and uncreased in incidence at 4W old mice. The apoptotic granulosa cells were phagocytosed by neighboring normal cells. Such a phagocytotic activity of granulosa cells seems to regulate the follicular atresia in the mouse ovary. The present study suggests that the macrophage will not be involved in the follicular atresia at least in the mouse ovary.
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