1999 Fiscal Year Final Research Report Summary
Cell death and luteinization of ovarian granulosa cells
| Project/Area Number |
10671521
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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 |
ASAKAI Rei Tokyo Med & Dent Univ, Med Res Inst, Res. assistant, 難治疾患研究所・機能調節疾患, 助手 (20167224)
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| Co-Investigator(Kenkyū-buntansha) |
YAMAGUCHI Tokio Tokyo Med & Dent Univ, Med Res Inst, Assistant professor, 難治疾患研究所, 助教授 (30134745)
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| Project Period (FY) |
1998 – 1999
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| Keywords | atresia / granulosa cells / death / prostaglandin / calcium ion / Fenton reaction |
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| Research Abstract |
Most of ovarian follicles during development undergo cell death (it is called atresia), and thus it is important to elucidate the underlying mechanism. To gain insights into atresia, a cultured granulosa cell system in the presence of follicle stimulating hormone (FSH) plus luteinizing hormone (LH) in defined medium has been newly established, mimicking three stages of differentiation, maturation, as evaluated by the ability of progesterone secretion, and finally necrotic cell death. Recombinant FSH alone was found to be sufficient for inducing the three stages, whereas in the absence of FSH such stage changes did not occurred. The cell death was inhibited by the cyclooxygenase inhibitor indomethacin and cyclooxygenase 2 was detected immuno-histochemically only prior to cell death. Moreover, prostaglandin E2 was able to induce cell death only when it was added at the maturation stage, suggesting the role of prostaglandin synthesis as a death trigger. Investigation of the dying process revealed that cell death was effectively blocked by nifedipine, an inhibitor for Ca2+ channels and by two iron ion chelators presumably through inhibition of the Fenton reaction. These data provide the first evidence that FSH-primed prostaglandin synthesis in the maturation stage may be responsible for granulosa cell death during the atresia at antral stages.
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