| Project/Area Number |
62440068
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| Research Category |
Grant-in-Aid for General Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MIZUNO Masahiko Dept. of Otolaryngology, University of Tokyo Professor., 医学部(病)・産婦人科, 教授 (10010175)
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| Co-Investigator(Kenkyū-buntansha) |
RYO Yoshimitsu Dept. of Otolaryngology, University of Tokyo Assistant., 医学部(病)・産婦人科, 助手 (20220808)
ISHIHARA Satoko Dept. of Otolaryngology, University of Tokyo Assistant., 医学部(病)・産婦人科, 助手 (30201320)
YANO Tetsu Dept. of Otolaryngology, University of Tokyo Assistant., 医学部(病)・産婦人科, 助手 (50182390)
TSUTSUMI Osamu Dept. of Otolaryngology, University of Tokyo Assistant., 医学部(病)・産婦人科, 助手 (60134574)
TAKETANI Yuji Dept. of Otolaryngology, University of Tokyo Associate Professor., 医学部(病)・産婦人科, 助教授 (10114539)
久具 宏司 東京大学, 医学部, 助手 (20177976)
綾部 琢哉 東京大学, 医学部, 助手 (50184247)
桑原 慶紀 東京大学, 医学部, 助教授 (20010324)
石川 弘子 東京大学, 医学部・産婦人科, 助手 (50191870)
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| Project Period (FY) |
1987 – 1989
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| Project Status |
Completed (Fiscal Year 1989)
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| Budget Amount *help |
¥23,100,000 (Direct Cost: ¥23,100,000)
Fiscal Year 1989: ¥4,100,000 (Direct Cost: ¥4,100,000)
Fiscal Year 1988: ¥10,000,000 (Direct Cost: ¥10,000,000)
Fiscal Year 1987: ¥9,000,000 (Direct Cost: ¥9,000,000)
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| Keywords | epidermal growth factor / human endometrium / growth and differentiation of human endometrium / follicular maturation / egg maturation / endometriosis / infertility / interleukin 1 / prostaglandin E_2 / aromatase / progesterone / EGF / 顆粒膜細胞 / インターロイキン1 / アロマターゼ / 子宮内膜 / グリコーゲン / (1)EGF / (2)EGF受容体 / (3)子宮内膜 / (4)グリコーゲン / (5)顆粒膜細胞 / (6)卵成熟 |
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| Research Abstract |
Endometrial tissues undergo drastic changes during menstrual cycle. After menstruation, they proliferate and differentiate into cells with secretory activity in the preparation for egg implantation. Although sex steroids play an important role in the development of endometrial tissues, sequential events occurring in the endometrium can not be fully explained. In this study, we offer evidences that epidermal growth factor(EGF) is released from human endometrial cells and they possess the receptors for EGF. Further. EGF is shown to elicit a variety of biological actions in human endometrial cells. For instance, EGF enhances both glycogenesis and glycogenolysis, thus increasing the supply of glucose for blastocysts. We further set forth that EGF augments the capacity of progestin binding and release of prostaglandin E_2 in endometrial cells. As for the mode of action of EGF, EGF is found to phosphorylate 170 KD potein immediately after binding the cells. These findings emphasize that EGF
… More
may participate in the development of human endometrial tissues in concert with sex steroids, thus contributing to the acquisition of receptivity of eggs in the endometrium.
EGF-like immunoreactivity was detected in human follicular fluid, activity of which increased along with the follicular maturation. EGF is shown to stimulate the proliferation of rat granulosa cells in the presence of insulin. FSH does not affect the mitogenic action of EGF. Granulosa cells possess two kinds of EGF receptors. The addition of PSH, estradiol and testosterone resulted in an increase in the amount of EGF binding to granulosa cells. EGF stimulates the release of both progesterone and prostaglandins from cultured follicles. These stimulatory effects of EGF is synergized with phosphodiesterase inhibitor. EGF is found to induce egg maturation by increasing the activity of phosphofructokinase, a key enzyme of glucose metabolism. Hence, suggestion is made that EGF as a local factor, may be involved in the follicular development, ovulation and oocyte maturation by modulating actions of gonadotropin.
Estadiol alone has no growth-promoting effect on both endometrial and endometriotic cells. EGF stimulates cell growth of both cell types. Endometrial cells but hot endometriotic cells produce and release EGP into culture media so that stimulatory effect of exogenously added EGF is blunted in endometrial cells. Estradiol exerts its mitogenic action by enhancing the mitogenic action of EGF in endometrium. By contrast, the effect of estradiol is minimal in endometriotic cells, pointing to less dependency on estradiol for their proliferation. Progesterone inhibits cell growth of both call types in the same manner. Less
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