| Project/Area Number |
01570930
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Department of obstetrics & Gynecology, Osaka University Medical School. |
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Principal Investigator |
TAKAGI Tetsu (1990) Osaka Univ. Med. School, Assistant prof., 医学部, 助手 (10150343)
亀田 隆 (1989) 大阪大学, 医学部, 助手 (70204641)
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| Co-Investigator(Kenkyū-buntansha) |
KOYAMA Masayasu Osaka Univ Med. School Assitant pof, 医学部, 助手 (00183351)
SAJI Fumitaka Osaka Univ Med School Locture, 医学部, 講師 (90093418)
MATSUZAKI Noboru Osaka Univ Med. School Assistant Prof., 医学部, 助手 (30199781)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1990: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1989: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Interleukin-6 / Interleukin-6 receptor / Human chorionic gonadotropin / Trophoblast / placenta / 絨毛性ゴナドトロピン刺激ホルモン / ヒト繊毛性ゴナドトロピン(hCG) / 繊毛細胞 / 繊毛性ゴナドトロピン刺激ホルモン / ヒト胎盤 / インタ-ロイキン6 |
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| Research Abstract |
We have already reported that placenta produces interleukin-6 (IL-6) constitutively during pregnancy. With this research grant support, we could find that trophoblast-derived IL-6 acts as an important factor in the regulation of placental hormonal functions, especially the regulation of human chorionic gonadotropin (hCG) release. We collected normal human chorionic tissue and prepared a single suspension of trophoblasts after the enzyme digestion. The trophoblasts released hCG in response to recombinant IL-6 (rIL-6) in a time- and dose-dependent manner. To examine whether the hCG release was dependent on IL-6 receptor (IL-6-R), we pre-treated trophoblasts with anti-IL-6-R monoclonal antibody, PM1. Trophoblast treated with PM1 failed to release hCG even after a large amount of rIL-6. The failure of hCG release was not due to PM1's cytotoxic effect on trophoblasts. GnRH is another molecule which has activity to release hCG through GnRH receptor (-R). To examine whether GnRH stimulated hCG release dependently of IL-6, we pre-treated trophoblasts with PM1 and then stimulated trophoblasts. Trophoblasts released hCG regardless of the presence or absence of PM1, suggesting that GnRH and GnRH-R system acts on trophoblasts independently of IL-6 and IL-6-R system.
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