| Project/Area Number |
06671693
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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 | Nihon University |
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Principal Investigator |
SAKAMOTO Hideki NIHON UNIVERSITY MEDICAL SCHOOL OBSTETRICS AND GYNECOLOGY ASSISTANT PROFESSOR, 医学部, 講師 (80158922)
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| Co-Investigator(Kenkyū-buntansha) |
FURUYA Kiyohide NIHON UNIVERSITY MEDICAL SCHOOL OBSTETRICS AND GYNECOLOGY ASSISTANT PROFESSOR, 医学部, 講師 (00096893)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1995: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1994: ¥1,400,000 (Direct Cost: ¥1,400,000)
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| Keywords | preeclampsia / HUVEC / apoptosis / 臍帯血管内皮 / アポトーシス |
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| Research Abstract |
The goal of the research was to test a hypothesis that the intrauterine growth retardation (IUGR) in toxemia of pregnancy is due at least in part to umbilical endothelial failure. We used serum from preeclamptic patients, mild pregnancy induced hypertensive patients and normal pregnant patients. The serum was added to HUVEC in vitro and production of prostaglandins (PG) was studied by RIA.The results showed that serum from preeclamptic patients with IUGR showed significant stimulation on 6-keto-PGF1alpha and PGE2 production from HUVEC.Immunohistochemical study of cyclooxygenase (COX) showed increased expression of the enzyme after the serum challenge. No such effects were observed when serum of mild pregnancy induced hypertensive patients or normal pregnant patients was used. Western blot analysis and RT-PCR analysis of COX sub-type (COX I,II) showed they were both increased in transcription after preeclamptic serum challenge. These changes were reproduced by adding IL8 in the culture media which caused increased apoptosis in HUVEC.
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