| Project/Area Number |
03670777
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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 | Nagoya University |
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Principal Investigator |
KURAUCHI Osamu Nagoya University Obstetrics Gynecology Lecturer, 医学部, 講師 (80195528)
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| Co-Investigator(Kenkyū-buntansha) |
MIZUTANI Shigehiko Nagoya University Obstetrics Gynecology associate professor, 医学部, 助教授 (00159162)
TANAKA Masashi Nagoya University Biomedical Chemistry associate professor, 医学部, 助教授 (60155166)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | placenta / overterm / IUGR / mitochondria gene / accumulation of mutation / cytochrome oxidase / DNA copy / promotor / 子定日超過 / 子宮内胎児発育遅延 / チトクロ-ムオキシダ-ゼ / DNAコピ- / プロモ-タ- |
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| Research Abstract |
To elucidate possible relation between mitchondrial gene expression and placental dysfunction, we excamined the expression of CoL and its activity as well as mitochondrial DNA (mtDNA) mutation and copy number in human placentas from appropriate for gestational age (AGA), Intrauterine growth retardation, and preeclamptic pregnancies.
1)No mutant mtDNA with the 4977-bp deletion could not be found in all of the placenta.
2)The gene expression and enzyme activity of CoL were decreased in the placenta of IUGR and preeclamptic pregnancy.
3)Although the levels of mtDNA were gradually decreased with gestation, they were not different between AGA placenta and that of IUGR or preclamptic pregnancy. The present results suggested that the mitchondria of IUGR or preclamptic placenta showed the low expression of its gene which might cause a falure of cell energy production.
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