| Project/Area Number |
14571574
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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 | Sapporo Medical University |
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Principal Investigator |
ENDO Toshiaki Sapporo Medical University, School of Medicine, Associate Professor, 医学部, 助教授 (90213595)
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| Co-Investigator(Kenkyū-buntansha) |
CHIBA Hideki Sapporo Medical University, School of Medicine, Assistant Professor, 医学部, 講師 (00295346)
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| Project Period (FY) |
2002 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥4,000,000 (Direct Cost: ¥4,000,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2002: ¥2,500,000 (Direct Cost: ¥2,500,000)
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| Keywords | corous Luteum / ovarian hyperstimulation syndrome / vascular permeability / vascular endothelial growth factor / tight junction / claudin-5 / occludin / 血管新生 |
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| Research Abstract |
Vascular endothelial growth factor(VEGF) is well known to stimulate both the growth of endothelium and vascular permeability. VEGF expression in the ovary is also reported to increase during normal luteal formation. In this study we investigated the mechanisms of the occurrence of ovarian hyperstimulation syndrome(OHSS).
The expression of VEGE and VEGF receptors(R) was extremely stimulated in the ovaries of OHSS rat models compared with corpora lutea of pseudopregnant rats. Vascular permeability examined with Evans blue was markedly increased in the ovaries of OHSS rats. Gonadotropin releasing hormone agonist(GnRHa) treatment blocked the increase of VEGF-VEGFR expression and vascular permeability of the ovaries of OHSS rats.
Tight junction proteins of endothelium are reported to play a pivotal role in vascular permeability. As there are known to be several sorts of tight junction proteins, we checked the expression of such proteins in the ovaries of OHSS rats.
Claudin-5 and occludin protein were significantly decreased in the ovaries OHSS rats. However, GnRHa treatment blocked the decrease in both proteins. Moreover, we clinically experienced that the continuation at GnRHa prevented the occurrence of OHSS during in vitro fertilization and embryo transfer.
In summary, the decreased expression of claudin-5 and occludin caused by excess expression of VEGF-VEGFR was speculated to change from normal luteal formation into the occurrence of OHSS.
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