| Project/Area Number |
23592426
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Obstetrics and gynecology
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| Research Institution | Kansai Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
YASUDA Katsuhiko 関西医科大学, 医学部, 准教授 (90174507)
OKADA Hidetaka 関西医科大学, 医学部, 准教授 (80330182)
NAKAJIMA Tatsuya 関西医科大学, 医学部, 講師 (70288827)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2011: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | 生殖医学 / 子宮内膜 / 血管新生因子 / 低酸素 |
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| Research Abstract |
The aim of this study is to investigate the effects of hypoxic stress on the regulation of vascular endothelial growth factor (VEGF) and stromal cell-derived factor-1 (SDF-1), and the potential role of hypoxia-inducible factor-1 (HIF-1) in the endometrium. Hypoxia simultaneously induced expression of mRNA and production of VEGF and attenuated the expression and production of SDF-1 in a time-dependent manner. With regard to the interaction of estradiol and hypoxia, estradiol did not affect the regulation of VEGF under hypoxic conditions. Echinomycin, a small-molecule inhibitor of HIF-1 activity, inhibited hypoxia-induced VEGF production. Hypoxia simultaneously acts to increase VEGF via HIF-1. These results indicate a potential mechanism for the action of hypoxic conditions that could influence angiogenesis in the human endometrium.
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