| Project/Area Number |
13671733
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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 | Oita University (2004)
大分医科大学 (2001-2003) |
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Principal Investigator |
MIYAKAWA Isao Oita Univ., Dept.of Obstet. & Gynecol., Professor, 医学部, 教授 (70040607)
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| Co-Investigator(Kenkyū-buntansha) |
KAWANO Yasushi Oita Univ., Dept.of Obstet. & Gynecol., Instructor, 医学部, 助手 (40274758)
FUKUDA Junichiro Oita Univ., Dept.of Obstet. & Gynecol., Instructor, 医学部, 助手 (20381048)
嶺 真一郎 大分大学, 医学部, 助手 (00336273)
西田 欣広 大分医科大学, 医学部, 助手 (10336274)
高井 教行 大分医科大学, 医学部, 助手 (50295185)
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| Project Period (FY) |
2001 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 2003: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥2,000,000 (Direct Cost: ¥2,000,000)
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| Keywords | Vascular endothelial growth factor / Endometrial stromal cells / Amniotic cells / 血管新生 |
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| Research Abstract |
Our objective was to clarify the physiological role of vascular endothelial growth factor(VEGF) by endometrial stromal cells(ESC) and amnion-derived(WISH) cells. ESC were cultured, and VEGF production was increased by epidermal growth factor(EGF) and was decreased by interferon(IFN)-γ in a dose-dependent manner. VEGF production and VEGF mRNA expression were also increased by medroxyprogesterone(MPA) and cyclic AMP during in vitro decidualization. IP-10 production and IP-10 mRNA expression were increased by interleukin-1β or tumor necrosis factor-α.
WISH cells were cultured, and VEGF production was increased by EGF or insulin-like growth factor(IGF)-1 in a dose-dependent manner. The activation of MAP kinase and akt, which is phosphorylated by PI 3-kinase, were detected by western blot analysis. VEGF production was significantly decreased following pretreatment with MEK inhibitor(U0126) or PI 3-kinase inhibitor(wortmannin), and then treated with EGF or IGF-1.
It is suggested that VEGF may contribute to the neovascularization and proliferation of the uterine endometrium, placenta and gestational tissue.
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