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The production and regulation of angiogenic factor or anti-angiogenic factor by ovary and uterine endometrial tissues.

卵巢和子宫内膜组织血管生成因子或抗血管生成因子的产生和调节。

基本信息

批准号：
15591766
负责人：
KAWANO Yasushi
金额：
$ 2.3万
依托单位：
Oita University (2004-2006)大分医科大学 (2003)
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2003
资助国家：
日本
起止时间：
2003 至 2006
项目状态：
已结题

项目摘要

Our objective was to clarify the physiological role of angiogenic factor or anti-angiogenic factor by ovarian granulosa cell, endometrial stromal cells (ESC) and amnion-derived (WISH) cells.Several angiogenic factors were present in human follicular fluid. macrophage colony-stimulating factor, monocyte chemoattractait protein-1 and macrophage inflammatory protein-3 a were secreted by granulosa cells. These factors were up-regulared by interleukin-1 a and tumor necrosis factor-a by these cells.We reported that VEGF was produced by ESC. In adition thrombospondin (TSP)-1 production was increased by interferon (IFN)-γ and was decreased by epidermal growth factor (EGF) in a dose-dependent manner. TSP-1 production and TSP-1 mRNA expression were also increased by medroxyprogesterone (MPA) and cyclic AMP during in vitro decidualization..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 suggest ed that angiogenic factor may contribute to the neovascularization and proliferation of the ovary, uterine endometrium, and placenta.

本研究的目的是通过卵巢颗粒细胞、子宫内膜基质细胞（ESC）和卵巢上皮细胞源性细胞（WISH）研究血管生成因子或抗血管生成因子的生理作用。颗粒细胞分泌巨噬细胞集落刺激因子、单核细胞趋化蛋白-1和巨噬细胞炎性蛋白-3a。IL-1 α和TNF-α可上调这些因子的表达。此外，干扰素（IFN）-γ可增加血小板反应蛋白（TSP）-1的产生，表皮生长因子（EGF）可降低TSP-1的产生，并呈剂量依赖性。在体外蜕膜化过程中，甲羟孕酮（MPA）和环磷酸腺苷（cAMP）也可增加TSP-1的产生和TSP-1 mRNA的表达。培养WISH细胞，EGF或胰岛素样生长因子（IGF）-1以剂量依赖性方式增加VEGF的产生。Westernblot检测MAP激酶和PI 3-激酶磷酸化的akt的活化。用MEK抑制剂（U 0126）或PI 3激酶抑制剂（wortmannin）预处理后，再用EGF或IGF-1处理，VEGF的生成明显减少。提示血管生成因子可能参与了卵巢、子宫内膜和胎盘的新生血管和增殖。