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LDL-Proteoglycans Complex as a fatty strek site in atherosclerosis.

LDL-Proteoglycans Complex as a fatty strek site in atherosclerosis.
低密度脂蛋白-蛋白聚糖复合物作为动脉粥样硬化中的脂肪运动部位。
批准号:
09670741
负责人:
HAMADA Masanori
金额:
$2.05万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
1997
资助国家:
日本
项目状态:
已结题
起止时间:
1997 至 1998

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中文摘要
翻译
目标:已经报告了一种低密度脂蛋白(LDL)生产的不相容复合体,该复合体与单硫代糖氨基葡萄糖(GAGs)。复合体也具有高亲和力与钙结合蛋白命名的osteopontin(OPN)。我们报告说,GAGs在大鼠中的实验性高血压模型中增加了。这个实验的主要目标是调查如何与LDL产生不稳定的GAGs-LDL复合物,以便在动脉粥样硬化部位以及OPN如何由血管紧张素II控制。设计和方法:一个96孔的微量滴定板被覆盖,有一定的LDL数量。生物素-结合蛋白质蛋白质蛋白酶(PrG)的有限数量允许在孵化期应用不同种类的GAGs或脂蛋白蛋白的竞争中绑定到每个涂层井。由生物碱磷酸酶-阿维丁法估计的光谱测量上保留的生物素-缀合的PrG的数量。OPN由文化媒介在文化中生产 ... more 用单克隆抗体对OPN进行Western blotting,结果:Lp(a)和非常低的密度脂蛋白(VLDL)显示出具有高亲和力的促性腺素-PrG低于LDL和高密度脂蛋白(HDL),但不显著。肝素显示出与氯代素-PrG的亲和力明显高于高硫代酸、肝素磺酸和氯代素硫酸盐。Divalent Cations(钙、镁或锰)在这种体外模型中具有不稳定的GAGS-低密度脂蛋白复合体是很重要的。Angiotensin II increased OPN protein in the medium in accordance with the concentrations between 10-D2 - 11-D2 - 7-D2 M。萨拉-阿拉-血管紧张素II没有。Angiotensin II receptor blockade supressed OPN increase produced by angiotensin II的concentration of 10-D2 - 5的D2M.Conclusions:Our results showed that GAGS and divalent cations are essential for LDL to remain in the atherosclerotic lesion。高血压可能有助于通过增强肾上腺素硫酸盐在有氧媒体中产生复合物。血管紧张素II可能增强羟基磷灰石形成在高毒性药理学方面。Less(低)
英文摘要
Objective : It has been reported that low density lipoprotein(LDL) produce insoluble complex with mono-sulfated glycosamino-glycans(GAGs). The complex also has a high affinity with calcium binding proteins namely osteopontin(OPN). We reported that the GAGs are increased in the aorta of experimental models of hypertension in rat. The main aim of this experiment was to investigate how the increased GAGs react with LDL to make insoluble GAGs-LDL complex at the site of atheroscleritic lesion and how the OPN is controled by angiotensin II.Design and Methods : 96-well microtiteation plate was coated with a certain amount of LDL. A limiting quantity of biotin-conjugated proteoglycans(PrG) is allowed to bind to each coated well in competition with different kind of GAGs or lipoproteins applied during incubation period. The amount of biotin-conjugated PrG retained on well was estimated spectrophotometrically by alkaline phosphatase-avidin method. The OPN produced in the culture medium by cultur … More ed vascular smooth muscle cells are measured by Western blotting with monoclonal antibody to OPN.Results : Lp(a) and very low density lipoprotein (VLDL) showed higher affinity with chondroitin-PrG than LDL and high density lipoprotein(HDL) but not significantly. Heparin showed significantly higher affinity with chondroitin-PrG than hiarulonic acid, heparan sulfate and chondroitin sulfate. Divalent cations(calcium, magnesium or manganese) were important to obtain insoluble GAGs-LDL complex in this in vitro model. Angiotensin II increased OPN protein in the medium in accordance with the concentrations between 10ィイD2-11ィエD2M to 10ィイD2-7ィエD2M. Whereas Sar-Ala angiotensin II did not. Angiotensin II receptor blockade supressed OPN increase produced by angiotensin II completely at a concentration of 10ィイD2-5ィエD2M.Conclusions : Our results showed that GAGs and divalent cations are essential for LDL to remain in the atherosclerotic lesion. Hypertension might contribute to make the complex by enhance production of chondroitin sulfate in the aortic media. Angiotensin II might enhance hydroxyapatite formation in hypertensive atherosclerotic lesion. Less
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会议论文
S.Booka,M.Hamada: "Glycosaminoglycans enhmces lipid accumulation in hypertension" J.of Hypertension. 61s. 321 (1998)
S.Booka,M.Hamada:“糖胺聚糖增强高血压中的脂质积累”J.of Hypertension。
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Study on liquefaction and lateral flow countermeasure technique due to use of wood
  • 批准号:
    20246078
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
  • 资助金额:
    $28.45万
  • 财政年份:
    2008
  • 负责人:
    HAMADA Masanori
  • 依托单位:
A study on Earthquake Resistance of Foundations against the flow of Liquefied Grond
  • 批准号:
    17206049
  • 项目类别:
    Grant-in-Aid for Scientific Research (A)
  • 资助金额:
    $20.63万
  • 财政年份:
    2005
  • 负责人:
    HAMADA Masanori
  • 依托单位:
Study on Earthquake Resistance of Infrastructures against Fault-Induced Ground Surfece Ruptures
Development of Assessment System for Liquefaction-Induced Ground Flow and Its Caused Damage to Lifeline
  • 批准号:
    13555135
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 资助金额:
    $6.66万
  • 财政年份:
    2001
  • 负责人:
    HAMADA Masanori
  • 依托单位:
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海外基金
胞外多糖分子在心脏发育过程中对关键信号通路的调节作用