Study on the mechanism of atherosclerotic lesion formation using cytokine-knockout mouse

细胞因子敲除小鼠研究动脉粥样硬化病变形成机制

基本信息

  • 批准号:
    13470517
  • 负责人:
  • 金额:
    $ 8.7万
  • 依托单位:
  • 依托单位国家:
    日本
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
  • 财政年份:
    2001
  • 资助国家:
    日本
  • 起止时间:
    2001 至 2003
  • 项目状态:
    已结题

项目摘要

1.In the study on the comparison of TNF-α^<-/-> apoE^<-/-> double KO mouse with apoE^<-/-> KO mice, the area of atherosclerotic lesion was significantly reduced in double KO mice. In addition, the expression of adhesion molecules such as ICAM-1and VCAM-1was also significantly suppressed in double KO mouse. These fidings suggest that augumented expression of adhesion molecules is, at least in part, involved in the atherosclerotic action of TNF-α.2.The atherosclerotic lesion was significantly reduced in IFN-γ^<-/-> apoE^<-/-> double KO mice compared with apoE^<-/-> KO mice and mRNA levels of ICAM-1 and VCAM-1 were significantly decreased in double KO mice. It is suggested that mononuclear cells including monocytes are recruited to arterial wall by IL-1β, resulting in the formation of atherosclerotic lesion.3.The atherosclerotic lesions of IFN-γ^<-/->BMT mice were larger than those of IFN-γ^<+/+>BMT mice at the aortic sinus, aortic arch and abdominal aorta. These findings show that IFN-γ produced by bone marrow-derived cells delays the progression of atherosclerosis without any effects on plasma lipids, and this suppression may be due to decreased extracellular matrix deposition.In this study, we clarified that TNF-α and IL-1β accelerate atherosclerosis via the augumented expression of adhesion molecules in vivo study. However, IFN-y derived from bone marrow rather suppressed atherosclerosis at least in the initial stage.
1.在TNF-α^<-/-> apoE^<-/->双基因敲除小鼠与apoE^<-/->敲除小鼠的比较研究中,双基因敲除小鼠的动脉粥样硬化病变面积明显减小。此外,双基因敲除小鼠细胞间粘附分子ICAM-1、VCAM-1的表达也明显受到抑制。2. IFN-γ^<-/-> apoE^<-/->双基因敲除小鼠的动脉粥样硬化病变较apoE ^<-/->敲除小鼠明显减轻,ICAM-1和VCAM-1的mRNA水平明显降低。提示IL-1β可募集单核细胞(包括单核细胞)至动脉壁,导致动脉粥样硬化病变的形成。3. IFN-γ^<-/->BMT小鼠的动脉粥样硬化病变在主动脉窦、主动脉弓和腹主动脉处均大于IFN-γ^<+/+>BMT小鼠。这些结果表明,骨髓源性细胞产生的IFN-γ可以延缓动脉粥样硬化的进展,而对血脂没有任何影响,这种抑制作用可能是由于减少了细胞外基质的沉积。然而,来自骨髓的IFN-γ至少在初始阶段相当抑制动脉粥样硬化。

项目成果

期刊论文数量(50)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
清島 満 他: "臨床検査項辞典"医歯薬出版株式会社. 219-225 (2003)
Mitsuru Kiyoshima等:《临床试验词典》石药出版有限公司219-225(2003)
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    0
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Fujigaki S, et al.: "L-tryptophan-L-Kynurenine pathway metabolism accelerated by Toxoplasma gondii infection is abolished in gamma interferon-gene-deficient mice : cross-regulation between Inducible nitric oxide Synthase and indoleamine-2,3-dioxygenas"Inf
Fujigaki S 等人:“弓形虫感染加速的 L-色氨酸-L-犬尿氨酸途径代谢在γ干扰素基因缺陷小鼠中被消除:诱导型一氧化氮合酶和吲哚胺-2,3-双加氧酶之间的交叉调节”
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    0
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Niwa T, et al.: "Interferon-γ produced by bone marrow-derived cells attenuates atherosclerotic lesion formation in LDLR-deficient mice"J Atheroscler Thromb. 11. 80-89 (2004)
Niwa T 等人:“骨髓来源细胞产生的干扰素-γ 可减弱 LDLR 缺陷小鼠的动脉粥样硬化病变形成”J Atheroscler Thromb. 11. 80-89 (2004)
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    0
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Iwasaki M, et al.: "Tumor necrosis factor-alpha from bone marrow-derived cells is not essential for the expression of adhesion molecules in lipopolysaccharide-induced nasal inflammation."Cytokine. 21(3). 129-136 (2003)
Iwasaki M 等人:“来自骨髓来源细胞的肿瘤坏死因子-α 对于脂多糖诱导的鼻部炎症中粘附分子的表达并不是必需的。”细胞因子。
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    0
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Maekawa N., et al.: "Improved myocardial ischemia/reperfusion injury in mice lacking tumor necrosis factor-α"J. Am. Coll. Cardiol.. 39. 1229-1235 (2002)
Maekawa N. 等人:“改善缺乏肿瘤坏死因子-α 的小鼠的心肌缺血/再灌注损伤”J. Am. Cardiol.. 39. 1229-1235 (2002)
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SEISHIMA Mitsuru其他文献

SEISHIMA Mitsuru的其他文献

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{{ truncateString('SEISHIMA Mitsuru', 18)}}的其他基金

The role of IDO in the HBV-related liver diseases.
IDO 在 HBV 相关肝脏疾病中的作用。
  • 批准号:
    24659361
  • 财政年份:
    2012
  • 资助金额:
    $ 8.7万
  • 项目类别:
    Grant-in-Aid for Challenging Exploratory Research
Screening and gene analysis for the protection from muscle damage by statin drugs
他汀类药物预防肌肉损伤的筛选和基因分析
  • 批准号:
    21390179
  • 财政年份:
    2009
  • 资助金额:
    $ 8.7万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
Study on analytical system for the etiology of autoimmune disease using two-dimensional nano LC/MS
二维纳米LC/MS自身免疫性疾病病因分析系统研究
  • 批准号:
    17390161
  • 财政年份:
    2005
  • 资助金额:
    $ 8.7万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
The method for determination of serum lipid-free apolipoprotein concentration and its clinical application
血清无脂载脂蛋白浓度的测定方法及其临床应用
  • 批准号:
    11557204
  • 财政年份:
    1999
  • 资助金额:
    $ 8.7万
  • 项目类别:
    Grant-in-Aid for Scientific Research (B)
The mechanism for synthesis and secretion of apo A-IV in CaCo-2 cells
CaCo-2细胞中apo A-IV的合成和分泌机制
  • 批准号:
    09672353
  • 财政年份:
    1997
  • 资助金额:
    $ 8.7万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)
Study on apo A-IV polymorphism in patients with hyperlipidemia.
高脂血症患者apo A-IV多态性研究
  • 批准号:
    07672485
  • 财政年份:
    1995
  • 资助金额:
    $ 8.7万
  • 项目类别:
    Grant-in-Aid for Scientific Research (C)

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