SAA and sPLA2 Role in Atherogenesis

SAA 和 sPLA2 在动脉粥样硬化形成中的作用

基本信息

  • 批准号:
    6779922
  • 负责人:
  • 金额:
    $ 31.5万
  • 依托单位:
  • 依托单位国家:
    美国
  • 项目类别:
  • 财政年份:
    2001
  • 资助国家:
    美国
  • 起止时间:
    2001-09-30 至 2006-07-31
  • 项目状态:
    已结题

项目摘要

DESCRIPTION (provided by applicant): Chronic inflammatory diseases, particularly rheumatic diseases, lead to accelerated atherosclerosis. At the same time, atherosclerosis itself is increasingly recognized as a chronic vascular inflammatory condition. These inflammatory processes induce a wide variety of metabolic changes with two of these changes relating specifically to atherogenesis. The first is the cytokine mediated induction of acute phase serum amyloid A protein (SAA) that increases hundreds of fold and can even become the major apolipoprotein on HDL. A second factor is the concomitant induction of an acute phase extracellular enzyme group II-A secretory phospholipase A2 (sPLA2). Like SAA, the concentration of sPLA2 can increase hundreds of fold in inflammatory fluids or the circulation. Circulating levels of both SAA and sPLA2 predict coronary events in patients with coronary artery disease. Using sPLA2 overexpressing transgenic mouse, direct evidence was presented that this enzyme promotes vascular lipid deposition, even in the absence of a high fat diet. In preliminary data, we present evidence that increased SAA is associated with vascular lipid deposition. Considerable effort was spent analyzing the concomitant influence of SAA and sPLA2 on systemic lipoprotein metabolism. Less emphasis was placed on the potentially important role that these molecules can play in the atherosclerotic lesion per se. Both avidly bind to proteoglycan and accumulate in lesions. Proteoglycan bound sPLA2 promote hydrolysis of a spectrum of lipoproteins, particularly LDL, generating bioactive entities that are proinflammatory. SAA can act as a co-factor for sPLA2. In addition amyloidogenic SAAs are the most fibrillogenic proteins known and can entrap lipoprotein in such networks. The major hypothesis of this proposal is that SAA and sPLA2 act interactively, predominantly at the vascular lesional level, to promote atherogenesis. We propose that SAA and sPLA2, respectively produced by macrophages and smooth muscle cells, is important in amplifying and perpetuating lesional inflammation ultimately promoting vascular lipid deposition.
描述(由申请人提供):

项目成果

期刊论文数量(0)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)

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FREDERICK C. DE BEER其他文献

FREDERICK C. DE BEER的其他文献

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{{ truncateString('FREDERICK C. DE BEER', 18)}}的其他基金

Serum Amyloid A, Inflammasome Activation, and Abdominal Aortic Aneurysms
血清淀粉样蛋白 A、炎症小体激活和腹主动脉瘤
  • 批准号:
    9213910
  • 财政年份:
    2017
  • 资助金额:
    $ 31.5万
  • 项目类别:
HDL Structure and Metabolism During Inflammation
炎症过程中 HDL 的结构和代谢
  • 批准号:
    7219726
  • 财政年份:
    2006
  • 资助金额:
    $ 31.5万
  • 项目类别:
Analytical and Preparative Core
分析和准备核心
  • 批准号:
    7219730
  • 财政年份:
    2006
  • 资助金额:
    $ 31.5万
  • 项目类别:
SR-BI MEDIATED SELECTIVE CHOLESTEROL ESTER UPTAKE
SR-BI 介导的选择性胆固醇酯摄取
  • 批准号:
    6509679
  • 财政年份:
    2001
  • 资助金额:
    $ 31.5万
  • 项目类别:
SAA and sPLA2 Role in Atherogenesis
SAA 和 sPLA2 在动脉粥样硬化形成中的作用
  • 批准号:
    6618079
  • 财政年份:
    2001
  • 资助金额:
    $ 31.5万
  • 项目类别:
SR-BI MEDIATED SELECTIVE CHOLESTEROL ESTER UPTAKE
SR-BI 介导的选择性胆固醇酯摄取
  • 批准号:
    6866412
  • 财政年份:
    2001
  • 资助金额:
    $ 31.5万
  • 项目类别:
SAA and sPLA2 Role in Atherogenesis
SAA 和 sPLA2 在动脉粥样硬化形成中的作用
  • 批准号:
    6442685
  • 财政年份:
    2001
  • 资助金额:
    $ 31.5万
  • 项目类别:
SR-BI MEDIATED SELECTIVE CHOLESTEROL ESTER UPTAKE
SR-BI 介导的选择性胆固醇酯摄取
  • 批准号:
    6707547
  • 财政年份:
    2001
  • 资助金额:
    $ 31.5万
  • 项目类别:
SR-BI MEDIATED SELECTIVE CHOLESTEROL ESTER UPTAKE
SR-BI 介导的选择性胆固醇酯摄取
  • 批准号:
    6629853
  • 财政年份:
    2001
  • 资助金额:
    $ 31.5万
  • 项目类别:
SR-BI MEDIATED SELECTIVE CHOLESTEROL ESTER UPTAKE
SR-BI 介导的选择性胆固醇酯摄取
  • 批准号:
    6286827
  • 财政年份:
    2001
  • 资助金额:
    $ 31.5万
  • 项目类别:

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