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
- 来源:
- 关键词:
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)
数据更新时间:{{ journalArticles.updateTime }}
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
数据更新时间:{{ journalArticles.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ monograph.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ sciAawards.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ conferencePapers.updateTime }}
{{ item.title }}
- 作者:
{{ item.author }}
数据更新时间:{{ patent.updateTime }}
FREDERICK C. DE BEER其他文献
FREDERICK C. DE BEER的其他文献
{{
item.title }}
{{ item.translation_title }}
- DOI:
{{ item.doi }} - 发表时间:
{{ item.publish_year }} - 期刊:
- 影响因子:{{ item.factor }}
- 作者:
{{ item.authors }} - 通讯作者:
{{ item.author }}
{{ 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:
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:
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:
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:
相似海外基金
Development of aggregation inhibition strategy for pathogenic amyloid proteins
致病性淀粉样蛋白聚集抑制策略的开发
- 批准号:
16H06216 - 财政年份:2016
- 资助金额:
$ 31.5万 - 项目类别:
Grant-in-Aid for Young Scientists (A)
Elucidation of the mechanisms on aggregation and toxicity of plant amyloid proteins which are toxic in the presence of metals
阐明在金属存在下有毒的植物淀粉样蛋白的聚集和毒性机制
- 批准号:
23380192 - 财政年份:2011
- 资助金额:
$ 31.5万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Demonstration of the abnormal conformational transition of amyloid proteins and it's application as an early diagnostic tool
淀粉样蛋白异常构象转变的演示及其作为早期诊断工具的应用
- 批准号:
21200072 - 财政年份:2009
- 资助金额:
$ 31.5万 - 项目类别:
Grant-in-Aid for Scientific Research on Innovative Areas (Research a proposed research project)
Metabolism of amyloid proteins and methods for detecting amyloid proteins
淀粉样蛋白的代谢和检测淀粉样蛋白的方法
- 批准号:
21790541 - 财政年份:2009
- 资助金额:
$ 31.5万 - 项目类别:
Grant-in-Aid for Young Scientists (B)
Development of aggregation disrupters for amyloid proteins
淀粉样蛋白聚集破坏剂的开发
- 批准号:
17310132 - 财政年份:2005
- 资助金额:
$ 31.5万 - 项目类别:
Grant-in-Aid for Scientific Research (B)
Inhibition of axonal transport of hippocampal neurons by amyloid proteins: relation to Alzheimer's disease
淀粉样蛋白抑制海马神经元轴突运输:与阿尔茨海默病的关系
- 批准号:
11670638 - 财政年份:1999
- 资助金额:
$ 31.5万 - 项目类别:
Grant-in-Aid for Scientific Research (C)
RAB GTPASES AND TRAFFICKING OF BETA AMYLOID PROTEINS
RAB GTP 酶和 β 淀粉样蛋白的贩运
- 批准号:
6149928 - 财政年份:1998
- 资助金额:
$ 31.5万 - 项目类别: