SR-BI MEDIATED SELECTIVE CHOLESTEROL ESTER UPTAKE
SR-BI 介导的选择性胆固醇酯摄取
基本信息
- 批准号:6286827
- 负责人:
- 金额:$ 22.05万
- 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:2001-03-01 至 2006-02-28
- 项目状态:已结题
- 来源:
- 关键词:
项目摘要
DESCRIPTION: There is interest in understanding the factors that regulate HDL
and apoA-I levels in humans as these are inversely correlated with the risk for
atherosclerotic vascular disease. Plasma levels of HDL and apoA-I are related
to the rate of apoA-I catabolism rather than apoA-I production. Neither the
mechanisms underlying accelerated catabolism nor the site(s) of apoA-I removal
from plasma have been clearly delineated. This proposal focuses on the role of
the HDL receptor, SR-B1, in regulating apoA-I catabolic rate. SR-B1 delivers
cholesteryl ester to cells via a process that is fundamentally distinct from
receptor-mediated endocytosis. During this process, HDL binds to SR-B1 on the
cell surface and transfers cholesteryl ester from the core of the particle to
the cell without internalization of the apolipoprotein moiety. Despite the
absence of apolipoprotein uptake, increased selective lipid uptake in the liver
mediated by SR-B1 is associated with increased catabolism of apoA-I, and at
least some of this catabolism occurs in the kidney. Thus, a central hypothesis
of this proposal is that SR-B1 interaction with HDL initiates changes in the
lipoprotein particle that promotes subsequent catabolism by a mechanism that is
independent of SR-B1. SR-B1 binds with high affinity a number of different
lipoprotein particles in addition to HDL, including VLDL, LDL, and oxidized
LDL. The important metabolic event subsequent to lipoprotein binding by SR-B1
is the selective delivery of CE from the core of particles to cells. We propose
that apoA-I is a critical ligand for SR-B1-mediated selective uptake, and that
apoA-I conformation on the HDL particle can influence its interaction with
SR-B1 to impede or promote receptor binding and/or selective uptake. The
efficiency of selective uptake mediated by SR-B1:apoA-I interaction can be
modulated by properties of the HDL particle (lipid composition, apolipoprotein
content, or the structure of apoA-I itself). These hypotheses will be tested by
defining: 1) the sub-population of HDL particles that are the preferred
substrate for SR-B1-mediated lipid transfer; 2) the structure and composition
of HDL particles after processing by SR-B1 (including the potential for apoA-I
proteolysis); and 3) the metabolic fate of HDL particles after SR-B1
processing. Understanding the role of SR-B1 in HDL metabolism could define new
areas for potential therapeutic assault.
描述:人们对了解调节HDL的因素很感兴趣
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:
$ 22.05万 - 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:
$ 22.05万 - 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:
$ 22.05万 - 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:
$ 22.05万 - 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:
$ 22.05万 - 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:
$ 22.05万 - 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:
$ 22.05万 - 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:
6779922 - 财政年份:2001
- 资助金额:
$ 22.05万 - 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:
$ 22.05万 - 项目类别:
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