Lesion Development in Apolipoprotein E Inactivation of Macrophage Scavenger Receptor Class B Type I Promotes Atherosclerotic
نویسندگان
چکیده
Wenwu Zhang, Patricia G. Yancey, Yan Ru Su, Vladimir R. Babaev, Yuomin Zhang, Sergio Deficient Mice − Lesion Development in Apolipoprotein E Inactivation of Macrophage Scavenger Receptor Class B Type I Promotes Atherosclerotic Print ISSN: 0009-7322. Online ISSN: 1524-4539 Copyright © 2003 American Heart Association, Inc. All rights reserved. is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Circulation doi: 10.1161/01.CIR.0000093189.97429.9D 2003;108:2258-2263; originally published online October 27, 2003; Circulation. http://circ.ahajournals.org/content/108/18/2258 World Wide Web at: The online version of this article, along with updated information and services, is located on the
منابع مشابه
Inactivation of macrophage scavenger receptor class B type I promotes atherosclerotic lesion development in apolipoprotein E-deficient mice.
BACKGROUND Scavenger receptor class B type I (SR-BI) is expressed in macrophages, where it has been proposed to facilitate cholesterol efflux. However, direct evidence that the expression of macrophage SR-BI is protective against atherosclerosis is lacking. In this study, we examined the in vivo role of macrophage SR-BI in atherosclerotic lesion development in the apolipoprotein (apo) E-deficie...
متن کاملScavenger receptor class B type I (SR-BI) is an HDL re- ceptor that promotes bidirectional fl ux of free cholesterol between cells and HDL, as well as selective uptake of HDL cholesteryl ester into hepatocytes and steroidogenic cells
Scavenger receptor class B type I (SR-BI) is an HDL receptor that promotes bidirectional fl ux of free cholesterol between cells and HDL, as well as selective uptake of HDL cholesteryl ester into hepatocytes and steroidogenic cells ( 1, 2 ). Single deletion of mouse SR-BI accelerates atherosclerosis, whereas combined deletion of SR-BI and ApoE mimics several features of human coronary disease, ...
متن کاملMolecular Medicine Enhanced Foam Cell Formation, Atherosclerotic Lesion Development, and Inflammation by Combined Deletion of ABCA1 and SR-BI in Bone Marrow–Derived Cells in LDL Receptor Knockout Mice on Western-Type Diet
Rationale: Macrophages cannot limit the uptake of lipids and rely on cholesterol efflux mechanisms for maintaining cellular cholesterol homeostasis. Important mediators of macrophage cholesterol efflux are ATP-binding cassette transporter 1 (ABCA1), which mediates the efflux of cholesterol to lipid-poor apolipoprotein AI, and scavenger receptor class B type I (SR-BI), which promotes efflux to m...
متن کاملEnhanced foam cell formation, atherosclerotic lesion development, and inflammation by combined deletion of ABCA1 and SR-BI in Bone marrow-derived cells in LDL receptor knockout mice on western-type diet.
RATIONALE macrophages cannot limit the uptake of lipids and rely on cholesterol efflux mechanisms for maintaining cellular cholesterol homeostasis. Important mediators of macrophage cholesterol efflux are ATP-binding cassette transporter 1 (ABCA1), which mediates the efflux of cholesterol to lipid-poor apolipoprotein AI, and scavenger receptor class B type I (SR-BI), which promotes efflux to ma...
متن کاملTargeted disruption of the class B scavenger receptor CD36 protects against atherosclerotic lesion development in mice.
Macrophage scavenger receptors have been implicated as key players in the pathogenesis of atherosclerosis. To assess the role of the class B scavenger receptor CD36 in atherogenesis, we crossed a CD36-null strain with the atherogenic apo E-null strain and quantified lesion development. There was a 76.5% decrease in aortic tree lesion area (Western diet) and a 45% decrease in aortic sinus lesion...
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