Cholesteryl ester synthesis in macrophages: stimulation by beta-very low density lipoproteins from cholesterol-fed animals of several species.
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TLDR
It is demonstrated that beta-VLDL obtained from cholesterol-fed animals of several other species, including monkeys, rabbits, and rats, also causes cholesteryl ester accumulation in monolayers of mouse peritoneal macrophages, as monitored by an increase in the rate at which the cells incorporate exogenous [14C]oleate into cholesterymoleate.About:
This article is published in Journal of Lipid Research.The article was published on 1980-11-01 and is currently open access. It has received 271 citations till now. The article focuses on the topics: Cholesteryl ester & Cholesterylester transfer protein.read more
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Lipoprotein receptors and cholesterol homeostasis
Journal ArticleDOI
Postprandial lipoprotein metabolism in normolipidemic men with and without coronary artery disease.
P H Groot,W. A. H. J. Van Stiphout,X.H. Krauss,Hans Jansen,A. van Tol,E. van Ramshorst,S Chin-On,Albert Hofman,S R Cresswell,Louis M. Havekes +9 more
TL;DR: The data indicate that the clearance of postprandial lipoproteins in normolipidemic CAD patients as selected in the present study is delayed as compared with that of controls without coronary atherosclerosis and suggest that postpr andial lipiproteins may play a role in the etiology of their disease.
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Lipoproteins and atherogenesis. Current concepts
TL;DR: The frontiers in atherosclerosis research are moving from lipoprotein metabolism and control of hyperlipidemia to the cellular events in the artery wall, and emerging hypotheses, including the oxidative modification hypothesis, are already suggesting new approaches that could complement and be additive to control ofhypercholesterolemia in the prevention of Atherosclerosis.
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Decrease in reactive amino groups during oxidation or endothelial cell modification of LDL. Correlation with changes in receptor-mediated catabolism.
TL;DR: These studies demonstrate that all of the changes associated with endothelial cell modification of LDL can be attributed to oxidation, and the cells can, however, promote oxidation under conditions where it would otherwise occur very slowly.
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Cholesterol and coronary heart disease. A new era.
TL;DR: A new class of cholesterollowering drugs, namely, competitive inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase, the rate-limiting enzyme in cholesterol synthesis, has been shown to markedly lower cholesterol levels.
References
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Journal Article
Protein Measurement with the Folin Phenol Reagent
TL;DR: Procedures are described for measuring protein in solution or after precipitation with acids or other agents, and for the determination of as little as 0.2 gamma of protein.
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Binding Site on Macrophages that Mediates Uptake and Degradation of Acetylated Low Density Lipoprotein, Producing Massive Cholesterol Deposition
TL;DR: It is hypothesized that this macrophage uptake mechanism may mediate the degradation of denatured LDL in the body and thus serve as a "backup" mechanism for the previously described receptor-mediated degradation of native LDL that occurs in parenchymal cells.
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The Low-Density Lipoprotein Pathway and its Relation to Atherosclerosis
Joseph L. Goldstein,M. S. Brown +1 more
TL;DR: The LDL Pathway is a Vehicle for Normal Human PhySIOLOGY and the PATHOGENESIS of ATHEROSCLEROSIS and its implications for normal human physiology and the pathogenesis of AtherOSCLerosis are discussed.
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Binding and Degradation of Low Density Lipoproteins by Cultured Human Fibroblasts COMPARISON OF CELLS FROM A NORMAL SUBJECT AND FROM A PATIENT WITH HOMOZYGOUS FAMILIAL HYPERCHOLESTEROLEMIA
TL;DR: It is raised that a prerequisite for the regulation of cholestero-genesis in cultured fibroblasts is the initial binding of low density lipoproteins to the high affinity surface receptor sites and that a defect in this process represents the primary genetic abnormality in the disorder familial hypercholesterolemia.