Degradation of low density lipoprotein . dextran sulfate complexes associated with deposition of cholesteryl esters in mouse macrophages.
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TLDR
These experiments indicate that macrophages have the capacity to ingest large amounts of LDL in association with high molecular weight-sulfated polysaccharides and that this ingestion leads to cholesteryl ester deposition in these cells.About:
This article is published in Journal of Biological Chemistry.The article was published on 1979-08-10 and is currently open access. It has received 138 citations till now. The article focuses on the topics: Deposition (chemistry) & Low-density lipoprotein.read more
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Low Density Lipoprotein Oxidation and Its Pathobiological Significance
TL;DR: In this article, it was shown that LDL modification induced by cells appeared to be a biologically plausible modification of LDL that could account for foam cell formation and the initiation, or at least acceleration, of the atherosclerotic process.
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Lipoprotein receptors and cholesterol homeostasis
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The scavenger cell pathway for lipoprotein degradation: specificity of the binding site that mediates the uptake of negatively-charged LDL by macrophages.
TL;DR: It is possible that the site that binds negatively-charged LDL may be responsible for the massive accumulation of cholesteryl esters that occurs in vivo in macrophages and other scavenger cells in patients with high levels of circulating plasma LDL.
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Enhanced macrophage degradation of biologically modified low density lipoprotein.
TL;DR: A biologically generated modification of LDL is described that markedly alters cholesterol metabolism of macrophages and, consequently, may play a role in foam cell formation during atherogenesis.
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Cell biology of arterial proteoglycans.
TL;DR: The importance of proteoglycans in regulating several key events in normal and pathophysiological processes in the vascular tissue is emphasized, because these events pertain to atherogenesis.
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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.
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Degradation of cationized low density lipoprotein and regulation of cholesterol metabolism in homozygous familial hypercholesterolemia fibroblasts.
TL;DR: Although the cationized LDL entered the cell through a mechanism independent of the LDL receptor, the cholesterol liberated from the degradation of the lipoprotein became available for suppression of cholesterol synthesis and stimulation of cholesteryl ester formation in the homozygous familial hypercholesterolemia fibroblasts.