Receptors for oxidized low density lipoprotein

High Affinity Saturable Uptake of Oxidized Low Density Lipoprotein by Macrophages from Mice Lacking the Scavenger Receptor Class A Type I/II

To determine whether scavenger receptors are susceptible to regulation by granulocyte macrophage colony-stimulating factor (GM-CSF), a macrophage-specific cytokine, human monocytes were differentiated into macrophages in the absence or presence of 20 U/mL GM-CSF. Binding, uptake, and degradation of acetylated LDL (Ac-LDL) and oxidized LDL (Ox-LDL) were measured. Treatment with GM-CSF resulted in a significant twofold to threefold decrease in the number of binding sites for Ac-LDL and Ox-LDL on the surface of macrophages without affecting the affinity of the receptor for these ligands. Competition experiments revealed that two binding sites were responsible for the recognition and uptake of Ac-LDL: one specific for Ac-LDL and one that recognized both Ac-LDL and Ox-LDL. No binding site specific for Ox-LDL could be detected in either control or GM-CSF–treated macrophages. Treatment of human monocyte–derived macrophages with GM-CSF resulted in a decrease of the Ac-LDL/Ox-LDL receptor but did not affect the binding site specific for Ac-LDL. Northern blot analysis showed that mRNA levels of both types I and II scavenger receptor were reduced in macrophages differentiated in the presence of GM-CSF. Human macrophages that were differentiated in the presence of GM-CSF accumulated ≈50% fewer cholesteryl esters. Taken together, these results indicate that GM-CSF can downregulate both types I and II scavenger receptor in human monocyte–derived macrophages, which might have implications for foam cell formation.

Decrease in Scavenger Receptor Expression in Human Monocyte–Derived Macrophages Treated With Granulocyte Macrophage Colony-Stimulating Factor

LDL receptor-independent and -dependent uptake of lipoproteins.

The emerging dogma that low density lipoprotein (LDL) oxidation is a contributing cause and not simply a consequence of atherosclerosis is based on three lines of experimental evidence: (i) lipid peroxidation products and oxidized LDLs are present in atherosclerotic lesions; (ii) oxidized LDL has an array of potentially proatherogenic properties in vitro, including uptake by macrophages via a number of distinct "scavenger" receptors; and (iii) treatment of hypercholesterolemic animals with potent antioxidant drugs can retard the development of atherosclerosis. Additional support for the role of lipoprotein oxidation in atherogenesis was provided by cross-cultural dietary comparisons, which suggested an inverse correlation between antioxidant vitamin intake and coronary mortality. As well, several large case-control studies indicated that antioxidant vitamin intake, particularly vitamin E, was associated with reduced coronary risk. However, these studies do not indicate whether this association is causal, or if vitamin supplementation is merely a marker for some other protective factor. To test this properly, randomized controlled intervention studies are required. In several animal models, a number of different antioxidant drugs have been shown to retard atherosclerosis, but results with vitamin supplementation are unclear. Results of intervention trials in humans show no benefit to long-term beta-carotene supplementation, and the only published study of vitamin E found a reduction of nonfatal myocardial infarction but no reduction (actually an increase) in fatal myocardial infarction and total mortality. Several other large antioxidant intervention trials are underway. Until the results of these studies are available, there appears to be insufficient evidence on which to base recommendations regarding antioxidant supplements for the prevention of atherosclerosis.

Dietary antioxidants and cardioprotection--fact or fallacy?

Different expression of modified low density lipoprotein receptors in rabbit peritoneal macrophages and Kupffer cells

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Different expression of modified low density lipoprotein receptors in rabbit peritoneal macrophages and Kupffer cells