Key result
Macrophage CD36 selectively mediates lipid uptake from oxidized HDL, potentially driving atheroma formation.
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Atherosclerotic plaques result from the excessive deposition of cholesterol esters derived from lipoproteins and lipoprotein fragments. Tissue macrophage within the intimal space of major arterial vessels have been shown to play an important role in this process. We demonstrate in a transfection system using two human cell lines that the macrophage scavenger receptor CD36 selectively elicited lipid uptake from Cu(2+)-oxidized high density lipoprotein (HDL) but not from native HDL or low density lipoprotein (LDL). The uptake of oxHDL displayed morphological and biochemical similarities with the CD36-dependent uptake of oxidized LDL. CD36-mediated uptake of oxidized HDL by macrophage may therefore contribute to atheroma formation.
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Thorne et al. (2007) studied Atherosclerosis. Cu(2+)-oxidized high density lipoprotein (HDL) vs. Native HDL or low density lipoprotein (LDL) was evaluated on Lipid uptake. The macrophage scavenger receptor CD36 selectively elicited lipid uptake from Cu(2+)-oxidized HDL, but not from native HDL or LDL, suggesting a potential contribution to atheroma formation.
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