Lipoprotein metabolism of human and rabbit arterial cells in primary culture.
The early atherosclerotic lesion, the fatty streak, consists of cholesteryl ester-containing foam cells originating mainly from monocyte-macrophages and to a lesser extent from smooth muscle cells. In this study, we describe lipoprotein uptake and cholesterol accumulation into enzyme-dispersed primary cell cultures from cholesterol-fed rabbit aortas and human aortic fatty streaks. Uptake of fluorescently labelled acetylated low density lipoprotein (acetyl-LDL) was demonstrable in macrophage-derived foam cells and in many smooth muscle cells in early primary cultures. The uptake of acetyl-LDL led to significantly enhanced cellular esterification of cholesterol. Fluorescent beta-migrating very low density lipoprotein (beta-VLDL) was internalized by a considerable number of lesion macrophages and also by smooth muscle cells. Also beta-VLDL uptake stimulated cholesterol esterification, although the effect was milder than that of acetyl-LDL. These findings lend support to the assumption that, during atherogenesis, arterial macrophages are capable of accumulating cholesteryl esters by receptor-mediated uptake of beta-VLDL and modified LDL. The internalization of modified LDL by smooth muscle cells represents a mechanism potentially contributing to the formation of foam cells in the atherosclerotic lesion.
Jaakkola
O
O
Department of Biomedical Sciences, University of Tampere, Finland.
Kallioniemi
O P
OP
Nikkari
T
T
D000818:Animals; D001011:Aorta / Q000378:metabolism; D001158:Arteries / Q000378:metabolism*; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000378:metabolism*; D006801:Humans; D008074:Lipoproteins / Q000378:metabolism*; D011817:Rabbits
D008074:Lipoproteins