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[Stimulation of cholesterol ester synthesis in macrophages by lipoproteins from normal and atherosclerotic human aorta intima].

A buffer extract from homogenized human aorta was applied to a Bio-Gel A-15m column, and two cholesterol-containing peaks were resolved. Both fractions of aortic lipoproteins present in the extracts from normal and atherosclerotic intima and stimulated cholesteryl ester (CE) synthesis in J774 mouse macrophages caused unregulated loading with CE. The Vmax of CE formation in the presence of both fractions correlated with the degree of intimal atherosclerosis. An excess of both fractions did not inhibit the uptake of malondialdehyde-treated low density lipoproteins by macrophages; their interaction with the cells was not inhibited either by fucoidin or by dextran sulfate. The uptake of labeled LDL by human fibroblasts was markedly decreased with excess of both fractions. Aortic lipoprotein-mediated CE synthesis (for both fractions) was completely blocked by EDTA in fibroblasts, being decreased by 50% in macrophages.