Abstract

Monkey arterial smooth muscle cell binding, incorporation and degradation of low density lipoproteins (LDL) from normal or hyperlipemic rhesus monkey plasma were examined by labeling lipoproteins with 125I. Specific and nonspecific binding of both lipoproteins occurred. Although the dissociation constant for the normal LDL was twice as high as for hyperlipemic LDL, indicating a higher binding affinity for hyperlipemic LDL, the maximal binding capacity of the smooth muscle cells for normal [ 125I]LDL was 2-fold higher than for hyperlipemic [ 125I]LDL. In competition experiments where the two types of LDL competed with normal [ 125I]LDL for binding to smooth muscle cells, LDL isolated from hyperlipemic plasma was a more effective competitor than normal LDL. Receptors for normal LDL were reduced to a greater extent by preincubation with hyperlipemic LDL than by the same protein concentration of normal LDL. Under conditions where nonspecific uptake of lipoproteins would occur predominantly, the cells showed higher incorporation and degradation of normal LDL than hyperlipemic LDL. The corresponding cellular cholesterol ester levels showed an inverse pattern, with higher accumulation of cholesterol ester in the cells grown in hyperlipemic LDL. The results suggest that binding and incorporation of LDL by specific receptors or through the nonspecific pathway play a role in the changes of cellular cholesterol content but cannot totally account for the enhanced accumulation of cellular cholesterol esters produced by hyperlipemic monkey LDL.

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