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Research Article Free access | 10.1172/JCI116257

Lipoprotein-proteoglycan complexes induce continued cholesteryl ester accumulation in foam cells from rabbit atherosclerotic lesions.

P Vijayagopal, S R Srinivasan, J H Xu, E R Dalferes Jr, B Radhakrishnamurthy, and G S Berenson

Department of Medicine, Louisiana State University Medical Center, New Orleans 70112.

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Department of Medicine, Louisiana State University Medical Center, New Orleans 70112.

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Department of Medicine, Louisiana State University Medical Center, New Orleans 70112.

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Department of Medicine, Louisiana State University Medical Center, New Orleans 70112.

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Department of Medicine, Louisiana State University Medical Center, New Orleans 70112.

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Department of Medicine, Louisiana State University Medical Center, New Orleans 70112.

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Published March 1, 1993 - More info

Published in Volume 91, Issue 3 on March 1, 1993
J Clin Invest. 1993;91(3):1011–1018. https://doi.org/10.1172/JCI116257.
© 1993 The American Society for Clinical Investigation
Published March 1, 1993 - Version history
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Abstract

We studied the metabolism of lipoprotein-proteoglycan complexes by macrophage-derived foam cells. Foam cells were isolated from atherosclerotic rabbit aortas. ApoB-lipoprotein-proteoglycan complex was isolated from human aorta fibrous plaque lesions and LDL-proteoglycan complex was formed in vitro. Both in vitro and in vivo complexes stimulated cholesteryl ester synthesis in foam cells by a dose-dependent, saturable process that resulted in the intracellular accumulation of cholesteryl ester. Stimulation of cholesteryl ester synthesis was linear with time over a 32-h period. Polyinosinic acid inhibited the stimulation of cholesteryl ester synthesis by the complexes by 32-37%, whereas cytochalasin D only produced a 6-16% inhibition. Foam cells degraded 125I-LDL-proteoglycan complex and 125I-acetyl LDL in a saturable, dose-dependent manner. Excess unlabeled acetyl-LDL inhibited the degradation of 125I-LDL-proteoglycan complex by 52%, while LDL had no effect. Similarly, excess unlabeled complex suppressed the degradation of 125I-acetyl-LDL by 48%. Foam cells degraded 125I-methyl-LDL-proteoglycan complex to the same extent as 125I-LDL-proteoglycan complex. These results show that foam cells from atherosclerotic lesions metabolize lipoprotein-proteoglycan complexes predominantly via receptor-mediated endocytosis and consequently continue to accumulate intracellular cholesteryl ester.

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