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Cited by 2,448

The DOI matches its Crossref record.

Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition

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Goldstein, Joseph L., Ho, Y. K., Basu, Sandip K., Brown, Michael S.·1979·Proceedings of the National Academy of Sciences
DOI 10.1073/pnas.76.1.333
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Abstract

Resident mouse peritoneal macrophages were shown to take up and degrade acetylated 125 I-labeled low density lipoprotein ( 125 I-acetyl-LDL) in vitro at rates that were 20-fold greater than those for the uptake and degradation of 125 I-LDL. The uptake of 125 I-acetyl-LDL and its subsequent degradation in lysosomes were attributable to a high-affinity, trypsin-sensitive, surface binding site that recognized acetyl-LDL but not native LDL. When 125 I-acetyl-LDL was bound to this site at 4°C and the macrophages were subsequently warmed to 37°C, 75% of the cell-bound radioactivity was degraded to mono[ 125 I]iodotyrosine within 1 hr. The macrophage binding site also recognized maleylated LDL, maleylated albumin, and two sulfated polysaccharides (fucoidin and dextran sulfate) indicating that negative charges were important in the binding reaction. A similar binding site was present on rat peritoneal macrophages, guinea pig Kupffer cells, and cultured human monocytes but not on human lymphocytes or fibroblasts, mouse L cells or Y-1 adrenal cells, or Chinese hamster ovary cells. Uptake and degradation of acetyl-LDL via this binding site stimulated cholesterol esterification 100-fold and produced a 38-fold increase in the cellular content of cholesterol in mouse peritoneal macrophages. Although the physiologic significance, if any, of this macrophage uptake mechanism is not yet known, we hypothesize that it may mediate the degradation of denatured LDL in the body and thus serve as a “backup” mechanism for the previously described receptor-mediated degradation of native LDL that occurs in parenchymal cells. Such a scavenger pathway might account for the widespread deposition of LDL-derived cholesteryl esters in macrophages of patients with familial hypercholesterolemia in whom the parenchymal cell pathway for LDL degradation is blocked, owing to a genetic deficiency of receptors for native LDL.

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Authors
Goldstein, J. L., Ho, Y. K., Basu, S. K., & Brown, M. S.
Venue
Proceedings of the National Academy of Sciences
Publisher
Proceedings of the National Academy of Sciences
Published
1979-01
Volume
76
Issue
1
Pages
333-337
ISSN
  • 0027-8424 (ISSN-L)
  • 1091-6490
DOI
10.1073/pnas.76.1.333
OpenAlex
W2049401036
Cited by
2,448
References
0
FWCI
57.84
Type
journal article
Language
en
Open access
green

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