Effect of arterial proteoglycans on the interaction of LDL with human monocyte-derived macrophages

Hurt, Eva; Camejo, G

doi:10.1016/0021-9150(87)90272-3

Cited by 93 publications

(30 citation statements)

References 28 publications

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“…A similar observation was made by Hurt and Camejo 39 of human monocytes/macrophages incubated with LDL-proteoglycan complexes formed in vitro. In this respect the human cells seem to differ from mouse peritoneal macrophages.…”

supporting

confidence: 84%

Lipoprotein-proteoglycan complexes from atherosclerotic lesions promote cholesteryl ester accumulation in human monocytes/macrophages.

Vijayagopal

Srinivasan

Radhakrishnamurthy

et al. 1992

Arterioscler Thromb

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Lipoprotein-proteoglycan complexes from human atherosclerotic lesions were studied to determine their ability to stimulate cholesteryl ester accumulation in human monocytes/macrophages. Complexes containing apolipoprotein (apo) B lipoproteins and proteoglycans were extracted from fatty streaks and fibrous plaque lesions of human aortas by extraction with 0.15 M NaCl. Fractionation of the complex with Bio-Gel A-50m yielded a single fraction from fatty streaks and two fractions from fibrous plaques. The complexes were further purified by antl-apo B affinity chromatography and analyzed for apolipoproteins, lipids, and glycosaminoglycans. Apo B was the only apolipoprotein present in the complexes. Although the complexes from fatty streaks and fibrous plaques contained varying proportions of hyaluronic acid, chondroitin 6-sulfate, and dermatan sulfate, heparin was present in only the fibrous plaque complexes. All three lipoprotein-proteogtycan complexes increased the rate of incorporation of [ M C]oleate into cholesteryl [ 14 C]oleate and stimulated cholesteryl ester accumulation in monocytes/macrophages. However, the complexes from fibrous plaques were more potent than those from fatty streaks in this regard. Cholesteryl ester synthesis that is mediated by the uptake of the complexes was dose dependent and showed apparent saturation, suggesting that cell surface binding may be required. Chloroquine, a lysosomotropic agent, inhibited cholesteryl ester synthesis that is induced by the complexes, indicating that lysosomal hydrolysis was essential. Cholesteryl ester synthesis that is mediated by the complexes was inhibited 70-79% by polyinosinic acid. Furthermore, excess unlabeled fibrous plaque complexes significantly inhibited the binding and interaalization of in vitro In vitro, low density lipoprotein (LDL) does not induce cholesteryl ester accumulation in macrophages from different sources, including human

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supporting

confidence: 84%

Lipoprotein-proteoglycan complexes from atherosclerotic lesions promote cholesteryl ester accumulation in human monocytes/macrophages.

Vijayagopal

Srinivasan

Radhakrishnamurthy

et al. 1992

Arterioscler Thromb

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show abstract

“…This led to increased LDL internalization and stimulation of cholesteryl esterification in human monocyte-derived macrophages. 46 It has been proposed, therefore, that interaction with PG may result in alterations in the LDL particles, which allows their recognition and uptake by the cells. The process of recognition and involvement of a specific macrophage receptor is at present unclear.…”

Section: Resultsmentioning

confidence: 99%

Reduced proteoglycan binding of low density lipoproteins from monkeys (Macaca fascicularis) fed a fish oil versus lard diet.

Edwards

Gebre

Parks

1991

Arterioscler Thromb

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“…Furthermore, this study demonstrated that catabolism of the endocytosed LDLcomplex was greatly diminished, causing cholesterol ester to accumulate within these cells. More recently, Hurt and Camejo 245 demonstrated that incubation of human LDL with human arterial CSPG increased LDL uptake by human monocyte-derived macrophages, indicating that proteoglycan alone is capable of modifying LDL. It is interesting that sulfated polyanions such as dextran sulfate inhibit the fusion of phagosomes with lysosomes within macrophages by modifying membrane fluidity of the lysosome.…”

Section: Lipid Metabolismmentioning

confidence: 99%

Cell biology of arterial proteoglycans.

1989

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Effect of arterial proteoglycans on the interaction of LDL with human monocyte-derived macrophages

Cited by 93 publications

References 28 publications

Lipoprotein-proteoglycan complexes from atherosclerotic lesions promote cholesteryl ester accumulation in human monocytes/macrophages.

Lipoprotein-proteoglycan complexes from atherosclerotic lesions promote cholesteryl ester accumulation in human monocytes/macrophages.

Reduced proteoglycan binding of low density lipoproteins from monkeys (Macaca fascicularis) fed a fish oil versus lard diet.

Cell biology of arterial proteoglycans.

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