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Stimulation of Cholesteryl Ester Synthesis in Macrophages by Extracts of Atherosclerotic Human Aortas and Complexes of Albumin/Cholesteryl Esters

Stimulation of Cholesteryl Ester Synthesis in Macrophages by Extracts of Atherosclerotic Human... Cholesteryl ester-rich particles extracted from human atherosclerotic plaques were shown to increase the rate of incorporation of [14C]oleate into cholesteryl [14C]oleate and to cause massive accumulation of cholesteryl esters in monolayers of mouse peritoneal macrophages. This stimulation showed saturation kinetics and susceptibility to competition by polyanions (polylnosinic acid, fucoidin, dextran sulfate), suggesting that cell surface binding was required. Cellular uptake and lysosomal hydrolysis of the cholesteryl esters were also required, as Indicated by the finding that stimulation of cholesteryl ester formation was prevented by the lysosomal inhibitor, chloroqulne. The cholesterol esterlflcation-stlmulatlng activity of the aortic extracts was excluded on a 2% agarose column and floated In the density range of 1.006 to 1.063 g/ml. Cholesterol-rich extracts from human adrenal glands and liver did not stimulate cholesteryl ester formation In macrophages. The aortic extracts did not stimulate cholesteryl ester synthesis In human fibroblasts. Complexes of 126l-labeled albumin and cholesteryl llnoleate formed In vitro were taken up and degraded in macrophages, but not in fibroblasts, by a process resembling the uptake of the aortic extracts. The current data suggest that macrophages express mechanisms for internalizing certain types of cholesteryl ester-rich lipid/protein complexes, Including those present In atherosclerotic plaques. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Stimulation of Cholesteryl Ester Synthesis in Macrophages by Extracts of Atherosclerotic Human Aortas and Complexes of Albumin/Cholesteryl Esters

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Copyright
© 1981 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

Cholesteryl ester-rich particles extracted from human atherosclerotic plaques were shown to increase the rate of incorporation of [14C]oleate into cholesteryl [14C]oleate and to cause massive accumulation of cholesteryl esters in monolayers of mouse peritoneal macrophages. This stimulation showed saturation kinetics and susceptibility to competition by polyanions (polylnosinic acid, fucoidin, dextran sulfate), suggesting that cell surface binding was required. Cellular uptake and lysosomal hydrolysis of the cholesteryl esters were also required, as Indicated by the finding that stimulation of cholesteryl ester formation was prevented by the lysosomal inhibitor, chloroqulne. The cholesterol esterlflcation-stlmulatlng activity of the aortic extracts was excluded on a 2% agarose column and floated In the density range of 1.006 to 1.063 g/ml. Cholesterol-rich extracts from human adrenal glands and liver did not stimulate cholesteryl ester formation In macrophages. The aortic extracts did not stimulate cholesteryl ester synthesis In human fibroblasts. Complexes of 126l-labeled albumin and cholesteryl llnoleate formed In vitro were taken up and degraded in macrophages, but not in fibroblasts, by a process resembling the uptake of the aortic extracts. The current data suggest that macrophages express mechanisms for internalizing certain types of cholesteryl ester-rich lipid/protein complexes, Including those present In atherosclerotic plaques.

Journal

ArteriosclerosisWolters Kluwer Health

Published: May 1, 1981

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