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Modulating Effects of Canine High Density Lipoproteins on Cholesteryl Ester Synthesis Induced by B‐Very Low Density Lipoproteins in Macrophages Possible In Vitro Correlates with Atherosclerosis

Modulating Effects of Canine High Density Lipoproteins on Cholesteryl Ester Synthesis Induced by... We have previously observed that cholesterol-fed dogs with plasma cholesterol levels of 350 to 750 mg/dl failed to develop atherosclerosis (hyporesponders), whereas cholesterol-fed dogs with cholesterol levels greater than 750 mg/dl developed markedly accelerated atherosclerosis (hyperresponders). Two striking features of the hypercholesterolemia of the hyperresponders were the occurrence of cholesteryl ester-rich, β-mlgrating very low density llpoproteins (β-VLDL) In the d < 1.006 fraction and a decrease in plasma concentration of typical high density llpoproteins (HDL). Cholesterol-induced β-VLDL have been shown to cause massive accumulations of cholesteryl esters in mouse peritoneal macrophages in vitro, and HDL have been shown to remove cholesterol from these cells. In the present study, the mouse peritoneal macrophage system was used to explore the effects of high levels of cholesterol-Induced d < 1.006 llpoproteins and low levels of HDL In mediating cholesteryl ester synthesis and accumulation In these cells. It was found that the d < 1.006 lipoproteins from both the atherosclerotic hyperresponders and the nonatherosclerotlc hyporesponders stimulated cholesteryl [ http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Modulating Effects of Canine High Density Lipoproteins on Cholesteryl Ester Synthesis Induced by B‐Very Low Density Lipoproteins in Macrophages Possible In Vitro Correlates with Atherosclerosis

Arteriosclerosis , Volume 2 (2) – Mar 1, 1982

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Copyright
© 1982 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

We have previously observed that cholesterol-fed dogs with plasma cholesterol levels of 350 to 750 mg/dl failed to develop atherosclerosis (hyporesponders), whereas cholesterol-fed dogs with cholesterol levels greater than 750 mg/dl developed markedly accelerated atherosclerosis (hyperresponders). Two striking features of the hypercholesterolemia of the hyperresponders were the occurrence of cholesteryl ester-rich, β-mlgrating very low density llpoproteins (β-VLDL) In the d < 1.006 fraction and a decrease in plasma concentration of typical high density llpoproteins (HDL). Cholesterol-induced β-VLDL have been shown to cause massive accumulations of cholesteryl esters in mouse peritoneal macrophages in vitro, and HDL have been shown to remove cholesterol from these cells. In the present study, the mouse peritoneal macrophage system was used to explore the effects of high levels of cholesterol-Induced d < 1.006 llpoproteins and low levels of HDL In mediating cholesteryl ester synthesis and accumulation In these cells. It was found that the d < 1.006 lipoproteins from both the atherosclerotic hyperresponders and the nonatherosclerotlc hyporesponders stimulated cholesteryl [

Journal

ArteriosclerosisWolters Kluwer Health

Published: Mar 1, 1982

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