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Effects of High Density Lipoprotein Subfractions on Cholesterol Homeostasis in Human Fibroblasts and Arterial Smooth Muscle Cells

Effects of High Density Lipoprotein Subfractions on Cholesterol Homeostasis in Human Fibroblasts... Ultracentrifugally isolated high density lipoprotein (HDL) particles of d > 1.125 g/ml promote net transport of cholesterol from cultured cells. Consequently, when cultured human fibroblasts and arterial smooth muscle cells were incubated with HDL3(d = 1.125-1.21 g/ml) and "very high" density lipoprotein (VHDL, d = 1.21-1.25 g/ml), low density lipoprotein (LDL) receptor activity was induced and the rate of LDL degradation by the cells was increased. Enhancement of LDL degradation by HDL3and VHDL was sustained over incubation periods of 5 days at medium LDL concentrations greater than needed to saturate the LDL receptors. Even during these long-term incubations with LDL, HDL3and VHDL caused marked reductions in cellular cholesterol content. Thus, an increase in the rate of cholesterol transport from cells may lead to a steady-state decrease in cellular cholesterol content and a sustained increase in the rate of clearance of LDL from the extracellular fluid. In contrast to the effects of HDL3and VHDL, the major subclasses of HDL2(HDL2b, d = 1.063-1.100 g/ml; HDL2a, d = 1.100-1.125 g/ml) did not promote net cholesterol transport from cells. Moreover, by apparent direct blockage of the effects that HDL3and VHDL had on cholesterol transport, HDL2reversed the increased rate of LDL degradation induced by HDL3and VHDL. These results suggest that the relative proportion of HDL subfractions in the extracellular fluid may be an important determinant of both the rate of cholesterol transport from cells and the rate of receptormediated catabolism of LDL. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Arteriosclerosis Wolters Kluwer Health

Effects of High Density Lipoprotein Subfractions on Cholesterol Homeostasis in Human Fibroblasts and Arterial Smooth Muscle Cells

Arteriosclerosis , Volume 3 (5) – Sep 1, 1983

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Copyright
© 1983 by American Heart Association, Inc.
ISSN
0276-5047

Abstract

Ultracentrifugally isolated high density lipoprotein (HDL) particles of d > 1.125 g/ml promote net transport of cholesterol from cultured cells. Consequently, when cultured human fibroblasts and arterial smooth muscle cells were incubated with HDL3(d = 1.125-1.21 g/ml) and "very high" density lipoprotein (VHDL, d = 1.21-1.25 g/ml), low density lipoprotein (LDL) receptor activity was induced and the rate of LDL degradation by the cells was increased. Enhancement of LDL degradation by HDL3and VHDL was sustained over incubation periods of 5 days at medium LDL concentrations greater than needed to saturate the LDL receptors. Even during these long-term incubations with LDL, HDL3and VHDL caused marked reductions in cellular cholesterol content. Thus, an increase in the rate of cholesterol transport from cells may lead to a steady-state decrease in cellular cholesterol content and a sustained increase in the rate of clearance of LDL from the extracellular fluid. In contrast to the effects of HDL3and VHDL, the major subclasses of HDL2(HDL2b, d = 1.063-1.100 g/ml; HDL2a, d = 1.100-1.125 g/ml) did not promote net cholesterol transport from cells. Moreover, by apparent direct blockage of the effects that HDL3and VHDL had on cholesterol transport, HDL2reversed the increased rate of LDL degradation induced by HDL3and VHDL. These results suggest that the relative proportion of HDL subfractions in the extracellular fluid may be an important determinant of both the rate of cholesterol transport from cells and the rate of receptormediated catabolism of LDL.

Journal

ArteriosclerosisWolters Kluwer Health

Published: Sep 1, 1983

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