Reverse Cholesterol Transport

Hoeg, Jeffrey M.; Remaley, Alan T.

doi:10.1007/978-94-011-1130-0_25

Cited by 5 publications

(4 citation statements)

References 130 publications

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“…Excess cholesterol in peripheral cells is returned to the liver for excretion by a process referred to as reverse cholesterol transport (1,2). Defects in this pathway lead to an accumulation of cholesterol in peripheral cells, and the accelerated development of atherosclerosis.…”

mentioning

confidence: 99%

Apolipoprotein Specificity for Lipid Efflux by the Human ABCAI Transporter

Remaley

Stonik

Demosky

et al. 2001

Biochemical and Biophysical Research Communications

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307

223

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mentioning

confidence: 99%

Apolipoprotein Specificity for Lipid Efflux by the Human ABCAI Transporter

Remaley

Stonik

Demosky

et al. 2001

Biochemical and Biophysical Research Communications

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307

223

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“…This process, termed reverse cholesterol transport (4), was proposed to facilitate the removal of cholesterol from the body. Thus reverse cholesterol transport is one of several proposed mechanisms by which HDL provides protection from cardiovascular disease (5)(6)(7)(8)(9)(10).…”

mentioning

confidence: 99%

Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis.

Hoeg

Santamarina-Fojo

Bérard

et al. 1996

Proc. Natl. Acad. Sci. U.S.A.

217

121

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Lecithin:cholesterol acyltransferase (LCAT) is a key plasma enzyme in cholesterol and high density lipoprotein (HDL) metabolism. Transgenic rabbits overexpressing human LCAT had 15-fold greater plasma LCAT activity than nontransgenic control rabbits. This degree of overexpression was associated with a 6.7-fold increase in the plasma HDL cholesterol concentration in LCAT transgenic rabbits. On a 0.3% cholesterol diet, the HDL cholesterol concentrations increased from 24 ± 1 to 39 + 3 mg/dl in nontransgenic control rabbits (n = 10; P < 0.05) and increased from 161 + 5 to 200 ± 21 mg/dl (P < 0.001) in the LCAT transgenic rabbits (n = 9). Although the baseline non-HDL concentrations of control (4 ± 3 mg/dl) and transgenic rabbits (18 ± 4 mg/dl) were similar, the cholesterol-rich diet raised the non-HDL cholesterol concentrations, reflecting the atherogenic very low density, intermediate density, and low density lipoprotein particles observed by gel filtration chromatography. The non-HDL cholesterol rose to 509 + 57 mg/dl in controls compared with only 196 ± 14 mg/dl in the LCAT transgenic rabbits (P < 0.005). The differences in the plasma lipoprotein response to a cholesterol-rich diet observed in the transgenic rabbits paralleled the susceptibility to developing aortic atherosclerosis. Compared with nontransgenic controls, LCAT transgenic rabbits were protected from diet-induced atherosclerosis with significant reductions determined by both quantitative planimetry (-86%; P < 0.003) and quantitative immunohistochemistry (-93%; P < 0.009). Our results establish the importance of LCAT in the metabolism of both HDL and apolipoprotein B-containing lipoprotein particles with cholesterol feeding and the response to diet-induced atherosclerosis. In addition, these findings identify LCAT as a new target for therapy to prevent atherosclerosis.

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“…6). Two different mechanisms have been proposed for HDL-mediated cholesterol efflux from cells (9). Cholesterol can desorb from cells into the aqueous compartment and then bind to HDL or to other acceptors in a process referred to as aqueous diffusion (11).…”

Section: Discussionmentioning

confidence: 99%

“…Reverse cholesterol transport is the process whereby cholesterol is removed from peripheral tissues and is delivered to the liver for subsequent excretion into bile (9)(10)(11). High density lipoprotein (HDL) has been proposed to play a protective role in preventing atherosclerosis by being the principal acceptor of cholesterol that effluxes from peripheral cells.…”

mentioning

confidence: 99%

Differential rate of cholesterol efflux from the apical and basolateral membranes of MDCK cells

Remaley

Farsi

Shirali

et al. 1998

Journal of Lipid Research

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Epithelial cells contain two distinct membrane surfaces, the apical and basolateral plasma membranes, which have different lipid and protein compositions. In order to assess the effect of the compositional differences of the apical and basolateral membranes on their ability to undergo cholesterol efflux, MDCK cells were radiolabeled with [ 3 H]cholesterol and grown as a polarized monolayer on filter inserts, that separate the upper apical compartment from the lower basolateral compartment. The rate of cholesterol efflux from the basolateral membrane into media containing HDL in the basolateral compartment was 6.3%/h Ϯ 0.7, whereas HDL-mediated efflux from the apical membrane was approximately 3-fold slower (1.9%/h Ϯ 0.3). In contrast, Fu5AH cells, which do not form distinct polarized membrane domains, had a similar rate of HDLmediated cholesterol efflux into the apical and basolateral compartments. Similar to HDL, other cholesterol acceptors, namely LDL, bovine serum albumin, and a lipid emulsion, also showed a decreased rate of cholesterol efflux from the apical membrane surface versus the basolateral membrane. Compared to the basolateral membrane, the apical membrane was also found to be more resistant to cholesterol oxidase treatment, to bind less HDL, and to take up less cholesterol from the medium. In conclusion, cholesterol efflux occurred less readily from the apical membrane than from the basolateral membrane for all types of acceptors tested. These results suggest that differences in the composition of the apical and basolateral membrane lead to a relative decrease in cholesterol desorption from the apical membrane and hence a reduced rate of cholesterol efflux.-

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Reverse Cholesterol Transport

Cited by 5 publications

References 130 publications

Apolipoprotein Specificity for Lipid Efflux by the Human ABCAI Transporter

Apolipoprotein Specificity for Lipid Efflux by the Human ABCAI Transporter

Overexpression of lecithin:cholesterol acyltransferase in transgenic rabbits prevents diet-induced atherosclerosis.

Differential rate of cholesterol efflux from the apical and basolateral membranes of MDCK cells

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