Apolipoprotein-mediated removal of cellular cholesterol and phospholipids

Oram, John F.; Yokoyama, Shinji

doi:10.1016/s0022-2275(20)37453-8

Cited by 318 publications

(51 citation statements)

References 153 publications

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“…Considerable interest has been focused recently on the ability of lipid-free or lipid-poor apolipoproteins to partic-ipate in the process of cell cholesterol efflux (3,15,16). Studies have demonstrated the presence of essentially lipid-free apolipoproteins in serum (17)(18)(19).…”

Section: Lipid-free/lipid-poor Apolipoproteinsmentioning

confidence: 99%

“…Among the most responsive cells are macrophages (29,62) whereas smooth muscle cells are among the most resistant cells (63). Thus, exposure of macrophages, CHO cells, L-cells, and fibroblasts to apoA-I, apoA-II, apoE, or apoA-IV results in the release of both cellular cholesterol and cellular phospholipid (3,27,29,64). In most systems the efflux of cell cholesterol is closely paralleled by the release of phospholipid.…”

Section: Observation 6: Lipid-free Apolipoproteins Can Stimulate the Efflux Of Cellular Cholesterol And Phospholipidmentioning

confidence: 99%

“…This model will focus only on the steps thought to be involved in the movement of free cholesterol (FC) molecules between the plasma membrane and extracellular acceptors. The movement of cholesterol between intracellular sites and the plasma membrane will not be addressed in any detail, and the reader is referred to a number of recent reviews on this important subject (3,4).…”

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confidence: 99%

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Cell cholesterol efflux: integration of old and new observations provides new insights

Rothblat

Llera-Moya

Atger

et al. 1999

Journal of Lipid Research

443

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Numerous studies using a variety of cell/acceptor combinations have demonstrated differences in cholesterol efflux among cells. These studies also show that different acceptors, ranging from simple molecules like cyclodextrins to serum, stimulate efflux through a variety of mechanisms. By combining early observations with data derived from recent studies, it is now possible to formulate a model for cell cholesterol efflux which proposes that an array of different mechanisms, including aqueous diffusion, lipid-free apolipoprotein membrane microsolubilization, and SR-BI-mediated cholesterol exchange contribute to cholesterol flux. In this model the relative importance of each mechanism would be determined both by the cell type and the nature of the extracellular cholesterol acceptor. -Rothblat, G.

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Section: Lipid-free/lipid-poor Apolipoproteinsmentioning

confidence: 99%

Section: Observation 6: Lipid-free Apolipoproteins Can Stimulate the Efflux Of Cellular Cholesterol And Phospholipidmentioning

confidence: 99%

mentioning

confidence: 99%

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Cell cholesterol efflux: integration of old and new observations provides new insights

Rothblat

Llera-Moya

Atger

et al. 1999

Journal of Lipid Research

443

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“…[1][2][3] The primary antiatherogenic function of HDL was suggested to play a key role in reverse cholesterol transport by mobilizing cholesterol from the peripheral cells to the liver for elimination in the bile. 4,5 The ATP-binding cassette transporter A1 (ABCA1) mediates the rate-controlling step in HDL particle formation and in the assembly of free cholesterol and phospholipids with lipid-poor apolipoprotein A-I (apoA-I). 6 Mutations in ABCA1 can cause an autosomal recessive genetic disorder called Tangier disease, which is characterized by the absence of HDL and premature atherosclerosis.…”

Section: Introductionmentioning

confidence: 99%

Identification of Upregulators of Human ATP-Binding Cassette Transporter A1 via High-Throughput Screening of a Synthetic and Natural Compound Library

et al. 2008

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“…Once the sterol leaves the peripheral cells, the pathways involved in its delivery to the liver are better understood and are also shown in Fig. 1 (for reviews see references [11][12][13][14]. The unesterified cholesterol is probably taken up from the plasma membrane by a lipid-poor high density lipoprotein (HDL) containing apolipoprotein A-I (apoA-I) with pre-␤ -mobility (15), although an alternative lipoprotein acceptor containing only apolipoprotein E (apoE) ( ␥ -LpE) has also been described (16).…”

mentioning

confidence: 99%

Centripetal cholesterol flux to the liver is dictated by events in the peripheral organs and not by the plasma high density lipoprotein or apolipoprotein A-I concentration

Jolley

Woollett

Turley

et al. 1998

Journal of Lipid Research

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The major net flux of cholesterol in the intact animal or human is from the peripheral organs to the liver. This flux is made up of cholesterol that is either synthesized in these peripheral tissues or taken up as lipoprotein cholesterol. This study investigates whether it is the concentration of apolipoprotein (apo) A-I or high density lipoprotein in the plasma that determines the magnitude of this flux or, alternatively, whether events within the peripheral cells themselves regulate this important process. In mice that lack apoA-I and have very low concentrations of circulating high density lipoprotein, it was found that there was no accumulation of cholesterol in any peripheral organ so that the mean sterol concentration in these tissues was the same (2208 ؎ 29 mg/kg body weight) as in control mice (2176 ؎ 50 mg/kg). Furthermore, by measuring the rates of net cholesterol acquisition in the peripheral organs from de novo synthesis and uptake of low density lipoprotein, it was demonstrated that the magnitude of centripetal sterol movement from the peripheral organs to the liver was virtually identical in control animals (78 ؎ 5 mg/day per kg) and in those lacking apoA-I (72 ؎ 4 mg/day per kg). These studies indicate that the magnitude of net sterol flux through the body is not related to the concentration of high density lipoprotein or apolipoprotein A-I in the plasma, but is probably determined by intracellular processes in the peripheral organs that dictate the rate of movement of cholesterol from the endoplasmic reticulum to the plasma membrane.-Jolley, C. D., L. A. Woollett, S. D. Turley, and J. M. Dietschy. Centripetal cholesterol flux to the liver is dictated by events in the peripheral organs and not by the plasma high density lipoprotein or apolipoprotein A-I concentration.

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Apolipoprotein-mediated removal of cellular cholesterol and phospholipids

Cited by 318 publications

References 153 publications

Cell cholesterol efflux: integration of old and new observations provides new insights

Cell cholesterol efflux: integration of old and new observations provides new insights

Identification of Upregulators of Human ATP-Binding Cassette Transporter A1 via High-Throughput Screening of a Synthetic and Natural Compound Library

Centripetal cholesterol flux to the liver is dictated by events in the peripheral organs and not by the plasma high density lipoprotein or apolipoprotein A-I concentration

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