Role of the plasma membrane in the mechanism of cholesterol efflux from cells

Bellini, F.; Phillips, Michael C.; Pickell, C.; Rothblat, George H.

doi:10.1016/0005-2736(84)90422-x

Cited by 46 publications

(17 citation statements)

References 29 publications

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“…However, the rate of cholesterol release varies significantly among different cell types (9,33,42). This may be for several reasons, such as variability in the fluidity or cholesterol content of the plasma membrane (43), in the thickness or composition of the extracellular matrix, which might prevent the access of cholesterol acceptors to the plasma membrane, or in different expression levels of a lipoprotein receptor, such as SR-BI (44), in the plasma membranes of different cell types.…”

Section: Discussionmentioning

confidence: 97%

Scavenger Receptor Class B Type I as a Mediator of Cellular Cholesterol Efflux to Lipoproteins and Phospholipid Acceptors

Jiang¹,

Llera-Moya²,

Ji³

et al. 1998

Journal of Biological Chemistry

275

220

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We recently reported that the rate of efflux of cholesterol from cells to high density lipoprotein (HDL) was related to the expression level of scavenger receptor class B type I (SR-BI). Moreover, the expression of this receptor in atheromatous arteries raises the possibility that SR-BI mediates cholesterol efflux in the arterial wall (Ji, Y., Jian, B., Wang, N., Sun, Y., de la Llera Moya, M., Phillips, M. C., Rothblat, G. H., Swaney, J. B., and Tall, A. R. (1997) J. Biol. Chem. 272, 20982-20985). In this paper we describe studies that suggest that the presence of phospholipid on acceptor particles plays an important role in modulating interaction with the SR-BI. Specifically, enrichment of serum with phospholipid resulted in marked stimulation of cholesterol efflux from cells that had higher levels of SR-BI expression, like Fu5AH or Y1-BS1 cells, and little or no stimulation in cells with low SR-BI levels, such as Y-1 cells. Stimulation of efflux by phospholipid enrichment was also a function of SR-BI levels in Chinese hamster ovary cells transfected with the SR-BI gene. Efflux to protein-free vesicles prepared with 1-palmitoyl-2-oleoylphosphatidyl-choline also correlated with SR-BI levels, suggesting that phospholipid, as well as protein, influences the interaction that results in cholesterol efflux. By contrast, cholesterol efflux from a non-cell donor showed no stimulation consequent to phospholipid enrichment of the serum acceptor. These results may help to explain observations in the literature that document an increased risk of atherosclerosis in patients with depressed levels of HDL phospholipid even in the face of normal HDL cholesterol levels.

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Section: Discussionmentioning

confidence: 97%

Scavenger Receptor Class B Type I as a Mediator of Cellular Cholesterol Efflux to Lipoproteins and Phospholipid Acceptors

Jiang¹,

Llera-Moya²,

Ji³

et al. 1998

Journal of Biological Chemistry

275

220

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“…Cells were treated with 10 n m mifepristone to express ABCA1 and incubated with apoA-I (10 μg/ml) to induce lipid efflux and formation of nascent HDL particles (7, 12). Plasma membrane vesicles were produced by incubating the cells with 50 m m formaldehyde and 2 m m dithiothreitol for 90 min (13). Detergent-free plasma membrane lipid raft and non-raft domains were obtained from cell lysates by flotation in an OptiPrep gradient (14).…”

Section: Methodsmentioning

confidence: 99%

Mechanisms Responsible for the Compositional Heterogeneity of Nascent High Density Lipoprotein

Lund‐Katz

Lyssenko

Nickel

et al. 2013

Journal of Biological Chemistry

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Background: The molecular basis for heterogeneity in nascent HDL particle cholesterol content is unknown.Results: Apolipoprotein A-I-mediated solubilization of phospholipid/cholesterol membranes creates large cholesterol-rich and small cholesterol-poor HDL particles.Conclusion: Variations in cholesterol distribution between nanoscale HDL discs are due to particle size-dependent molecular packing constraints.Significance: This explains the origin of HDL particles with different cholesterol contents.

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“…It is remarkable that the cell can redistribute such a marked amount of its cholesterol from the cell surface and still remain apparently viable over a long period of time in serum-free medium. cellular acceptors is known to be cell-specific and dependent on the protein composition of the membranes (Bellini et al, 1984). A similar difference in membrane protein composition of the endoleaflet of the plasma membrane may exist for the two different cell types.…”

Section: Discussionmentioning

confidence: 99%

Reversible effects of sphingomyelin degradation on cholesterol distribution and metabolism in fibroblasts and transformed neuroblastoma cells

Pörn

Slotte

1990

Biochemical Journal

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Plasma-membrane sphingomyelin appears to be one of the major determinants of the preferential allocation of cell cholesterol into the plasma-membrane compartment, since removal of sphingomyelin leads to a dramatic redistribution of cholesterol within the cell [Slotte & Bierman (1988) Biochem. J. 250, 653-658]. In the present study we examined the long-term effects of sphingomyelin degradation on cholesterol redistribution in cells and determined the reversibility of the process. In a human lung fibroblast-cell line, removal of 80 % of the sphingomyelin led to a rapid and transient upregulation (3-fold) of acyl-CoA cholesterol acyltransferase (ACAT) activity, and also, within 30 h, to the translocation of about 50 % of the cell non-esterified cholesterol from a cholesterol oxidase-susceptible compartment (i.e. the cell surface) to oxidase-resistant compartments. At 49 h after the initial sphingomyelin degradation, the cell sphingomyelin level was back to 45 % of the control level, and the direction of cell cholesterol flow was toward the cell surface, although the original distribution was not achieved. In a transformed neuroblastoma cell line (SH-SY5Y), the depletion of sphingomyelin led to a similarly rapid and transient up-regulation of ACAT activity, and to the translocation of about 25 % of cell-surface cholesterol into internal membranes (within 3 h). The flow of cholesterol back to the cholesterol oxidase-susceptible pool was rapid, and a pretreatment cholesterol distribution was reached within 20-49 h. Also, the resynthesis of sphingomyelin was faster in SH-SY5Y neuroblastoma cells and reached control levels within 24 h. The findings of the present study show that the cellular redistribution of cholesterol, as induced by sphingomyelin degradation, is reversible and suggest that the normalization of cellular cholesterol distribution is linked to the re-synthesis of sphingomyelin.

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Role of the plasma membrane in the mechanism of cholesterol efflux from cells

Cited by 46 publications

References 29 publications

Scavenger Receptor Class B Type I as a Mediator of Cellular Cholesterol Efflux to Lipoproteins and Phospholipid Acceptors

Scavenger Receptor Class B Type I as a Mediator of Cellular Cholesterol Efflux to Lipoproteins and Phospholipid Acceptors

Mechanisms Responsible for the Compositional Heterogeneity of Nascent High Density Lipoprotein

Reversible effects of sphingomyelin degradation on cholesterol distribution and metabolism in fibroblasts and transformed neuroblastoma cells

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