Quantifying Cellular Cholesterol Efflux

2019 ◽  
pp. 111-133 ◽  
Author(s):  
Sabrina Robichaud ◽  
Mireille Ouimet
Keyword(s):  
Cholesterol Efflux ◽  
Cellular Cholesterol ◽  
Cellular Cholesterol Efflux

scholarly journals Cellular cholesterol efflux is modulated by phospholipid-derived signaling molecules in familial HDL deficiency/Tangier disease fibroblasts

2001 ◽  
Vol 42 (2) ◽  
pp. 249-257 ◽  
Author(s):  
Bassam Haidar ◽  
Stephanie Mott ◽  
Betsie Boucher ◽  
Ching Yin Lee ◽  
Michel Marcil ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Signaling Molecules ◽  
Tangier Disease ◽  
Cellular Cholesterol ◽  
Cellular Cholesterol Efflux

Decreased cellular cholesterol efflux is a common cause of familial hypoalphalipoproteinemia: role of the ABCA1 gene mutations

2000 ◽  
Vol 152 (2) ◽  
pp. 457-468 ◽  
Author(s):  
Stephanie Mott ◽  
Lu Yu ◽  
Michel Marcil ◽  
Betsie Boucher ◽  
Colette Rondeau ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Gene Mutations ◽  
Cellular Cholesterol ◽  
Common Cause ◽  
Abca1 Gene ◽  
Cellular Cholesterol Efflux

scholarly journals Serum Amyloid A Promotes Cholesterol Efflux Mediated by Scavenger Receptor B-I

2005 ◽  
Vol 280 (43) ◽  
pp. 35890-35895 ◽  
Author(s):  
Deneys R. van der Westhuyzen ◽  
Lei Cai ◽  
Maria C. de Beer ◽  
Frederick C. de Beer
Keyword(s):  
Acute Phase ◽  
Cholesterol Efflux ◽  
Serum Amyloid A ◽  
Acute Phase Protein ◽  
Scavenger Receptor ◽  
Dependent Manner ◽  
Cellular Cholesterol ◽  
Amyloid A ◽  
Phase Protein ◽  
Cellular Cholesterol Efflux

Serum amyloid A (SAA) is an acute phase protein whose expression is markedly up-regulated during inflammation and infection. The physiological function of SAA is unclear. In this study, we reported that SAA promotes cellular cholesterol efflux mediated by scavenger receptor B-I (SR-BI). In Chinese hamster ovary cells, SAA promoted cellular cholesterol efflux in an SR-BI-dependent manner, whereas apoA-I did not. Similarly, SAA, but not apoA-I, promoted cholesterol efflux from HepG2 cells in an SR-BI-dependent manner as shown by using the SR-BI inhibitor BLT-1. When SAA was overexpressed in HepG2 cells using adenovirus-mediated gene transfer, the endogenously expressed SAA promoted SR-BI-dependent efflux. To assess the effect of SAA on SR-BI-mediated efflux to high density lipoprotein (HDL), we compared normal HDL, acute phase HDL (AP-HDL, prepared from mice injected with lipopolysaccharide), and AdSAA-HDL (HDL prepared from mice overexpressing SAA). Both AP-HDL and AdSAA-HDL promoted 2-fold greater cholesterol efflux than normal HDL. Lipid-free SAA was shown to also stimulate ABCA1-dependent cholesterol efflux in fibroblasts, in line with an earlier report (Stonik, J. A., Remaley, A. T., Demosky, S. J., Neufeld, E. B., Bocharov, A., and Brewer, H. B. (2004) Biochem. Biophys. Res. Commun. 321, 936–941). When added to cells together, SAA and HDL exerted a synergistic effect in promoting ABCA1-dependent efflux, suggesting that SAA may remodel HDL in a manner that releases apoA-I or other efficient ABCA1 ligands from HDL. SAA also facilitated efflux by a process that was independent of SR-BI and ABCA1. We conclude that the acute phase protein SAA plays an important role in HDL cholesterol metabolism by promoting cellular cholesterol efflux through a number of different efflux pathways.

scholarly journals Fibroblast cholesterol efflux to plasma from metabolic syndrome subjects is not defective despite low high-density lipoprotein cholesterol

2008 ◽  
Vol 158 (1) ◽  
pp. 53-60 ◽  
Author(s):  
Robin P F Dullaart ◽  
Albert K Groen ◽  
Geesje M Dallinga-Thie ◽  
Rindert de Vries ◽  
Wim J Sluiter ◽  
...  
Keyword(s):  
Metabolic Syndrome ◽  
High Density Lipoprotein ◽  
Cholesterol Efflux ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
Cholesterol Esterification ◽  
Cellular Cholesterol ◽  
Apo E ◽  
Pltp Activity ◽  
Cellular Cholesterol Efflux

ObjectiveWe tested whether in metabolic syndrome (MetS) subjects the ability of plasma to stimulate cellular cholesterol efflux, an early step in the anti-atherogenic reverse cholesterol transport pathway, is maintained despite low high-density lipoprotein (HDL) cholesterol.DesignIn 76 subjects with and 94 subjects without MetS based on the National Cholesterol Education Program Adult Treatment Panel III (NCEP ATP III) criteria, we determined plasma (apo)lipoproteins, pre-β-HDL formation, phospholipid transfer protein (PLTP) activity, cholesterol esterification (EST), cholesteryl ester transfer (CET), adiponectin, and the ability of plasma from each subject to stimulate cholesterol efflux out of cultured fibroblasts obtained from a single donor.ResultsApo E, PLTP activity, EST, and CET were higher (P=0.04 to <0.001), whereas adiponectin was lower in MetS subjects (P<0.01). Pre-β-HDL and pre-β-HDL formation were not different between subjects with and without MetS. Cellular cholesterol efflux to plasma from MetS subjects was slightly higher versus plasma from subjects without MetS (8.8±1.0 vs 8.5±0.9%,P=0.05), but the difference was not significant after age, sex, and diabetes adjustment. Cellular cholesterol efflux was positively related to pre-β-HDL formation, EST, PLTP activity, and apo E (P<0.05 for all by multiple linear regression analysis), without an independent association with MetS and diabetes status.ConclusionsThe ability of plasma from MetS subjects to promote fibroblast cholesterol efflux is not defective, although HDL cholesterol is decreased. Higher cholesterol esterification, PLTP activity, and apo E levels may contribute to the maintenance of cholesterol efflux in MetS.

Increased postprandial plasma capacity of cellular cholesterol efflux in normolipidemic subjects

1999 ◽  
Vol 144 ◽  
pp. 41
Author(s):  
C. Senault ◽  
B. Le Roy ◽  
D.F. Sayed ◽  
A. Thaminy ◽  
F. Mendy ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Cellular Cholesterol ◽  
Cellular Cholesterol Efflux
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