scholarly journals The Establishment of Telomerase-immortalized Tangier Disease Cell Lines Indicates the Existence of an Apolipoprotein A-I-inducible but ABCA1-independent Cholesterol Efflux Pathway

2004 ◽  
Vol 279 (20) ◽  
pp. 20866-20873 ◽  
Author(s):  
Michael Walter ◽  
Nicholas R. Forsyth ◽  
Woodring E. Wright ◽  
Jerry W. Shay ◽  
Michael G. Roth
Keyword(s):  
Cell Lines ◽  
Cholesterol Efflux ◽  
Tangier Disease ◽  
Apolipoprotein A ◽  
Efflux Pathway ◽  
Disease Cell

scholarly journals Cholesterol Efflux-Independent Modification of Lipid Rafts by AIBP (Apolipoprotein A-I Binding Protein)

2020 ◽  
Vol 40 (10) ◽  
pp. 2346-2359
Author(s):  
Hann Low ◽  
Nigora Mukhamedova ◽  
Luciano dos Santos Aggum Capettini ◽  
Yining Xia ◽  
Irena Carmichael ◽  
...  
Keyword(s):  
Lipid Rafts ◽  
Nicotinamide Adenine Dinucleotide ◽  
Metabolic Pathways ◽  
Cholesterol Efflux ◽  
Binding Protein ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Underlying Mechanism ◽  
Atp Binding Cassette Transporter ◽  
Apolipoprotein A ◽  
Phosphatidylinositol 3

Objective: AIBP (apolipoprotein A-I binding protein) is an effective and selective regulator of lipid rafts modulating many metabolic pathways originating from the rafts, including inflammation. The mechanism of action was suggested to involve stimulation by AIBP of cholesterol efflux, depleting rafts of cholesterol, which is essential for lipid raft integrity. Here we describe a different mechanism contributing to the regulation of lipid rafts by AIBP. Approach and Results: We demonstrate that modulation of rafts by AIBP may not exclusively depend on the rate of cholesterol efflux or presence of the key regulator of the efflux, ABCA1 (ATP-binding cassette transporter A-I). AIBP interacted with phosphatidylinositol 3-phosphate, which was associated with increased abundance and activation of Cdc42 and rearrangement of the actin cytoskeleton. Cytoskeleton rearrangement was accompanied with reduction of the abundance of lipid rafts, without significant changes in the lipid composition of the rafts. The interaction of AIBP with phosphatidylinositol 3-phosphate was blocked by AIBP substrate, NADPH (nicotinamide adenine dinucleotide phosphate), and both NADPH and silencing of Cdc42 interfered with the ability of AIBP to regulate lipid rafts and cholesterol efflux. Conclusions: Our findings indicate that an underlying mechanism of regulation of lipid rafts by AIBP involves PIP-dependent rearrangement of the cytoskeleton.

scholarly journals Plasma and fibroblasts of Tangier disease patients are disturbed in transferring phospholipids onto apolipoprotein A-I

1998 ◽  
Vol 39 (5) ◽  
pp. 987-998 ◽  
Author(s):  
Arnold von Eckardstein ◽  
Ali Chirazi ◽  
Susanne Schuler-Lüttmann ◽  
Michael Walter ◽  
John J.P. Kastelein ◽  
...  
Keyword(s):  
Tangier Disease ◽  
Apolipoprotein A

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

scholarly journals Lipoprotein Lipase Regulates Microglial Lipid Droplet Accumulation

Cells ◽  
2021 ◽  
Vol 10 (2) ◽  
pp. 198
Author(s):  
Bailey A. Loving ◽  
Maoping Tang ◽  
Mikaela C. Neal ◽  
Sachi Gorkhali ◽  
Robert Murphy ◽  
...  
Keyword(s):  
Lipoprotein Lipase ◽  
Cholesterol Efflux ◽  
Acid Oxidation ◽  
Lipid Uptake ◽  
Expression Of Genes ◽  
Ppar Signaling ◽  
Ppar Agonists ◽  
Inflammatory State ◽  
Excessive Secretion ◽  
Efflux Pathway

Microglia become increasingly dysfunctional with aging and contribute to the onset of neurodegenerative disease (NDs) through defective phagocytosis, attenuated cholesterol efflux, and excessive secretion of pro-inflammatory cytokines. Dysfunctional microglia also accumulate lipid droplets (LDs); however, the mechanism underlying increased LD load is unknown. We have previously shown that microglia lacking lipoprotein lipase (LPL KD) are polarized to a pro-inflammatory state and have impaired lipid uptake and reduced fatty acid oxidation (FAO). Here, we also show that LPL KD microglia show excessive accumulation of LD-like structures. Moreover, LPL KD microglia display a pro-inflammatory lipidomic profile, increased cholesterol ester (CE) content, and reduced cholesterol efflux at baseline. We also show reduced expression of genes within the canonical cholesterol efflux pathway. Importantly, PPAR agonists (rosiglitazone and bezafibrate) rescued the LD-associated phenotype in LPL KD microglia. These data suggest that microglial-LPL is associated with lipid uptake, which may drive PPAR signaling and cholesterol efflux to prevent inflammatory lipid distribution and LD accumulation. Moreover, PPAR agonists can reverse LD accumulation, and therefore may be beneficial in aging and in the treatment of NDs.

Abstract: P444 TRANS INTESTINAL CHOLESTEROL EFFLUX PATHWAY IS NOT MEDIATED THROUGH HDL

2009 ◽  
Vol 10 (2) ◽  
pp. e754
Author(s):  
C Vrins ◽  
M van Eck ◽  
R Ottenhoff ◽  
P Rensen ◽  
A Groen
Keyword(s):  
Cholesterol Efflux ◽  
Efflux Pathway

Abstract 104: Serum from Patients with Aortic Valvular Stenosis Shows Decreased Cholesterol Efflux Capacities Despite Similar High-Density Lipoprotein Cholesterol Levels

2012 ◽  
Vol 32 (suppl_1) ◽  
Author(s):  
Benoit J Arsenault ◽  
Mathieu R Brodeur ◽  
David Rhainds ◽  
Anne-Elen Kernaleguen ◽  
Véronique Lavoie ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Pearson Correlation ◽  
Hdl Cholesterol ◽  
P Value ◽  
Aortic Valvular Stenosis ◽  
Cholesterol Efflux Capacity ◽  
Cholesterol Levels ◽  
Apolipoprotein A ◽  
Valvular Stenosis ◽  
Jet Velocity

Background: Studies have shown that low HDL-cholesterol levels may be associated with the progression of aortic valvular calcium and aortic valvular stenosis (AVS), but whether patients with AVS have impaired cholesterol efflux capacities is unknown. Methods and results: We have measured four parameters of cholesterol efflux capacity in apolipoprotein B-depleted serum samples from 48 patients with (aortic jet velocity ≥2.5 m/s, mean age = 72 ± 7 years and 72.7% men) and 51 patients without AVS (aortic jet velocity ≤ 1.7 m/s, mean age 71 ± 7 years and 70.6% men). Cholesterol efflux capacity was measured using J774 macrophages with and without stimulation of ABCA1 expression by cAMP (non-stimulated efflux, total efflux and ABCA1-mediated efflux), and HepG2 hepatocytes to measure SR-BI-mediated efflux. Mean HDL-cholesterol and apolipoprotein A-I levels as well as efflux are shown in the table for patients with vs. without AVS. The Pearson correlation coefficient between HDL-cholesterol levels and SR-B1-dependent efflux was 0.39 (p=0.007) in patients with AVS and 0.68 (<0.0001) in controls (P-value for the difference between the correlation coefficients obtained with Fisher’s test = 0.04). Conclusions: This study provides evidence that serum from patients with AVS may have impaired cholesterol efflux capacities, especially through the SR-B1 pathway. Table. Mean HDL-cholesterol and apolipoprotein A-I levels as well as non-stimulated-, total-, ABCA1-, and SR-B1-dependent cholesterol efflux obtained from patients’ serum with vs. without AVS. Data is shown as mean ± SD. Differences between categories were assessed using a Student unpaired t-test.

scholarly journals The Role of Apolipoprotein A-I Helix 10 in Apolipoprotein-mediated Cholesterol Efflux via the ATP-binding Cassette Transporter ABCA1

2002 ◽  
Vol 277 (42) ◽  
pp. 39477-39484 ◽  
Author(s):  
Stacey E. Panagotopulos ◽  
Scott R. Witting ◽  
Erica M. Horace ◽  
David Y. Hui ◽  
J. Nicholas Maiorano ◽  
...  
Keyword(s):  
Cholesterol Efflux ◽  
Atp Binding ◽  
Atp Binding Cassette Transporter ◽  
Apolipoprotein A ◽  
Atp Binding Cassette
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