Cholesterol efflux from normal and Tangier disease fibroblasts into normal, high-density lipoprotein-deficient, and apolipoprotein E-deficient plasmas

Metabolism ◽  
2000 ◽  
Vol 49 (6) ◽  
pp. 770-777 ◽  
Author(s):  
S. Schuler-Lüttmann ◽  
Y. Zhu ◽  
M. Hoffmann ◽  
W. März ◽  
G. Feussner ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Apolipoprotein E ◽  
Cholesterol Efflux ◽  
Density Lipoprotein ◽  
High Density ◽  
Tangier Disease

Cholesterol efflux regulatory protein, Tangier disease and familial high-density lipoprotein deficiency

2000 ◽  
Vol 11 (2) ◽  
pp. 117-122 ◽  
Author(s):  
Michael R. Hayden ◽  
Susanne M. Clee ◽  
Angela Brooks-Wilson ◽  
Jacques Genest ◽  
Alan Attie ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Cholesterol Efflux ◽  
Regulatory Protein ◽  
Density Lipoprotein ◽  
High Density ◽  
Tangier Disease

Characterization of the cholesterol efflux of apolipoprotein E-containing high-density lipoprotein in THP-1 cells

2019 ◽  
Vol 400 (2) ◽  
pp. 209-218 ◽  
Author(s):  
Yuna Horiuchi ◽  
Ryunosuke Ohkawa ◽  
Shao-Jui Lai ◽  
Azusa Yamazaki ◽  
Hayato Ikoma ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Apolipoprotein E ◽  
Cholesterol Efflux ◽  
Density Lipoprotein ◽  
High Density ◽  
Response To Treatment ◽  
Atp Binding Cassette Transporter ◽  
A Minor

Abstract High-density lipoprotein (HDL), also known as antiatherogenic lipoprotein, consists of heterogeneous particles in terms of size, density and composition, suggesting differences among HDL subclasses in characteristics and functions. We investigated the role of apolipoprotein E (apoE)-containing HDL, a minor HDL subclass, in the cholesterol efflux capacity (CEC) of HDL, which is its predominant atheroprotective function. The CEC of apoE-containing HDL was similar to that of apoE-deficient HDL, but the former exhibited a greater rate increase (1.48-fold) compared to that of the latter (1.10-fold) by the stimulation of THP-1 macrophages with the Liver X Receptor (LXR) agonist. No difference in CEC was observed without the LXR agonist between apoA-I, the main apolipoprotein in HDL, and apoE, whereas the increase in CEC in response to treatment with the LXR agonist was greater for apoA-I (4.25-fold) than for apoE (2.22-fold). Furthermore, the increase in the CEC of apoE-containing HDL induced by the LXR agonist was significantly reduced by treatment with glyburide, an inhibitor of ATP-binding cassette transporter A1 (ABCA1). These results suggest that apoE-containing HDL, unlike apoE-deficient HDL, is involved in cholesterol efflux via ABCA1.

scholarly journals High Density Lipoprotein Cholesterol Efflux Capacity and Atherosclerosis in Cardiovascular Disease: Pathophysiological Aspects and Pharmacological Perspectives

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 574
Author(s):  
Maria Pia Adorni ◽  
Nicoletta Ronda ◽  
Franco Bernini ◽  
Francesca Zimetti
Keyword(s):  
High Density Lipoprotein ◽  
Cholesterol Efflux ◽  
Current Knowledge ◽  
Density Lipoprotein ◽  
Hdl Cholesterol ◽  
High Density ◽  
Current Evidence ◽  
Endocrine Disorders ◽  
Lifestyle Modifications ◽  
Cholesterol Efflux Capacity

Over the years, the relationship between high-density lipoprotein (HDL) and atherosclerosis, initially highlighted by the Framingham study, has been revealed to be extremely complex, due to the multiple HDL functions involved in atheroprotection. Among them, HDL cholesterol efflux capacity (CEC), the ability of HDL to promote cell cholesterol efflux from cells, has emerged as a better predictor of cardiovascular (CV) risk compared to merely plasma HDL-cholesterol (HDL-C) levels. HDL CEC is impaired in many genetic and pathological conditions associated to high CV risk such as dyslipidemia, chronic kidney disease, diabetes, inflammatory and autoimmune diseases, endocrine disorders, etc. The present review describes the current knowledge on HDL CEC modifications in these conditions, focusing on the most recent human studies and on genetic and pathophysiologic aspects. In addition, the most relevant strategies possibly modulating HDL CEC, including lifestyle modifications, as well as nutraceutical and pharmacological interventions, will be discussed. The objective of this review is to help understanding whether, from the current evidence, HDL CEC may be considered as a valid biomarker of CV risk and a potential pharmacological target for novel therapeutic approaches.

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