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

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

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.

scholarly journals High Density Lipoprotein Biogenesis, Cholesterol Efflux, and Immune Cell Function

2012 ◽  
Vol 32 (11) ◽  
pp. 2561-2565 ◽  
Author(s):  
Mary G. Sorci-Thomas ◽  
Michael J. Thomas
Keyword(s):  
High Density Lipoprotein ◽  
Cholesterol Efflux ◽  
Cell Function ◽  
Immune Cell ◽  
Density Lipoprotein ◽  
High Density ◽  
Immune Cell Function

scholarly journals Synthetic High-Density Lipoprotein (sHDL) Inhibits Steroid Production in HAC15 Adrenal Cells

Endocrinology ◽  
2016 ◽  
Vol 157 (8) ◽  
pp. 3122-3129 ◽  
Author(s):  
Matthew J. Taylor ◽  
Aalok R. Sanjanwala ◽  
Emily E. Morin ◽  
Elizabeth Rowland-Fisher ◽  
Kyle Anderson ◽  
...  
Keyword(s):  
High Density Lipoprotein ◽  
Coenzyme A ◽  
Culture Media ◽  
Regulatory Protein ◽  
Density Lipoprotein ◽  
High Density ◽  
Plaque Burden ◽  
Dependent Manner ◽  
Steroid Production ◽  
Coenzyme A Reductase

High density lipoprotein (HDL) transported cholesterol represents one of the sources of substrate for adrenal steroid production. Synthetic HDL (sHDL) particles represent a new therapeutic option to reduce atherosclerotic plaque burden by increasing cholesterol efflux from macrophage cells. The effects of the sHDL particles on steroidogenic cells have not been explored. sHDL, specifically ETC-642, was studied in HAC15 adrenocortical cells. Cells were treated with sHDL, forskolin, 22R-hydroxycholesterol, or pregnenolone. Experiments included time and concentration response curves, followed by steroid assay. Quantitative real-time RT-PCR was used to study mRNA of 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase, lanosterol 14-α-methylase, cholesterol side-chain cleavage enzyme, and steroid acute regulatory protein. Cholesterol assay was performed using cell culture media and cell lipid extracts from a dose response experiment. sHDL significantly inhibited production of cortisol. Inhibition occurred in a concentration- and time-dependent manner and in a concentration range of 3μM–50μM. Forskolin (10μM) stimulated cortisol production was also inhibited. Incubation with 22R-hydroxycholesterol (10μM) and pregnenolone (10μM) increased cortisol production, which was unaffected by sHDL treatment. sHDL increased transcript levels for the rate-limiting cholesterol biosynthetic enzyme, 3-hydroxy-3-methyl-glutaryl-coenzyme A reductase. Extracellular cholesterol assayed in culture media showed a positive correlation with increasing concentration of sHDL, whereas intracellular cholesterol decreased after treatment with sHDL. The current study suggests that sHDL inhibits HAC15 adrenal cell steroid production by efflux of cholesterol, leading to an overall decrease in steroid production and an adaptive rise in adrenal cholesterol biosynthesis.

Sign in / Sign up

Export Citation Format

Share Document