Plasma-derived and synthetic high-density lipoprotein inhibit tissue factor in endothelial cells and monocytes

2016 ◽  
Vol 473 (2) ◽  
pp. 211-219 ◽  
Author(s):  
Alice Ossoli ◽  
Alan T. Remaley ◽  
Boris Vaisman ◽  
Laura Calabresi ◽  
Monica Gomaraschi
Keyword(s):  
Endothelial Cells ◽  
High Density Lipoprotein ◽  
Tissue Factor ◽  
Density Lipoprotein ◽  
High Density ◽  
Coagulation Cascade ◽  
High Density Lipoproteins

Atheroprotection mediated by high-density lipoproteins could also be related to their ability to inhibit the expression of tissue factor, the main activator of the coagulation cascade, in endothelial cells and in monocytes.

scholarly journals High-Density Lipoproteins and Cardiovascular Disease: The Good, the Bad and the Future

Biomedicines ◽  
2021 ◽  
Vol 9 (8) ◽  
pp. 857
Author(s):  
Josep Julve ◽  
Joan Carles Escolà-Gil
Keyword(s):  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
Epidemiological Studies ◽  
High Density ◽  
High Density Lipoproteins ◽  
Atherosclerotic Cardiovascular Disease ◽  
Plasma High Density ◽  
Low Levels

Epidemiological studies have shown that low levels of plasma high-density lipoprotein cholesterol (HDL-C) are associated with increased atherosclerotic cardiovascular disease (CVD) [...]

Determination of high-density lipoprotein phospholipids in serum.

1980 ◽  
Vol 26 (9) ◽  
pp. 1275-1277 ◽  
Author(s):  
Y Yamaguchi
Keyword(s):  
High Density Lipoprotein ◽  
Density Lipoprotein ◽  
Mean Value ◽  
High Density ◽  
High Density Lipoproteins ◽  
Low Density ◽  
Very Low Density Lipoproteins ◽  
Color Development ◽  
The Mean

Abstract I describe a method for measuring high-density lipoprotein phospholipids. Magnesium chloride and dextran sulfate are used to precipitate all low-density and very-low-density lipoproteins. The supernate contains only high-density lipoproteins, the phospholipid concentration of which is determined by an enzymic method. The precision of the method (CV) is 2.35% (10 repeated assays), and the mean value for HDL-phospholipids was 1006 (SD 248) mg/L for 30 apparently healthy subjects. I used electrophoresis and enzymic color development to confirm the presence of HDL-phospholipids. Results are compared with those obtained by an ultracentrifugation method.

scholarly journals Featured Article: Depletion of HDL3 high density lipoprotein and altered functionality of HDL2 in blood from sickle cell patients

2017 ◽  
Vol 242 (12) ◽  
pp. 1244-1253 ◽  
Author(s):  
Eric Soupene ◽  
Sandra K Larkin ◽  
Frans A Kuypers
Keyword(s):  
Sickle Cell Disease ◽  
High Density Lipoprotein ◽  
Sickle Cell ◽  
Acute Phase ◽  
Whole Blood ◽  
Density Lipoprotein ◽  
High Density ◽  
High Density Lipoproteins ◽  
Mrna Levels ◽  
Cell Disease

In sickle cell disease (SCD), alterations of cholesterol metabolism is in part related to abnormal levels and activity of plasma proteins such as lecithin cholesterol acyltransferase (LCAT), and apolipoprotein A-I (ApoA-I). In addition, the size distribution of ApoA-I high density lipoproteins (HDL) differs from normal blood. The ratio of the amount of HDL2 particle relative to the smaller higher density pre-β HDL (HDL3) particle was shifted toward HDL2. This lipoprotein imbalance is exacerbated during acute vaso-occlusive episodes (VOE) as the relative levels of HDL3 decrease. HDL3 deficiency in SCD plasma was found to relate to a slower ApoA-I exchange rate, which suggests an impaired ABCA1-mediated cholesterol efflux in SCD. HDL2 isolated from SCD plasma displayed an antioxidant capacity normally associated with HDL3, providing evidence for a change in function of HDL2 in SCD as compared to HDL2 in normal plasma. Although SCD plasma is depleted in HDL3, this altered capacity of HDL2 could account for the lack of difference in pro-inflammatory HDL levels in SCD as compared to normal. Exposure of human umbilical vein endothelial cells to HDL2 isolated from SCD plasma resulted in higher mRNA levels of the acute phase protein long pentraxin 3 (PTX3) as compared to incubation with HDL2 from control plasma. Addition of the heme-scavenger hemopexin protein prevented increased expression of PTX3 in sickle HDL2-treated cells. These findings suggest that ApoA-I lipoprotein composition and functions are altered in SCD plasma, and that whole blood transfusion may be considered as a blood replacement therapy in SCD. Impact statement Our study adds to the growing evidence that the dysfunctional red blood cell (RBC) in sickle cell disease (SCD) affects the plasma environment, which contributes significantly in the vasculopathy that defines the disease. Remodeling of anti-inflammatory high density lipoprotein (HDL) to pro-inflammatory entities can occur during the acute phase response. SCD plasma is depleted of the pre-β particle (HDL3), which is essential for stimulation of reverse cholesterol from macrophages, and the function of the larger HDL2 particle is altered. These dysfunctions are exacerbated during vaso-occlusive episodes. Interaction of lipoproteins with endothelium increases formation of inflammatory mediators, a process counteracted by the heme-scavenger hemopexin. This links hemolysis to lipoprotein-mediated inflammation in SCD, and hemopexin treatment could be considered. The use of RBC concentrates in transfusion therapy of SCD patients underestimates the importance of the dysfunctional plasma compartment, and transfusion of whole blood or plasma may be warranted.

High-density Lipoprotein Cholesterol: Current Perspective for Clinicians

Angiology ◽  
2009 ◽  
Vol 60 (5) ◽  
pp. 644-649 ◽  
Author(s):  
Thomas F. Whayne
Keyword(s):  
Cardiovascular Risk ◽  
High Density Lipoprotein ◽  
Nicotinic Acid ◽  
Cholesteryl Ester Transfer Protein ◽  
High Density Lipoprotein Cholesterol ◽  
Density Lipoprotein ◽  
High Density ◽  
Lipoprotein Cholesterol ◽  
High Density Lipoproteins ◽  
Transfer Protein

High-density lipoproteins are regarded as “good guys” but not always. Situations involving high-density lipoproteins are discussed and medication results are considered. Clinicians usually consider high-density lipoprotein cholesterol. Nicotinic acid is the best available medication to elevate high-density lipoprotein cholesterol and this appears beneficial for cardiovascular risk. The major problem with nicotinic acid is that many patients do not tolerate the associated flushing. Laropiprant decreases this flushing and has an approval in Europe but not in the United States. The most potent medications for increasing high-density lipoprotein cholesterol are cholesteryl ester transfer protein inhibitors. The initial drug in this class, torcetrapib, was eliminated by excess cardiovascular problems. Two newer cholesteryl ester transfer protein inhibitors, R1658 and anacetrapib, initially appear promising. High-density lipoprotein cholesterol may play an important role in improving cardiovascular risk in the 60% of patients who do not receive cardiovascular mortality/morbidity benefit from low-density lipoproteins reduction by statins.

Glycated high-density lipoprotein regulates reactive oxygen species and reactive nitrogen species in endothelial cells

Metabolism ◽  
2003 ◽  
Vol 52 (1) ◽  
pp. 42-49 ◽  
Author(s):  
Toshiyuki Matsunaga ◽  
Takanori Nakajima ◽  
Takashi Miyazaki ◽  
Iwao Koyama ◽  
Shigeru Hokari ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
High Density Lipoprotein ◽  
Reactive Nitrogen Species ◽  
Density Lipoprotein ◽  
Reactive Oxygen ◽  
High Density ◽  
Reactive Nitrogen ◽  
Oxygen Species ◽  
Nitrogen Species
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