scholarly journals Proteomic profiling following immunoaffinity capture of high-density lipoprotein: Association of acute-phase proteins and complement factors with proinflammatory high-density lipoprotein in rheumatoid arthritis

2012 ◽  
Vol 64 (6) ◽  
pp. 1828-1837 ◽  
Author(s):  
Junji Watanabe ◽  
Christina Charles-Schoeman ◽  
Yunan Miao ◽  
David Elashoff ◽  
Yuen Yin Lee ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
High Density Lipoprotein ◽  
Acute Phase ◽  
Acute Phase Proteins ◽  
Density Lipoprotein ◽  
High Density ◽  
Proteomic Profiling ◽  
Complement Factors ◽  
Lipoprotein Association

scholarly journals Paraoxonase 1 Activity Is Modulated by the rs662 Polymorphism and IgG Anti-High-Density Lipoprotein Antibodies in Patients With Rheumatoid Arthritis: Potential Implications for Cardiovascular Disease

2016 ◽  
Vol 68 (6) ◽  
pp. 1367-1376 ◽  
Author(s):  
Javier Rodríguez-Carrio ◽  
Raquel López-Mejías ◽  
Mercedes Alperi-López ◽  
Patricia López ◽  
Francisco J. Ballina-García ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Disease ◽  
High Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density ◽  
Paraoxonase 1

HYPOCHOLESTEROLAEMIA AND ABNORMAL HIGH-DENSITY LIPOPROTEIN IN RHEUMATOID ARTHRITIS

Rheumatology ◽  
1985 ◽  
Vol 24 (3) ◽  
pp. 250-255 ◽  
Author(s):  
M. LORBER ◽  
M. AVIRAM ◽  
S. LINN ◽  
Y. SCHARF ◽  
J. G. BROOK
Keyword(s):  
Rheumatoid Arthritis ◽  
High Density Lipoprotein ◽  
Density Lipoprotein ◽  
High Density

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.

scholarly journals Heparan Sulfate Dissociates Serum Amyloid A (SAA) from Acute-phase High-density Lipoprotein, Promoting SAA Aggregation

2012 ◽  
Vol 287 (30) ◽  
pp. 25669-25677 ◽  
Author(s):  
Fredrik Noborn ◽  
John B. Ancsin ◽  
Wimal Ubhayasekera ◽  
Robert Kisilevsky ◽  
Jin-Ping Li
Keyword(s):  
High Density Lipoprotein ◽  
Heparan Sulfate ◽  
Acute Phase ◽  
Serum Amyloid A ◽  
Density Lipoprotein ◽  
High Density ◽  
Serum Amyloid ◽  
Amyloid A
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