Low-density lipoprotein (LDL)-induced monocyte-endothelial cell adhesion, soluble cell adhesion molecules, and autoantibodies to oxidized-LDL in chronic renal failure patients on dialysis therapy

O’Byrne, Dawn; Devaraj, Sridevi; Islam, Kazi Nazrul; Collazo, Roberto; McDonald, Lauren; Grundy, Scott M.; Jialal, Ishwarlal

doi:10.1053/meta.2001.19486

Cited by 49 publications

(32 citation statements)

References 67 publications

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“…It therefore seems tempting to relate the increased LDL oxidation levels found in FH and in ESRD patients on hemodialysis in the present study to increased oxidative stress. However, recently it was reported that supplementation with alpha-tocopherol dose dependently decreased urinary F2 isoprostanes in hypercholesterolemic subjects (Davi et al, 1997) and reduced LDL oxidizability (Islam et al, 2000) but did not affect the elevated atherogenicity of LDL (which is a measure of oxidative modification) of renal failure patients on dialysis (O'Byrne et al, 2001). Thus these data also suggest that plasma oxLDL does not result from oxidative processes in the circulation.…”

Section: Resultsmentioning

confidence: 99%

“…However, with respect to oxidative modification of LDL as assessed by indirect measurements, findings are not consistent. Although some groups report elevated levels of autoantibodies to oxLDL (Maggi et al, 1994a(Maggi et al, , 1994b, increased LDL oxidizability (Maggi et al, 1994a;Panzetta et al, 1995), and reduced alpha-tocopherol content of LDL (Panzetta et al, 1995) in dialysis patients compared with healthy controls, others could not confirm these differences but did demonstrate that LDL of chronic renal failure patients was more atherogenic (Islam et al, 2000;O'Byrne et al, 2001). It has been suggested that these inconsistencies are partly a result of the variable methodologies used and of abnormal LDL composition in dialysis patients (Devaraj and Jialal, 1997;Loughrey et al, 1994b).…”

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confidence: 99%

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Increased Levels of Low-Density Lipoprotein Oxidation in Patients with Familial Hypercholesterolemia and in End-Stage Renal Disease Patients on Hemodialysis

Tits

Graaf

Hak-Lemmers

et al. 2003

Laboratory Investigation

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SUMMARY:Patients with familial hypercholesterolemia (FH) and patients with end-stage renal disease (ESRD) undergoing dialysis suffer from accelerated atherosclerosis. Oxidation of low-density lipoprotein (LDL) cholesterol is crucial in atherogenesis. In the present study, we determined the LDL oxidation level and oxidizability of isolated LDL of 11 male patients with FH, 15 male ESRD patients on hemodialysis, and 15 age-matched male normolipidemic healthy controls. FH patients were without lipid-lowering medication for at least 4 weeks and were reassessed after 2 years of cholesterol-lowering therapy (statins). LDL oxidation level was measured by ELISA using monoclonal antibody 4E6 to oxidized LDL (oxLDL) as the capture antibody and anti-human apoB antibody for detection; results were expressed as percentage oxLDL. In FH patients and in ESRD patients on hemodialysis, both groups having a higher percentage of cardiovascular disease, mean plasma LDL oxidation levels were significantly elevated compared with controls (4.9 Ϯ 1.3; 3.7 Ϯ 2.0; 1.7 Ϯ 0.6%, respectively). Within each group of subjects, LDL oxidation level was not associated with history of cardiovascular disease. Furthermore, in neither group was a significant correlation found between plasma concentration of LDL cholesterol and LDL oxidation level. After cholesterol-lowering therapy, LDL oxidation level in FH patients had not changed significantly and remained elevated compared with controls, despite a reduction of LDL cholesterol by 55% on average. Also, absolute plasma oxLDL concentrations, obtained by multiplying LDL oxidation level with plasma LDL cholesterol concentration, were significantly higher in FH patients before and after cholesterollowering therapy and in ESRD patients on hemodialysis than in controls (489 Ϯ 145; 189 Ϯ 122; 100 Ϯ 65; and 59 Ϯ 27 moles/L, respectively). No correlation was found between plasma oxLDL concentration and parameters of LDL oxidizability, LDL fatty acids, and LDL alpha-tocopherol content. We conclude that cholesterol-lowering therapy does not normalize elevated LDL oxidation levels in FH patients and elevated LDL oxidation level in FH and in ESRD might mirror atherosclerosis. (Lab Invest 2003, 83:13-21).

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Section: Resultsmentioning

confidence: 99%

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confidence: 99%

Increased Levels of Low-Density Lipoprotein Oxidation in Patients with Familial Hypercholesterolemia and in End-Stage Renal Disease Patients on Hemodialysis

Tits

Graaf

Hak-Lemmers

et al. 2003

Laboratory Investigation

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“…29 A population study showed that ␣-tocopherol supplementation in healthy individuals increases plasma levels of ␣-tocopherol and reduces LDL oxidative susceptibility and circulating oxidized LDL. 30 In contrast, several other clinical studies have reported that supplementation with ␣-tocopherol has no effect on autoantibodies against Ox-LDL in hyperlipidemic patients, 31 in patients with chronic renal failure, 32 or in chronic smokers. 33 In agreement with the latter results, the plasma levels of Ox-LDL were increased in affected FCHL family members, despite the elevation of plasma ␣-tocopherol.…”

Section: Circulating Ox-ldl 8-isoprostane and Antioxidantsmentioning

confidence: 91%

Circulating Oxidized Low-Density Lipoprotein and Its Association With Carotid Intima-Media Thickness in Asymptomatic Members of Familial Combined Hyperlipidemia Families

Liu

Ylitalo

Salonen

et al. 2004

ATVB

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Objective-Oxidized low-density lipoprotein (Ox-LDL)is implicated in the pathogenesis of atherosclerosis. Circulating oxidation-specific epitopes on plasma Ox-LDL has been linked with coronary artery disease, but its determinants and its association with early development of atherosclerosis in familial combined hyperlipidemia (FCHL) has not been very well studied. This study aimed to investigate the determinants of the circulating Ox-LDL and the association between Ox-LDL and carotid intima-media thickness (IMT) in asymptomatic members of FCHL families. Methods and Results-Ox-LDL, susceptibility of LDL to oxidation in vitro, plasma 8-isoprostane and antioxidants, lipids and lipoproteins, LDL particle size, and carotid IMT were measured in 150 asymptomatic FCHL family members. Affected FCHL family members had reduced LDL particle size and lag time for LDL oxidation, increased plasma levels of Ox-LDL, increased plasma urate and ␣-tocopherol, and a trend for the increase of 8-isoprostane as compared with nonaffected FCHL. Ox-LDL was independently associated with serum LDL cholesterol, apoB, and 8-isoprostane in multivariate analysis but only univariately correlated with LDL particle size and lag time for LDL oxidation. In addition, Ox-LDL was significantly associated with carotid mean IMT independently of other clinical and biochemical variables in a multivariate model. Conclusion-Serum LDL cholesterol, apoB levels, and 8-isoprostane were the most important determinants of Ox-LDL.Ox-LDL is independently associated with carotid IMT in asymptomatic FCHL family members and can be used as a marker of early atherosclerosis in FCHL. Key Words: carotid arteries Ⅲ hyperlipoproteinemia Ⅲ familial combined Ⅲ lipoproteins Ⅲ low-denisty lipoprotein Ⅲ oxygen radical Ⅲ ultrasonography T here is substantial evidence that oxidized low-density lipoprotein (Ox-LDL) is present in vivo within atherosclerotic lesions of arteries. 1 Under the oxidative stress, oxidative modification of LDL may take place in the subendothelial space of the arterial wall, 1 and a small amount of Ox-LDL may also be released into the circulation. 2 When "fully oxidized LDL" enters the circulation in minor quantities, it will be rapidly cleared by the reticuloendothelial system, particularly in the liver, or it will be removed by the preexisting circulating autoantibodies to In contrast, the "minimally modified LDL," in which oxidative modification has not been sufficient to cause changes recognized by scavenger receptors, can be found in circulation. 4,5 Other studies have defined the presence of oxidationspecific epitopes on plasma LDL 6 -8 or baseline levels of conjugated dienes in lipids extracted from LDL (LDL-BDC) as measures of LDL oxidation in vivo. 9 Recently, several groups have developed several specific methods to measure circulating Ox-LDL using different anti-Ox-LDL antibodies. 6 -8 As a sensitive biochemical marker, Ox-LDL has been related to coronary artery disease (CAD) in several clinical studies. 6,10 -12 Plasma Ox-LDL has also been associ...

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“…The interaction with their receptors (RAGE) present on macrophage cells [21] , T lymphocytes [22] and mesangial cells [23] induces, through activation of NF-kB, transcription of cytokines such as IL-1, IL-6 and TNF-␣ [24] , which are responsible of infl ammation and, therefore, of oxidative stress. AGEs might modify LDL cholesterol, making it more atherogenic [25] , inducing a bigger expression of endothelial adhesion molecules and reducing endothelial function. Vitamin E supplementation in human subjects and animal models has been shown to decrease lipid peroxidation, superoxide (O 2 -) production and decrease the expression of scavenger receptors (SR-A and CD36), important in the formation of foam cells.…”

Section: Discussionmentioning

confidence: 99%

Role of Vitamin E-Coated Membrane in Reducing Advanced Glycation End Products in Hemodialysis Patients: A Pilot Study

Baragetti

Furiani²,

Vettoretti³

et al. 2006

Blood Purif

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Introduction: Advanced glycation end products (AGEs) are markers of oxidative stress. Aims: To assess if a vitamin-E-coated dialyzer affects plasma AGE levels and endothelial function in hemodialysis patients. Methods: 16 patients were dialyzed with a synthetic modified cellulose membrane (SMC, n = 8) or a vitamin E-coated dialyzer (n = 8), respectively. At week 32 endothelial function was determined as brachial artery flow-mediated dilatation (FMD). Total AGEs, free pentosidine (FP), protein-bound pentosidine (BP) and autoantibodies against oxidized LDL (ox-LDL-autoantibodies) were assessed at baseline (T0) and at 16, 32, 40 and 42 weeks (T16, T32, T40 and T42). Results: At T16 and T32 FP and BP were lower in vitamin E than in SMC (T 16: 88.7 ± 8.96 vs. 124.2 ± 11.90 pmol/ml plasma; p = 0.04, and 22.9 ± 2.99 vs. 32.8 ± 2.98 pmol/mg proteins; p = 0.04. T32: 78.7 ± 8.54 vs. 123.7 ± 10.15 pmol/ml plasma; p = 0.007, and 19.9 ± 2.0 vs. 33.67 ± 2.41 pmol/mg proteins; p = 0.001). In vitamin E, AGEs were lower at T32, T40 and T42 (946.7 ± 80.91 vs. 1,351.2 ± 179.33 AU/ml, p = 0.05; 986.9 ± 59.63 vs. 1,509.9 ± 154.17 AU/ml, p = 0.013; 890.3 ± 73.70 vs. 1,453.9 ± 153.16 AU/ml, p = 0.009). At T32 AGEs, ox-LDL autoantibodies and FMD were inversely correlated (R = –0.70 p = 0.007 and R = –0.59, p = 0.04, respectively). Conclusions: Vit E-coated membrane reduces plasma AGEs levels and AGEs values are negatively correlated with FMD.

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Low-density lipoprotein (LDL)-induced monocyte-endothelial cell adhesion, soluble cell adhesion molecules, and autoantibodies to oxidized-LDL in chronic renal failure patients on dialysis therapy

Cited by 49 publications

References 67 publications

Increased Levels of Low-Density Lipoprotein Oxidation in Patients with Familial Hypercholesterolemia and in End-Stage Renal Disease Patients on Hemodialysis

Increased Levels of Low-Density Lipoprotein Oxidation in Patients with Familial Hypercholesterolemia and in End-Stage Renal Disease Patients on Hemodialysis

Circulating Oxidized Low-Density Lipoprotein and Its Association With Carotid Intima-Media Thickness in Asymptomatic Members of Familial Combined Hyperlipidemia Families

Role of Vitamin E-Coated Membrane in Reducing Advanced Glycation End Products in Hemodialysis Patients: A Pilot Study

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