Characteristics of ten charge-differing subfractions isolated from human native low-density lipoproteins (LDL). No evidence of peroxidative modifications

Chappey, B.; Myara, I.; Benoit, Marie-Odile; Mazière, Cécile; Mazière, Jean‐Claude; Moatti, N.

doi:10.1016/0005-2760(95)00172-7

Cited by 42 publications

(35 citation statements)

References 34 publications

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“…10,11 LDL(Ϫ) isolated from normolipidemic human plasma may or may not produce more conjugated dienes than LDL(ϩ). 11,13 In hypercholesterolemic human plasma, Sevanian et al 12 found significantly higher conjugated dienes in LDL(Ϫ) than in LDL(ϩ). The proinflammatory and cytotoxic effects of LDL(Ϫ) on ECs included release of interleukin 8, monocyte chemotactic protein, and lactate dehydrogenase.…”

Section: Discussionmentioning

confidence: 99%

“…4 -9 Electronegative human LDL, LDL(Ϫ), has been found in vitro to be proinflammatory and cytotoxic to ECs, as reported by Demuth et al 10 and others. [11][12][13] Because induction of apoptosis by circulating LDL has not been demonstrated previously, we sought to elucidate the mechanism of apoptosis in vascular ECs treated by an electronegative LDL species similar to LDL(Ϫ).…”

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confidence: 99%

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Low-Density Lipoprotein in Hypercholesterolemic Human Plasma Induces Vascular Endothelial Cell Apoptosis by Inhibiting Fibroblast Growth Factor 2 Transcription

et al. 2003

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Low-Density Lipoprotein in Hypercholesterolemic Human Plasma Induces Vascular Endothelial Cell Apoptosis by Inhibiting Fibroblast Growth Factor 2 Transcription

et al. 2003

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“…24 Collected LDL was dialyzed for 24 hours at ϩ4°C against four changes of 100 vol 10 mmol/L Tris-HCl buffer, pH 7.4, containing 1 mmol/L EDTA, and was stored at ϩ4°C in the dark. For in vitro studies, LDL was isolated by preparative ultracentrifugation from normolipidemic plasma pools according to a procedure previously described in detail 6,29 and then dialyzed as indicated above. The absence of contaminating lipoproteins (VLDL and HDL) in LDL preparations was checked by agarose gel electrophoresis.…”

Section: Methodsmentioning

confidence: 99%

“…1,2 However, LDL comprises a continuum of particles differing in their chemicophysical [3][4][5][6] and biological [6][7][8] properties, and some subfractions have been more strongly incriminated than others in the development of atherosclerosis. 9,10 Sialic acid is a component of both the protein and lipid moieties of LDL.…”

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confidence: 99%

Sialic Acid Content of LDL in Coronary Artery Disease: No Evidence of Desialylation in Subjects With Coronary Stenosis and Increased Levels in Subjects With Extensive Atherosclerosis and Acute Myocardial Infarction

Chappey

Beyssen

Foos

et al. 1998

ATVB

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Abstract-We recently showed that sialic acid content of LDL was not a marker of early cardiovascular disease (Arterioscler Thromb Vasc Biol. 1995;15:334 -339). Here, we investigated this parameter in patients with advanced coronary artery disease (CAD). We first examined 100 patients having undergone coronary angiography. The distribution of LDL sialic acid values was very similar in subjects with no coronary stenosis (31.3Ϯ3.7 nmol/mg LDL protein, meanϮSD) and those with Ն75% stenosis in at least one main coronary artery or Ն50% stenosis in at least two main coronary arteries (32.1Ϯ5.5 nmol/mg LDL protein). In contrast, LDL sialic acid content was significantly increased in patients with both coronary stenosis and peripheral arterial atherosclerotic lesions compared with those with either no lesion or only one or the other type of lesion. We then examined LDL sialic acid content in 20 patients with acute myocardial infarction. LDL sialic acid content was significantly higher (35.9Ϯ3.2 nmol/mg LDL protein) than that in the CAD(Ϫ) control group. These data suggest that LDL sialic acid content increases with the extension of atherosclerosis and its progression to acute complications. To explain the discordance with Orekhov and coworkers (Atherosclerosis. 1991;86:153-161), who showed that LDL sialic acid content in patients with advanced CAD was lower than that in healthy subjects, we studied the time courses of sialic acid, TBARS, and vitamin E levels in LDL dialyzed in different experimental conditions. A continuous decrease in both sialic acid and vitamin E levels and an increase in TBARS levels were observed in LDL samples containing less than 1 mmol/L EDTA, the intensity and rapidity of which varied with the EDTA concentration in the buffer. Our data support the idea that desialylation may result from in vitro peroxidation of LDL. (Arterioscler Thromb Vasc Biol. 1998;18:876-883.)

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“…Because LDL( Ϫ ) separated by anion-exchange chromatography techniques has been shown to contain higher TG content than the major LDL subfraction (7)(8)(9), it is possible that there may be a relation between insulin resistance and LDL( Ϫ ). However, this has not yet been examined.…”

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Relation between insulin resistance and fast-migrating LDL subfraction as characterized by capillary isotachophoresis

Zhang

Kaneshi

Ohta

et al. 2005

Journal of Lipid Research

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The proportion of the electronegative low density lipoprotein [LDL( ؊ )] subfraction, which is atherogenic, is increased in type 2 diabetes but is not reduced by glycemic control. Therefore, we evaluated the ability of a new technique, capillary isotachophoresis (cITP), to quantify charge-based LDL subfractions and examined the relation between insulin resistance and the cITP fast-migrating (f) LDL levels. Seventy-five 10-year-old boys were included. The two cITP LDL subfractions, fLDL and major LDL subfractions, were proportional to the LDL protein content within the range of 0.1-0.8 mg/ml LDL protein. Levels of cITP fLDL were positively correlated with triglyceride (TG) levels and negatively correlated with LDL size. Insulin resistance as assessed by the homeostasis model assessment (HOMA-IR) was positively correlated ( P Ͻ 0.01) with cITP fLDL levels ( r ‫؍‬ 0.41). The relation between HOMA-IR and cITP fLDL levels depended on TG levels but was independent of body mass index and LDL size. cITP lipoprotein analysis is an accurate and sensitive method for quantifying charge-based LDL subfractions in human plasma, and insulin resistance is related to cITP fLDL independent of LDL size. -Zhang, B., T. Kaneshi, T. Ohta, and K. Saku. Relation between insulin resistance and fast-migrating LDL subfraction as characterized by capillary isotachophoresis. Electronegative low density lipoprotein [LDL( Ϫ )] subfraction in plasma has been shown to have various atherogenic properties [reviewed by Sánchez-Quesada, Benitez, and Ordonez-Llanos (1)]. Although in vitro oxidized LDL can only be taken up by scavenger receptors, LDL( Ϫ ) can also be taken up by LDL receptors to induce vascular cell adhesion molecule-1 expression through the activation of nuclear factor B and adaptor protein 1 (2).Both type 1 and type 2 diabetic patients have been shown to have an increased proportion of LDL( Ϫ ) (3, 4). However, LDL( Ϫ ) in type 1 and type 2 diabetes seems to be of different origins. In type 1 diabetes, nonenzymatic glycosylation has been shown to contribute to the increased proportion of LDL( Ϫ ): glycemic optimization decreased both the glycated LDL and the proportion of LDL( Ϫ ) (3, 4). However, in type 2 diabetes, glycemic control decreased glycated LDL but had no significant effects on the proportion of LDL( Ϫ ) (4, 5). It is not clear whether or not insulin resistance contributes to LDL( Ϫ ) generation in type 2 diabetes.Insulin resistance is known to be associated with increased levels of triglycerides (TGs) (6). Because LDL( Ϫ ) separated by anion-exchange chromatography techniques has been shown to contain higher TG content than the major LDL subfraction (7-9), it is possible that there may be a relation between insulin resistance and LDL( Ϫ ). However, this has not yet been examined. In addition, it would be interesting to know whether or not the relation between insulin resistance and LDL( Ϫ ) depends on TG levels.Insulin resistance is also linked to plasma levels of small, dense LDLs (pattern B lipoprotein phenot...

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Characteristics of ten charge-differing subfractions isolated from human native low-density lipoproteins (LDL). No evidence of peroxidative modifications

Cited by 42 publications

References 34 publications

Low-Density Lipoprotein in Hypercholesterolemic Human Plasma Induces Vascular Endothelial Cell Apoptosis by Inhibiting Fibroblast Growth Factor 2 Transcription

Low-Density Lipoprotein in Hypercholesterolemic Human Plasma Induces Vascular Endothelial Cell Apoptosis by Inhibiting Fibroblast Growth Factor 2 Transcription

Sialic Acid Content of LDL in Coronary Artery Disease: No Evidence of Desialylation in Subjects With Coronary Stenosis and Increased Levels in Subjects With Extensive Atherosclerosis and Acute Myocardial Infarction

Relation between insulin resistance and fast-migrating LDL subfraction as characterized by capillary isotachophoresis

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