LDL sialic acid content in patients with coronary artery disease

Ruelland, A.; Gallou, G; Legras, B; Paillard, François; Cloarec, L

doi:10.1016/0009-8981(93)90027-2

Cited by 40 publications

(26 citation statements)

References 16 publications

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“…Ruelland et al 25 found a far less marked decrease (23%) than that reported by Orekhov and coworkers. Melajärvi et al 26 found no difference between patients with and without CAD, either in diabetic or nondiabetic individuals.…”

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confidence: 59%

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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confidence: 59%

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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“…310 Downloaded by [University of Tasmania] at 14: 33 29 September 2015 Desialylation of LDL enhances uptake by aortic smooth muscle cells, 311,312 but not by fibroblasts or hepatocytes. 308,313 Low sialic acid content in LDL is associated with increased risk of coronary heart disease in some [314][315][316] but not in all studies. 317,318 Alcohol drinking might affect the metabolism of LDL by interfering with its sialylation, but this has not been studied so far.…”

Section: B Sialylation Of Lipoproteinsmentioning

confidence: 97%

Effect of Alcohol on Lipids and Lipoproteins in Relation to Atherosclerosis

Hannuksela

Liisanantti

Savolainen

2002

Critical Reviews in Clinical Laboratory Sciences

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Several studies indicate that light-to-moderate alcohol consumption is associated with a low prevalence of coronary heart disease. An increase in high-density lipoprotein (HDL) cholesterol is associated with alcohol intake and appears to account for approximately half of alcohol's cardioprotective effect. In addition to changes in the concentration and composition of lipoproteins, alcohol consumption may alter the activities of plasma proteins and enzymes involved in lipoprotein metabolism: cholesteryl ester transfer protein, phospholipid transfer protein, lecithin:cholesterol acyltransferase, lipoprotein lipase, hepatic lipase, paraoxonase-1 and phospholipases. Alcohol intake also results in modifications of lipoprotein particles: low sialic acid content in apolipoprotein components of lipoprotein particles (e.g., HDL apo E and apo J) and acetaldehyde modification of apolipoproteins. In addition, "abnormal" lipids, phosphatidylethanol, and fatty acid ethyl esters formed in the presence of ethanol are associated with lipoproteins in plasma. The effects of lipoproteins on the vascular wall cells (endothelial cells, smooth muscle cells, and monocyte/macrophages) may be modulated by ethanol and the alterations further enhanced by modified lipids. The present review discusses the effects of alcohol on lipoproteins in cholesterol transport, as well as the novel effects of lipoproteins on vascular wall cells.

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“…A minor fraction of circulating desialylated LDL (5%–10% of total LDL) could be detected in the blood of healthy subjects. In atherosclerotic patients, desialylated LDL levels are significantly increased (by 1.5- to 6-fold) compared to healthy individuals [158,159] and can account up to 60% of total LDL in CAD patients [154]. Small dense LDL particles exhibited a profound deficiency in sialylation rate correlated with increased atherogenicity of this subfraction [159].…”

Section: Ldl Modificationsmentioning

confidence: 99%

Modified Low Density Lipoprotein and Lipoprotein-Containing Circulating Immune Complexes as Diagnostic and Prognostic Biomarkers of Atherosclerosis and Type 1 Diabetes Macrovascular Disease

Orekhov

Bobryshev

Sobenin

et al. 2014

IJMS

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In atherosclerosis; blood low-density lipoproteins (LDL) are subjected to multiple enzymatic and non-enzymatic modifications that increase their atherogenicity and induce immunogenicity. Modified LDL are capable of inducing vascular inflammation through activation of innate immunity; thus, contributing to the progression of atherogenesis. The immunogenicity of modified LDL results in induction of self-antibodies specific to a certain type of modified LDL. The antibodies react with modified LDL forming circulating immune complexes. Circulating immune complexes exhibit prominent immunomodulatory properties that influence atherosclerotic inflammation. Compared to freely circulating modified LDL; modified LDL associated with the immune complexes have a more robust atherogenic and proinflammatory potential. Various lipid components of the immune complexes may serve not only as diagnostic but also as essential predictive markers of cardiovascular events in atherosclerosis. Accumulating evidence indicates that LDL-containing immune complexes can also serve as biomarker for macrovascular disease in type 1 diabetes.

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LDL sialic acid content in patients with coronary artery disease

Cited by 40 publications

References 16 publications

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

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

Effect of Alcohol on Lipids and Lipoproteins in Relation to Atherosclerosis

Modified Low Density Lipoprotein and Lipoprotein-Containing Circulating Immune Complexes as Diagnostic and Prognostic Biomarkers of Atherosclerosis and Type 1 Diabetes Macrovascular Disease

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