The structures of the asparagine-linked sugar chains of human apolipoprotein B-100

Taniguchi, Takahiro; Ishikawa, Yuichi; Tsunemitsu, Masahiko; Fukuzaki, Hisashi

doi:10.1016/0003-9861(89)90179-3

Cited by 50 publications

(30 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…LDL peroxidation could explain the paradoxical increase in negative charge of desialylated LDL. Indeed, sialic acid is a negatively charged component 46 and several groups, 11,15,18,19 including ourselves, 20 have shown that desialylation of LDL by neuraminidase treatment reduces its electrophoretic migration in agarose. One outstanding question is why the LDL desialylation was observed only in subjects with CAD.…”

Section: Discussionmentioning

confidence: 99%

“…9,10 Sialic acid is a component of both the protein and lipid moieties of LDL. [11][12][13][14] In vitro, the sialic acid content of LDL can modulate its receptor-mediated cell uptake, [15][16][17] its avidity for arterial proteoglycans, 18 and its susceptibility to oxidation. 19,20 Several investigators have reported large interindividual differences in LDL carbohydrate content.…”

mentioning

confidence: 99%

See 1 more Smart Citation

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

View full text Add to dashboard Cite

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.)

show abstract

Section: Discussionmentioning

confidence: 99%

mentioning

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

View full text Add to dashboard Cite

show abstract

“…As expected, the protein fraction produced a prominent GlycA signal, but we also observed in the lipoprotein fraction of this and similar experiments a small peak at 2.00 ppm that by deconvolution analysis never accounted for Ͼ10% of the measured serum/plasma GlycA signal. We presume that the small lipoprotein GlycA signal originates from the glycan attached to the apolipoprotein B (apoB) and/or apo(a) proteins on LDL and lipoprotein(a) particles, since both of these apolipoproteins are glycosylated (28,29 ). Because the GlycA signals originating from different plasma glycoproteins are not distinguishable, and the glycan on each is heterogeneous and varies dynamically, only a rough estimate can be made of how much each contributes to measured plasma GlycA concentrations.…”

Section: Glycoprotein Origins Of the Glyca Nmr Signalmentioning

confidence: 99%

GlycA: A Composite Nuclear Magnetic Resonance Biomarker of Systemic Inflammation

et al. 2015

View full text Add to dashboard Cite

BACKGROUND: Nuclear magnetic resonance (NMR) spectra of serum obtained under quantitative conditions for lipoprotein particle analyses contain additional signals that could potentially serve as useful clinical biomarkers. One of these signals that we named GlycA originates from a subset of glycan N-acetylglucosamine residues on enzymatically glycosylated acute-phase proteins. We hypothesized that the amplitude of the GlycA signal might provide a unique and convenient measure of systemic inflammation.

show abstract

“…Sixteen N-glycosylation sites in apoB-100 are glycosylated with high-mannose and complex forms of oligosaccharides. 97,98) ApoB is highly insoluble in aqueous solutions and remains at the lipoprotein particle throughout its metabolism. From the circular dichroism (CD) spectra of LDL, the secondary structure of apoB-100 is characterized by a large content of α-helix (ca.…”

Section: Foam Cell Formationmentioning

confidence: 99%

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Morita

2016

Biological & Pharmaceutical Bulletin

132

108

View full text Add to dashboard Cite

Increased levels of apolipoprotein B (apoB)-containing lipoproteins, such as low density lipoproteins (LDL) and chylomicron remnants, are associated with the development of atherosclerosis. Chylomicrons containing apoB-48 are secreted from the intestine during the postprandial state, whereas very low density lipoproteins (VLDL) containing apoB-100 are constitutively formed in the liver. Chylomicron remnants and VLDL remnants are produced by the lipoprotein lipase-mediated lipolysis of triglycerides, which is activated by apolipoprotein C-II bound on the particle surfaces. The hepatic uptake of these remnants is facilitated by apolipoprotein E (apoE), but is inhibited by apolipoproteins C-I, C-II and C-III. In the plasma, VLDL remnants are further converted into LDL by the hydrolysis of triglycerides. ApoB-100 is responsible for the hepatic uptake of LDL. LDL receptor, LDL receptor-related protein and heparan sulfate proteoglycans are involved in the hepatic clearance of lipoproteins containing apoB-100 and/or apoE. The subendothelial retention and modification of apoB-containing lipoproteins are crucial events in the initiation of atherosclerosis. In the subendothelium, the uptake of modified lipoproteins by macrophages leads to the formation of foam cells storing excess amounts of cholesteryl esters and subsequently to apoptosis. This review describes the current knowledge about the metabolism and modification of apoB-containing lipoproteins involved in dyslipidemia and atherogenesis. In particular, I focus on the effects of apolipoproteins, lipid composition and particle size on lipoprotein metabolism and on the roles of cholesterol, sphingomyelinase and apoB denaturation in macrophage foam cell formation and apoptosis. A detailed understanding of these mechanisms will help to develop new therapeutic strategies.

show abstract

The structures of the asparagine-linked sugar chains of human apolipoprotein B-100

Cited by 50 publications

References 39 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

GlycA: A Composite Nuclear Magnetic Resonance Biomarker of Systemic Inflammation

Metabolism and Modification of Apolipoprotein B-Containing Lipoproteins Involved in Dyslipidemia and Atherosclerosis

Contact Info

Product

Resources

About