Lipoprotein-matrix interactions in macrovascular disease in diabetes

Tannock, Lisa R.; Chait, Alan

doi:10.2741/1248

Cited by 24 publications

(13 citation statements)

References 53 publications

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“…Poor metabolic control and hyperglycemia may facilitate nonenzymatic glycation of extracellular matrix proteins and, therefore, reduce avidity of apolipoproteins for proteoglycans. 24 We showed by Western blotting that immune recognition of apoB and apoE by the antibodies used in this study is not affected by nonenzymatic glycation or other posttranslational modifications occurring in the blood. Diabetic patients have preferentially small LDL particles, 25 and these atherogenic lipoproteins have been shown to increase binding and uptake by monocyte-derived macrophages.…”

Section: Discussionmentioning

confidence: 98%

Increased Apolipoprotein Deposits in Early Atherosclerotic Lesions Distinguish Symptomatic From Asymptomatic Patients

Ballmoos

Dubler

Mirlacher

et al. 2006

ATVB

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Objective-Apolipoprotein E (apoE) and apolipoprotein B100 (apoB) are both involved in receptor-mediated uptake of atherogenic lipoproteins by the liver. Inefficient hepatic clearance of these lipoproteins leads to symptomatic atherosclerosis. Using arterial tissue microarrays, we tested the hypothesis that apoE and apoB accumulation in the arterial wall discriminates between patients with symptomatic atherosclerosis and patients who never experienced cardiovascular events. Methods and Results-In a postmortem study involving 49 patients (22 patients with symptomatic atherosclerosis), we quantified apolipoprotein deposits in arterial rings obtained from the left main coronary, the common carotid, the common iliac, and the renal artery applying tissue microarray technology and semiquantitative immunohistochemistry. In early atherosclerotic lesions, even before atheroma appeared, symptomatic patients had significantly more arterial apoE and apoB deposits than patients without cardiovascular events (PϽ0.001). Among the symptomatic patients, those without diabetes had more intense apolipoprotein deposits than diabetics. Large amounts of apoE and apoB were found in advanced atherosclerotic lesions, regardless of the activity of the disease. Conclusions-Increased

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Section: Discussionmentioning

confidence: 98%

Increased Apolipoprotein Deposits in Early Atherosclerotic Lesions Distinguish Symptomatic From Asymptomatic Patients

Ballmoos

Dubler

Mirlacher

et al. 2006

ATVB

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“…Most of the interactions of LDL with other macromolecules and cells, including those that contribute to its atherogenicity, are controlled by segments of the nonexchangeable apolipoprotein B-100 (apoB-100) exposed at the particle surface (1)(2)(3)(4). However, exchangeable apolipoproteins can also modulate some of these interactions when adsorbed at the LDL surface, as suggested in the pioneering work of Alaupovic (5) and Campos and colleagues (6).…”

mentioning

confidence: 96%

A proteomic study of the apolipoproteins in LDL subclasses in patients with the metabolic syndrome and type 2 diabetes

Davidsson

Hulthe

Fagerberg

et al. 2005

Journal of Lipid Research

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The exchangeable apolipoproteins present in small, dense LDL (sdLDL) and large, buoyant LDL subclasses were evaluated with a quantitative proteomic approach in patients with the metabolic syndrome and with type 2 diabetes, both with subclinical atherosclerosis and the B LDL phenotype. The analyses included surface-enhanced laser adsorption/ionization, time-of-flight mass spectrometry, and subsequent identification by mass spectrometry or immunoblotting and were carried out in LDL subclasses isolated by ultracentrifugation in deuterium oxide gradients with near physiological salt concentrations. The sdLDLs of both types of patients were enriched in apolipoprotein C-III (apoC-III) and were depleted of apoC-I, apoA-I, and apoE compared with matched healthy controls with the A phenotype. The LDL complexes formed in serum from patients with diabetes with the arterial proteoglycan (PG) versican were also enriched in apoC-III. In addition, there was a significant correlation between the apoC-III content in sdLDL in patients and the apparent affinity of their LDLs for arterial versican.The unique distribution of exchangeable apolipoproteins in the sdLDLs of the patients studied, especially high apoC-III, coupled with the augmented affinity with arterial PGs, may contribute to the strong association of the dyslipidemia of insulin resistance with increased risk for cardiovascular disease. -Davidsson, P., J. Hulthe, B. Fagerberg, B-M. Olsson, C. Hallberg, B. Dahllöf, and G. Camejo. A proteomic study of the apolipoproteins in LDL subclasses in patients with the metabolic syndrome and type 2 diabetes.

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“…41 The LDL binding affinity of proteoglycans synthesized by vascular smooth muscle cells stimulated with SAA was determined using a modified gel mobility shift assay. Proteoglycans synthesized by vascular cells stimulated with as little as 5 mg/L SAA had increased LDL binding affinity compared to proteoglycans synthesized by unstimulated cells (K d , 29 g/ml LDL versus 90 g/ml LDL, respectively; P Ͻ 0.0005) (Figure 2).…”

Section: Saa Stimulates the Production Of Proteoglycans With Increasementioning

confidence: 99%

Serum Amyloid A, but Not C-Reactive Protein, Stimulates Vascular Proteoglycan Synthesis in a Pro-Atherogenic Manner

Wilson

Thompson

Webb

et al. 2008

The American Journal of Pathology

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Inflammatory markers serum amyloid A (SAA) and C-reactive protein (CRP) are predictive of cardiac disease and are proposed to play causal roles in the development of atherosclerosis, in which the retention of lipoproteins by vascular wall proteoglycans is critical. The purpose of this study was to determine whether SAA and/or CRP alters vascular proteoglycan synthesis and lipoprotein retention in a pro-atherogenic manner. Vascular smooth muscle cells were stimulated with either SAA or CRP (1 to 100 mg/L) and proteoglycans were then isolated and characterized. SAA, but not CRP, increased proteoglycan sulfate incorporation by 50 to 100% in a dose-dependent manner (P < 0.0001), increased glycosaminoglycan chain length, and increased low-density lipoprotein (LDL) binding affinity (K d , 29 g/ml LDL versus 90 g/ml LDL for SAA versus control proteoglycans; P < 0.005). Furthermore, SAA up-regulated biglycan via the induction of endogenous transforming growth factor (TGF)-␤. To determine whether SAA stimulated proteoglycan synthesis in vivo, ApoE ؊/؊ mice were injected with an adenovirus expressing human SAA-1, a null virus, or saline. Mice that received adenovirus expressing SAA had increased TGF-␤ concentrations in plasma and increased aortic biglycan content compared with mice that received either null virus or saline. Thus, SAA alters vascular proteoglycans in a pro-atherogenic manner via the stimulation of TGF-␤ and may play a causal role in the development of atherosclerosis.

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Lipoprotein-matrix interactions in macrovascular disease in diabetes

Cited by 24 publications

References 53 publications

Increased Apolipoprotein Deposits in Early Atherosclerotic Lesions Distinguish Symptomatic From Asymptomatic Patients

Increased Apolipoprotein Deposits in Early Atherosclerotic Lesions Distinguish Symptomatic From Asymptomatic Patients

A proteomic study of the apolipoproteins in LDL subclasses in patients with the metabolic syndrome and type 2 diabetes

Serum Amyloid A, but Not C-Reactive Protein, Stimulates Vascular Proteoglycan Synthesis in a Pro-Atherogenic Manner

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