Effect of proteoglycans on lipoprotein-cell interactions: possible contribution to atherogenesis

Camejo, G; Hurt-Camejo, Eva; Bondjers, G.

doi:10.1097/00041433-199010000-00006

Cited by 29 publications

(11 citation statements)

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“…This association has been demonstrated in case-control studies of myocardial infarction survivors ( [5,8,11], the ECTIM study, personal results), 244 G. LUC et al and angiographically documented coronary disease [6,10]. Certain characteristics of small dense LDLs, such as a greater affinity for arterial wall proteoglycans [25] or a modification of the interaction with the arterial cells, might adversely affect vascular function [26][27][28]. Certain characteristics of small dense LDLs, such as a greater affinity for arterial wall proteoglycans [25] or a modification of the interaction with the arterial cells, might adversely affect vascular function [26][27][28].…”

Section: Discussionmentioning

confidence: 83%

Relationship between low‐density lipoprotein size and apolipoprotein A‐I‐containing particles: the ECTIM study

Luc

Bard

Poulain

et al. 1997

Eur J Clin Investigation

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It is now established that small dense low-density lipoproteins (LDLs) are more common among patients with coronary heart disease than among control individuals. Small LDL size is also associated with a high-risk profile, including increased levels of triglycerides and decreased high-density lipoprotein (HDL)-cholesterol. Furthermore, some human HDL particles contain both apolipoprotein (apo) A-I and apoA-II (LpA-I:A-II) while others contain apoA-I but are devoid of apoA-II (LpA-I). We have investigated the relationship between LDL size, measured by non-denaturing gradient-gel electrophoresis, and HDL parameters, particularly LpA-I and LpA-I:A-II levels, in healthy control subjects (n = 408). LDL size was positively and significantly correlated with HDL-cholesterol (r = 0.43), apoA-I (r = 0.32) and LpA-I (r = 0.29), whereas no correlation was observed with apoA-II and LpA-I:A-II. The determination of the mean apoA-I and LpA-I in the quintiles of LDL size distribution revealed a progressive increase in apoA-I and LpoA-I from the first quintile (small LDLs), 137 and 42 mg dL-1 respectively, to the fifth quintile (large LDLs), 161 and 54 mg dL-1 respectively. Conversely, no evolution of apoA-II and LpA-I:A-II was observed. Multivariate analysis showed that not only triglycerides, but also HDL-cholesterol, apoA-I and LpA-I, are determinants of LDL size, depending on the model used. Thus, part of the variation in size of LDLs is associated with the metabolism of HDL independently of that of triglycerides. Thus, a low concentration of LpA-I combined with the presence of small LDLs could contribute to the high-risk profile observed in subjects with small LDLs.

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Section: Discussionmentioning

confidence: 83%

Relationship between low‐density lipoprotein size and apolipoprotein A‐I‐containing particles: the ECTIM study

Luc

Bard

Poulain

et al. 1997

Eur J Clin Investigation

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“…Second, it may be questioned whether the method presently used to assess LDL-cholesterol reactivity by precipitation of serum with human arterial proteoglycan is of clinical importance. In this respect, previous studies using this method have demonstrated that there is a considerable variability between individuals in terms of LDL reactivity with proteoglycans [16] and that this variation seems to be associated with compositional characteristics of the LDL [3,4]. As regards manifest atherosclerotic disease, LDL was found to have higher affinity for proteoglycans in patients with coronary heart disease than in matched controls [14].…”

Section: Discussionmentioning

confidence: 96%

“…A hallmark of atherosclerosis is the accumulation of cholesterol in the intimal lesion [1]. Deposition of cholesterol is both related to the level of circulating low-density lipoprotein (LDL) and to the affinity of lipoproteins for mesenchymal proteoglycans in the intima [1][2][3]. A growing body of data indicates that the latter process is of great importance for modification of LDL and for the formation of foam cells [1][2][3].…”

Section: Introductionmentioning

confidence: 99%

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Multifactorial treatment of hypertensive men at high cardiovascular risk and low‐density lipoprotein cholesterol affinity to human arterial proteoglycans

Fagerberg

Wiklund

Agewall³

et al. 1996

Eur J Clin Investigation

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The purpose of this work was to examine in an open, randomized parallel-group study whether an intervention programme directed towards hypercholesterolaemia, smoking and diabetes mellitus in treated hypertensive men was associated with less complex formation between low-density lipoprotein (LDL) and human arterial proteoglycans than was the case with usual care. The intervention consisted mainly of non-pharmacological treatment, but drug therapy could be instituted to achieve the treatment goals in the intervention group. The intervention programme was associated with a significant reduction in body mass index, and 46% of the patients were on lipid-lowering medication at the follow-up examination. The net differences were (intervention--usual care): change in serum LDL-cholesterol, -0.48 mmol L-1 (95% confidence interval -0.84 to -0.11 mmol L-1), precipitated LDL-cholesterol, -5.5 micrograms (95% CI -9.0 to -1.1 micrograms). The latter remained after adjustment for the difference in serum LDL-cholesterol between groups. Our conclusion is that the multifactorial risk factor treatment programme was associated with a reduced tendency of LDL to form complexes with human arterial proteoglycans.

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“…The interactions of LDL particles with proteoglycans and GAGs have also been reported to cause changes in both the apoB100 component and the lipid pool of the particles. 26,30,[43][44][45] The interactions of LDL particles with GAGs have been shown to induce such conformational changes in apoB100 that increase the exposure of arginine-and lysine-containing segments 26 and, in contrast to the PLA 2 effect on the lipid pool of LDL, decrease the organization of the core and surface regions of the particles. 26,30 These structural changes induced by GAGs do not alone lead to aggregation or fusion of LDL, but they have been shown to accelerate both proteolytic 27,28 and oxidative modifications 28 of the particles.…”

Section: Discussionmentioning

confidence: 99%

Lipolytic Modification of LDL by Phospholipase A ₂ Induces Particle Aggregation in the Absence and Fusion in the Presence of Heparin

Hakala

Öörni

Ala‐Korpela

et al. 1999

ATVB

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Abstract-One of the first events in atherogenesis is modification of low density lipoprotein (LDL) particles in the arterial wall with ensuing formation of aggregated and fused lipid droplets. The accumulating particles are relatively depleted in phosphatidylcholine (PC). Recently, secretory phospholipase A 2 (PLA 2 ), an enzyme capable of hydrolyzing LDL PC into fatty acid and lysoPC molecules, has been found in atherosclerotic arteries. There is also evidence that both LDL and PLA 2 bind to the glycosaminoglycan (GAG) chains of extracellular proteoglycans in the arterial wall. Here we studied the effect of heparin GAG on the lipolytic modification of LDL by PLA 2 . Untreated LDL, heparin-treated LDL, and heparin-bound LDL were lipolyzed with bee venom PLA 2 . In the presence of albumin, lipolysis resulted in aggregation in all 3 preparations of the LDL particles. Lipolysis of untreated LDL did not result in aggregation if albumin was absent from the reaction medium, and the lipolytic products accumulated in the particles rendering them negatively charged. However, heparin-treated and heparin-bound lipolyzed LDL particles aggregated even in the absence of albumin. Importantly, in the presence of albumin, some of the heparin-treated and heparin-bound lipolyzed LDL particles fused, the proportion of fused particles being substantially greater when LDL was bound to heparin during lipolysis. In summary, lipolysis of LDL PC by PLA 2 under physiological conditions, which allow transfer of the lipolytic degradation products to albumin, leads to fusion of LDL particles in the presence, but not in the absence, of heparin. Thus, it is possible that within the GAG meshwork of the arterial intima, PLA 2 -induced modification of LDL is one source of the lipid droplets during atherogenesis.

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Effect of proteoglycans on lipoprotein-cell interactions: possible contribution to atherogenesis

Cited by 29 publications

References 0 publications

Relationship between low‐density lipoprotein size and apolipoprotein A‐I‐containing particles: the ECTIM study

Relationship between low‐density lipoprotein size and apolipoprotein A‐I‐containing particles: the ECTIM study

Multifactorial treatment of hypertensive men at high cardiovascular risk and low‐density lipoprotein cholesterol affinity to human arterial proteoglycans

Lipolytic Modification of LDL by Phospholipase A ₂ Induces Particle Aggregation in the Absence and Fusion in the Presence of Heparin

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Effect of proteoglycans on lipoprotein-cell interactions: possible contribution to atherogenesis

Cited by 29 publications

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Relationship between low‐density lipoprotein size and apolipoprotein A‐I‐containing particles: the ECTIM study

Relationship between low‐density lipoprotein size and apolipoprotein A‐I‐containing particles: the ECTIM study

Multifactorial treatment of hypertensive men at high cardiovascular risk and low‐density lipoprotein cholesterol affinity to human arterial proteoglycans

Lipolytic Modification of LDL by Phospholipase A 2 Induces Particle Aggregation in the Absence and Fusion in the Presence of Heparin

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Lipolytic Modification of LDL by Phospholipase A ₂ Induces Particle Aggregation in the Absence and Fusion in the Presence of Heparin