Glycosaminoglycan—Lipoprotein complexes from aortas of hypercholesterolemic rabbits

Mawhinney, Thomas P.; Augustyn, Joan M.; Fritz, Katherine

doi:10.1016/0021-9150(78)90161-2

Cited by 52 publications

(6 citation statements)

References 35 publications

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“…41 In vitro, chondroitin sulfate has a high affinity for very low and low density lipoprotein, 42 and complexes containing lipoprotein and chondroitin sulfate can be extracted from the aortas of hypercholesterolemic rabbits. 43 Increased binding of entered lipoprotein cholesteryl ester by greater amounts of chondroitin sulfate in the injured aorta, and the uptake and retention of some of the entered lipoprotein cholesteryl ester by the proliferating smooth muscle cells during the third to the fifth days after injury, which would be predicted by experiments in vitro, 44 would be consistent with the lower value of fractional loss calculated for the second through fifth days after injury.…”

supporting

confidence: 74%

Enhanced accumulation and turnover of esterified cholesterol in injured rabbit aorta.

Schwenke¹,

Zilversmit²

1987

Arteriosclerosis

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Several hypotheses have been advanced as possible explanations for the effects of injury. One of these 8 is that removal of the endothelium eliminates a barrier to influx of macromolecules from plasma. Others 9 argue that the endothelium prevents efflux of macromolecules from the artery. At present, relatively few studies have considered the contribution of plasma cholesteryl ester influx to the observed excess cholesteryl ester accumulating in the artery This work was supported by Research Grant HL10933 from the National Heart, Lung and Blood Institute of the United States Public Health Service. Donald B. Zilversmit is a Career Investigator of the American Heart Association. Dawn C. Schwenke held a National Science Foundation Graduate Fellowship during these studies.Received April 17, 1986; revision accepted March 18, 1987. after injury. Most of the measurements of cholesteryl ester influx 3 or lipoprotein accumulation 1011 into previously injured areas of the arterial wall have been made at relatively long times (months) after injury. At these times, the composition of the arterial wall In both reendothelialized areas and those remaining deendothelialized is considerably altered compared with uninjured areas.2 ' 7 1 2 1 3 Several studies suggest that the atherosclerosis risk factors, hypercholesterolemia 14 ' 15 and hypertension, 16 injure the arterial endothelium.Other studies 10 have measured the ability of acutely deendothelialized arterial tissue to limit the accumulation of low density lipoprotein (LDL) in vivo. Yet others 17 have studied the uptake of LDL by perfused vessels. The present investigation addresses the question of whether removal of aortic endothelium and perhaps underlying elements affect cholesteryl ester accumulation primarily by reducing the barrier to influx or to efflux of cholesteryl ester, or both. Specifically we have asked: 1) Does injury to the luminal surface of the artery result in enhanced cholesteryl ester influx in the injured artery? 2) If cholesteryl ester influx is elevated in injured areas, does the cholesteryl ester content of these areas increase concomitantly with the enhanced influx? 3) Is cholesteryl ester turnover altered in injured areas? Methods ChemicalsAll chemicals were reagent grade. Cholesterol methyl ether, 99% pure, (A 5 -cholesten-3G-ol-36-methyl) was pur-

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supporting

confidence: 74%

Enhanced accumulation and turnover of esterified cholesterol in injured rabbit aorta.

Schwenke¹,

Zilversmit²

1987

Arteriosclerosis

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“…Damage of proteoglycans can occur under exposure to atherogenic agents, such as oxidized LDL , hypercholesterolemia , and hyperglycemia . Glycosaminoglycans also form complexes with lipoproteins in the aortic wall and activate atherosclerotic mechanisms leading to cardiovascular disease . On the other hand, HDL inhibits proteoglycan synthesis and formation of complexes with lipoproteins , inhibiting atherogenesis.…”

Section: Discussionmentioning

confidence: 99%

Cardiovascular Risk and Serum Hyaluronic Acid: A Preliminary Study in a Healthy Population of Low/Intermediate Risk

Papanastasopoulou

Papastamataki

Karampatsis³

et al. 2016

Clinical Laboratory Analysis

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“…The demonstration of the existence of lipoprotein-proteoglycan complexes in vivo and their successful isolation from atherosclerotic lesions in humans and animals ( 15,16) have led to the hypothesis that the uptake of such complexes by macrophages could cause foam cell formation in vivo. Our recent studies have provided support to this hypothesis ( 17).…”

Section: Introductionmentioning

confidence: 99%

Lipoprotein-proteoglycan complexes induce continued cholesteryl ester accumulation in foam cells from rabbit atherosclerotic lesions.

Vijayagopal

Srinivasan²,

Xu³

et al. 1993

J. Clin. Invest.

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We studied the metabolism of lipoprotein-proteoglycan complexes by macrophage-derived foam cells. Foam cells were isolated from atherosclerotic rabbit aortas. ApoB-lipoproteinproteoglycan complex was isolated from human aorta fibrous plaque lesions and LDL-proteoglycan complex was formed in vitro. Both in vitro and in vivo complexes stimulated cholesteryl ester synthesis in foam cells by a dose-dependent, saturable process that resulted in the intracellular accumulation of cholesteryl ester. Stimulation ofcholesteryl ester synthesis was linear with time over a 32-h period. Polyinosinic acid inhibited the stimulation of cholesteryl ester synthesis by the complexes by 32-37%, whereas cytochalasin D only produced a 6-16% inhibition. Foam cells degraded '25I-LDL-proteoglycan complex and 125I-acetyl LDL in a saturable, dose-dependent manner. Excess unlabeled acetyl-LDL inhibited the degradation of '251-LDL-proteoglycan complex by 52%, while LDL had no effect. Similarly, excess unlabeled complex suppressed the degradation of '251-acetyl-LDL by 48%. Foam cells degraded 1251. methyl-LDL-proteoglycan complex to the same extent as 1251_ LDL-proteoglycan complex. These results show that foam cells from atherosclerotic lesions metabolize lipoprotein-proteoglycan complexes predominantly via receptor-mediated endocytosis and consequently continue to accumulate intracellular cholesteryl ester. (J. Clin. Invest. 1993. 91:1011-1018

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Glycosaminoglycan—Lipoprotein complexes from aortas of hypercholesterolemic rabbits

Cited by 52 publications

References 35 publications

Enhanced accumulation and turnover of esterified cholesterol in injured rabbit aorta.

Enhanced accumulation and turnover of esterified cholesterol in injured rabbit aorta.

Cardiovascular Risk and Serum Hyaluronic Acid: A Preliminary Study in a Healthy Population of Low/Intermediate Risk

Lipoprotein-proteoglycan complexes induce continued cholesteryl ester accumulation in foam cells from rabbit atherosclerotic lesions.

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