Accumulation of native and methylated low density lipoproteins by healing rabbit arterial wall.

Fischman, Alan J.; Lees, Ann M.; Lees, Robert S.; Barlai-Kovach, M; Strausś, H. William

doi:10.1161/01.atv.7.4.361

Cited by 28 publications

(14 citation statements)

References 20 publications

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“…Aortic accumulation was expressed as clearance of I25 I-LDL from the plasma by the aorta. Clearance (CL) represents the plasma volume equivalent of I25 I-LDL that was accumulated in a unit area of arterial wall (microliters per unit area) 11 and was determined by normalization of 125 I-LDL uptake per unit area of abdominal or thoracic aorta for mean plasma radioactivity as CL AA or TA=(RAA or TA/unit area AA OT TA )/(MPR)…”

Section: Image Analysis Of Photographsmentioning

confidence: 99%

Time course of 125I-labeled LDL accumulation in the healing, balloon-deendothelialized rabbit aorta.

Chang

Lees

1992

Arterioscler Thromb

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We previously showed by qualitative en face autoradiography that after 24 hours of circulation, 12S I-labeled low density lipoprotein (LDL) injected in tracer amounts accumulated focally at the edges of regenerating endothelial islands in the balloon catheter-deendothelialized aorta of the normocholesterolemic rabbit In the present study with the same animal model, we have used quantitative autoradiography to examine li5 I-LDL accumulation in the healing aorta as a function of LDL circulation time from 2.5 to 40 hours. The results demonstrated that '"I-LDL accumulation in the healing aorta occurred in two kinetically and biochemically distinct compartments, one of which was in equilibrium with plasma and one of which sequestered LDL. LDL accumulation in the still-deendothelialized aorta (DEA) was diffuse and only moderately intense on autoradiography. It peaked 4 hours after injection; over the following 36 hours the disappearance of IZ5 I-LDL from DEA paralleled the disappearance of IU

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Section: Image Analysis Of Photographsmentioning

confidence: 99%

Time course of 125I-labeled LDL accumulation in the healing, balloon-deendothelialized rabbit aorta.

Chang

Lees

1992

Arterioscler Thromb

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“…46 The consequence of endothelial injury could be an increase in endothelial permeability to macromolecules. The work done by Lees and coworkers (Roberts et al 47 and Fischman et al 48 ) suggested that low density lipoproteins were selectively accumulated in regions where the endothelium was actively regenerating after injury. Extracts of cigarette smoke have been shown to cause dose-dependent increases in albumin flux across the pulmonary endothelium in vitro through their effects on cytoskeletal elements.…”

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confidence: 99%

Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats.

Lin

Hong

Chang

et al. 1992

Arterioscler Thromb

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Repeated endothelial cell injury has been suggested as an initiating factor in atherogenesis. Dying or dead endothelial cells have been shown to make significant contributions to the local enhancement of transendothelial macromolecular transport. Since cigarette smoking is one of the major risk factors for atherosclerosis, we examined the hypothesis that smoking accelerates atherogenesis by increasing the frequency of endothelial cell death and hence transendothelial macromolecular transport. Sixteen male Sprague-Dawley rats were given nicotine at a weight-adjusted dose of 5 mg/kg body wt per day in their drinking water over a period of 6 weeks. A group of 16 age-matched male Sprague-Dawley rats not exposed to nicotine and maintained over the same time period served as the control group. In en face preparations of thoracic aorta, immunoglobulin G-containing dying or dead endothelial cells were identified by the indirect immunoperoxidase method, and endothelial leakage to Evans blue-albumin (EBA) complexes (5 minutes after intravenous injection) was visualized by fluorescence microscopy. The results showed that in nicotine-treated rats, 51% of dead endothelial cells were associated with EBA leakage, which was responsible for 57% of total EBA leaky foci. C igarette smoking is generally accepted to be one of the major risk factors for coronary heart disease. 1 -6 The potential for developing coronary heart disease in male cigarette smokers is approximately two times greater than in male nonsmokers. 7Large epidemiological surveys have shown that the incidence of morbidity and mortality from coronary heart disease increases progressively with the number of cigarettes smoked. 68 Smoking cessation has been demonstrated to be associated with a decline in cardiovascular death.9 Autopsy studies have also revealed the increased occurrence of advanced atherosclerotic le-

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“…• Lipoproteins (8,9), methylated (10) and oxidized (11) (35)(36)(37). These facts alone make a compelling argument to investigate 18 F-FDG as a marker of vulnerable plaque.…”

Section: Although the Process Was Recognizedmentioning

confidence: 99%

Radionuclide Techniques for Identifying Vulnerable Plaque

Dunphy

Schöder²,

Strausś³

2007

Journal of Nuclear Medicine

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Accumulation of native and methylated low density lipoproteins by healing rabbit arterial wall.

Cited by 28 publications

References 20 publications

Time course of 125I-labeled LDL accumulation in the healing, balloon-deendothelialized rabbit aorta.

Time course of 125I-labeled LDL accumulation in the healing, balloon-deendothelialized rabbit aorta.

Long-term nicotine exposure increases aortic endothelial cell death and enhances transendothelial macromolecular transport in rats.

Radionuclide Techniques for Identifying Vulnerable Plaque

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