Transendothelial transport of low density lipoprotein in association with cell mitosis in rat aorta.

Lin, Shing‐Jong; Jan, K M; Weinbaum, Sheldon; Chien, Shu

doi:10.1161/01.atv.9.2.230

Cited by 134 publications

(71 citation statements)

References 17 publications

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“…64 Alternatively, apoptosis induced by ChOx leads to increased endothelial cell turnover, which is associated with increased endothelial transcytosis or permeability. 65,66 Our previous studies with rabbits 25 demonstrated that ChOx injection led to increased vascular permeability. Therefore, circulating ChOx may increase arterial wall permeability and retention of particles such as LDL and VLDL, thus depositing more cholesterol and CEs into the vessel walls.…”

Section: Discussionmentioning

confidence: 99%

Cholesterol Oxidation Products Induce Vascular Foam Cell Lesion Formation in Hypercholesterolemic New Zealand White Rabbits

Rong

Shen

Chang

et al. 1999

ATVB

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Abstract-Circulating cholesterol oxidation products (ChOx) have long been implicated in the etiology of early atherosclerosis; however, direct in vivo evidence elucidating their role in atherogenesis is only recently becoming available. This study investigated ChOx effects on vascular lesion formation in New Zealand White rabbits under controlled hypercholesterolemic conditions. By closely monitoring plasma cholesterol levels and adjusting dietary cholesterol intake during a 78-day period, total plasma cholesterol exposures (cumulative plasma cholesterol levels over time) were controlled between 27 000 and 34 000 mg/dLϫday (final plasma cholesterol concentration, 467Ϯ77 mg/mL), representing a threshold range for sudanophilic lesion formation in the aorta. Twenty injections of a ChOx mixture (70 mg per injection) were made bearing an oxysterol composition similar to that found in circulating oxidatively modified low density lipoprotein. At sacrifice, the ChOx-injected rabbits (nϭ5) had (1) significantly higher plasma ChOx levels, (2) significantly increased cholesterol content in the aortas, mainly as esterified cholesterol, and (3) significantly greater sudanophilic lesion size and frequency in the aortas compared with vehicle-injected control rabbits (nϭ5). The aortic cholesterol content and extent of sudanophilic lesion area were correlated significantly with total plasma ChOx exposure (PϽ0.003 and PϽ0.0001, respectively) but not with total cholesterol exposure. The results indicate that for moderate experimental hypercholesterolemia, a situation more relevant to physiological hypercholesterolemia in humans, circulating ChOx may play an important role in inducing formation of early atherosclerotic lesions. Because ChOx are often present in cholesterol-containing diets, foam cell lesion formation induced by ChOx rather than cholesterol cannot be overlooked.

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Section: Discussionmentioning

confidence: 99%

Cholesterol Oxidation Products Induce Vascular Foam Cell Lesion Formation in Hypercholesterolemic New Zealand White Rabbits

Rong

Shen

Chang

et al. 1999

ATVB

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“…Lin et al (19) observed thoracic aortas of 10 rats to determine the total number of mitotic cells and the total number of LDL leakage sites. He found that 45.3% of total LDL leakage sites are formed by mitotic cells and that 80.5% of total mitotic cells are leaky.…”

Section: H911 Mass Transport Of Ldl With Effects Of Wall Shear Stressmentioning

confidence: 99%

“…Various experimental (2,19,21,37,38) and computational (1, 13-15, 25, 31, 33, 40) studies have been conducted to comprehend the pathways and mechanisms governing LDL transport from the artery lumen into the arterial wall and within the arterial wall. There are two pathways of LDL transport through the endothelium: by vesicular transcytosis, which is regulated by receptors on the endothelial cells (30), and through leaky junctions, most of which are located at the sites of dying or replicating cells (18,19).Early experimental studies on LDL transport were performed in animals. The main method was systemic injection of LDL solution with subsequent harvesting and examination of the animal's arteries.…”

mentioning

confidence: 99%

Computational modeling of coupled blood-wall mass transport of LDL: effects of local wall shear stress

Olgaç

Kurtcuoglu²,

Poulikakos³

2008

American Journal of Physiology-Heart and Circulatory Physiology

118

175

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Olgac U, Kurtcuoglu V, Poulikakos D. Computational modeling of coupled blood-wall mass transport of LDL: effects of local wall shear stress. Am J Physiol Heart Circ Physiol 294: H909-H919, 2008. First published December 14, 2007 doi:10.1152/ajpheart.01082.2007.-The work herein represents a novel approach for the modeling of lowdensity lipoprotein (LDL) transport from the artery lumen into the arterial wall, taking into account the effects of local wall shear stress (WSS) on the endothelial cell layer and its pathways of volume and solute flux. We have simulated LDL transport in an axisymmetric representation of a stenosed coronary artery, where the endothelium is represented by a three-pore model that takes into account the contributions of the vesicular pathway, normal junctions, and leaky junctions also employing the local WSS to yield the overall volume and solute flux. The fraction of leaky junctions is calculated as a function of the local WSS based on published experimental data and is used in conjunction with the pore theory to determine the transport properties of this pathway. We have found elevated levels of solute flux at low shear stress regions because of the presence of a larger number of leaky junctions compared with high shear stress regions. Accordingly, we were able to observe high LDL concentrations in the arterial wall in these low shear stress regions despite increased filtration velocity, indicating that the increase in filtration velocity is not sufficient for the convective removal of LDL.low-density lipoprotein transport; lipid accumulation; atherosclerosis; leaky junction MASS TRANSPORT of large molecules such as low-density lipoprotein (LDL) has received considerable interest in recent years because of its significance in the early stages of atherosclerosis. Locally elevated concentrations of LDL in the arterial wall are considered to be the initiator of atherosclerotic plaque formation (20,26). Various experimental (2,19,21,37,38) and computational (1, 13-15, 25, 31, 33, 40) studies have been conducted to comprehend the pathways and mechanisms governing LDL transport from the artery lumen into the arterial wall and within the arterial wall. There are two pathways of LDL transport through the endothelium: by vesicular transcytosis, which is regulated by receptors on the endothelial cells (30), and through leaky junctions, most of which are located at the sites of dying or replicating cells (18,19).Early experimental studies on LDL transport were performed in animals. The main method was systemic injection of LDL solution with subsequent harvesting and examination of the animal's arteries. Lin et al. (19) 2) used endothelial cell cultures to study LDL transport under pressurized conditions and found that LDL transport through leaky junctions constitutes the major part of total LDL transport (90.9%), whereas only a small portion occurs via the vesicular pathway (9.1%). Because the occurrence of leaky junctions is governed by the adjacent endothelial cells, and because the behavior o...

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“…A small fraction of clefts, however, are 'leaky' and provide a viable route for the paracellular transport of LDL (Lin et al, 1989). Since the domain Ω C considered here is periodic, all clefts within it must be identical i.e.…”

Section: Condition At Y = H − Bmentioning

confidence: 99%

The effect of the endothelial glycocalyx layer on concentration polarisation of low density lipoprotein in arteries

Vincent

Sherwin

Weinberg

2010

Journal of Theoretical Biology

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Transendothelial transport of low density lipoprotein in association with cell mitosis in rat aorta.

Cited by 134 publications

References 17 publications

Cholesterol Oxidation Products Induce Vascular Foam Cell Lesion Formation in Hypercholesterolemic New Zealand White Rabbits

Cholesterol Oxidation Products Induce Vascular Foam Cell Lesion Formation in Hypercholesterolemic New Zealand White Rabbits

Computational modeling of coupled blood-wall mass transport of LDL: effects of local wall shear stress

The effect of the endothelial glycocalyx layer on concentration polarisation of low density lipoprotein in arteries

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