Peroxidative stress and in vitro ageing of endothelial cells increases the monocyte-endothelial cell adherence in a human in vitro system

Molenaar, R.; Visser, W.J.; Verkerk, Anton; Koster, J.F.; Jongkind, J. F.

doi:10.1016/0021-9150(89)90103-2

Cited by 35 publications

(15 citation statements)

References 33 publications

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“…Increased peroxidative stress is similarly observed in aging endothelial cells in vitro. 24 However, in our study, PCOOH levels were not changed from baseline to 4 hours after methionine load in both younger and older groups. The inconsistency in lipid peroxidation between experimental and human studies may be that experimental studies have applied very high concentrations of reduced homocysteine, which generates excessive reactive oxygen species with consequent increase of lipid peroxidation.…”

Section: Discussionmentioning

confidence: 69%

“…16,21 However, conflicting results have been found in young healthy adults, who have no change in endotheliumdependent vasodilation or oxidative status after methionine load. 22 Aging is associated with progressive decrease of nitric oxide and increase of peroxidative stress 23,24 ; whether the effects of mild hyperhomocysteinemia on endotheliumdependent vasodilation and oxidative status are age-related remains less clear. To clarify the aging effect, we investigated the effects of methionine-induced hyperhomocysteinemia on the relationship between endothelium-dependent flowmediated vasodilation and oxidative status in different age groups.…”

mentioning

confidence: 99%

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Effects of Methionine-Induced Hyperhomocysteinemia on Endothelium-Dependent Vasodilation and Oxidative Status in Healthy Adults

2000

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Section: Discussionmentioning

confidence: 69%

mentioning

confidence: 99%

Effects of Methionine-Induced Hyperhomocysteinemia on Endothelium-Dependent Vasodilation and Oxidative Status in Healthy Adults

2000

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“…As the lesion advances, accumulated intimal macrophages engulf lipids by their scavenging function, and are converted to foam cells [27,35]. The expression of leukocyte adhesion molecules has been demonstrated in both human and experimental atherosclerosis [6,21] and Molenaar et al [17] have demonstrated that the adherence of monocytes to endothelial cells is significantly increased by in vitro aging of the endothelial cells. Prostacyclin, which is the most potent inhibitor of platelet aggregation (thrombus formation) [18], is produced by vascular tissue, primarily by the endothelium.…”

Section: Discussionmentioning

confidence: 99%

Endothelial cell heterogeneity in experimentally-induced rabbit atherosclerosis. Demonstration of multinucleated giant endothelial cells by scanning electron microscopy and cell culture

Tashiro

Shimokama

Haraoka

et al. 1994

Vichows Archiv A Pathol Anat

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We investigated the aortic endothelial cells of cholesterol-fed rabbits, using scanning electron microscopy and a cell culture technique. Rabbits were given a 1% cholesterol diet intermittently for up to 40 weeks. In these animals, the area of endothelial cells was increased and the cells showed polymorphism in relation to the progression of atherosclerosis. In animals fed the cholesterol diet for 12, 28 and 40 weeks, the average area of the endothelial cells was 436 +/- 15, 762 +/- 153, and 836 +/- 165 microns2, respectively. In the cholesterol-fed 40-week group, in particular, giant endothelial cells, measuring more than 1200 microns2, accounted for 14% of the population. In animals fed a standard diet there was no significant difference in endothelial cell morphology between control 0-week and control 40-week groups; in both, the luminal surface of the thoracic aorta formed a homogeneous sheet covered by small rhomboidal endothelial cells, the area of most being less than 400 microns2. Primary cultured endothelial cells harvested from those control groups were mononuclear typical small cells with a centrally located nucleus; the proportion of binucleated cells was less than 2% and no multinucleated giant cells with three or more nuclei were detected. Endothelial cells from the cholesterol-fed groups, however, contained larger numbers of binucleated cells, with the number increasing in proportion to the duration of cholesterol feeding. The major distinguishing feature of the endothelial cells in the cholesterol-fed groups was the presence of multinucleated giant cells with three or more nuclei; these accounted for 2.3% and 3.3% of the total cell population in the cholesterol-fed 28- and 40-week groups, respectively. No bromodeoxyuridine uptake was found in the nuclei of the cultured multinucleated giant cells. Heterogeneity of endothelial cells, with the concomitant appearance of multinucleated giant cells, emerges with the progression of diet-induced atherosclerosis. The morphological alterations of endothelial cells observed in the present study intimately reflect changes in their function associated with the progression of atherosclerotic lesions.

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“…65 Because nonmyocytic cells were less prevalent in AH than in YH lesions, we conclude that the age-related increase of lymphocytes is selective and not dependent on a possible, spontaneous, generalized increase of adhering mononuclear cells to the endothelial surface with aging. 13,66 Mechanisms responsible for this increased recruitment of T lymphocytes are still to be clarified. Because T lymphocytes have many relevant biological properties, including the secretion of inflammatory cytokines, 67 it is likely that greater lymphocyte infiltrates deliver locally increased amounts of cytokines, thus favoring the progression of lesions.…”

Section: Orlandi Et Almentioning

confidence: 99%

Aging Influences Development and Progression of Early Aortic Atherosclerotic Lesions in Cholesterol-Fed Rabbits

Orlandi

Marcellini

Spagnoli

2000

ATVB

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Abstract-The arterial wall in aged animals shows an increased susceptibility to develop atherosclerotic lesions, although the mechanisms by which aging acts are still unclear. We investigated early aortic lesions in aged rabbits (5 to 6 years old, AH group) and young rabbits (2 months old, YH group) after 2 months of 0.2% cholesterol feeding. Fatty streaks or spots mainly in the proximal segments occupied a relative surface area that was greater in AH than in YH rabbits, although plasma cholesterol and lipoprotein levels did not differ. YH lesions showed an irregular endothelial profile mainly from accumulations of large, rounded, RAM 11-positive macrophagic foam cells. There was a higher percentage of myocytic, CD-5-positive, proliferating, and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL)-positive cells and larger accumulation of glycosaminoglycans in AH fatty streaks than in YH lesions. Ligation-mediated polymerase chain reaction confirmed differences in apoptosis. Early fibromuscular coats and subendothelial plasma-like insudate were also observed in AH lesions. Aged-matched normocholesterolemic rabbits showed a diffuse aortic intimal thickening composed of myocytic cells with a synthetic phenotype and extracellular matrix rich in glycosaminoglycans. In addition, in aged rabbits, we observed a spontaneous increase of monocytes adhering to the endothelial surface and a reduced expression of endothelial nitric oxide synthase in areas distant from the branches. These plasma cholesterol-independent spontaneous changes in the aortic wall of aged rabbits seem to act as a multiple atherogenic risk factor. Moreover, age-related differences in the distribution, composition, and proliferative and apoptotic rates represent crucial events during the progression of early fatty streaks to advanced plaques. Key Words: atherosclerosis Ⅲ aging Ⅲ smooth muscle cells Ⅲ glycosaminoglycans Ⅲ endothelial nitric oxide synthase T he outset of severe or advanced fibroatheromatous plaques is a late event and represents the final result of a slow and complex phenomenon. 1,2 Human and animal studies suggest that atherosclerotic plaques begin as early lesions or fatty streaks, 2,3 although the mechanisms responsible for this progression are still unclear. In fact, advanced plaques are generally encountered after the fourth or fifth decade of life, 2,4 and their development is at first related to the chronic exposure of the arterial wall to exogenous risk factors, 1 in particular to hypercholesterolemia. 5 In rabbits receiving a hyperlipemic diet, the pattern of atherosclerotic lesions depends on cholesterol content 6 and duration of the diet. 7 In particular, a low-dose hypercholesterolemic diet, even when extended for a long period of time, induces the development of fatty streaks. 6 In addition to dietary habits, endogenous or intrinsic factors have been also considered in the pathogenesis of atherosclerosis. On the basis of the high incidence of cardiovascular disease in elderly people, McGill et al 8 ...

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Peroxidative stress and in vitro ageing of endothelial cells increases the monocyte-endothelial cell adherence in a human in vitro system

Cited by 35 publications

References 33 publications

Effects of Methionine-Induced Hyperhomocysteinemia on Endothelium-Dependent Vasodilation and Oxidative Status in Healthy Adults

Effects of Methionine-Induced Hyperhomocysteinemia on Endothelium-Dependent Vasodilation and Oxidative Status in Healthy Adults

Endothelial cell heterogeneity in experimentally-induced rabbit atherosclerosis. Demonstration of multinucleated giant endothelial cells by scanning electron microscopy and cell culture

Aging Influences Development and Progression of Early Aortic Atherosclerotic Lesions in Cholesterol-Fed Rabbits

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