Recruitment and dynamics of leukocytes in the formation of arterial intimal thickening — A comparative study with normo- and hypercholesterolemic rabbits

Kling, Dorothée; Holzschuh, Thomas; Betz, E.

doi:10.1016/0021-9150(93)90104-3

Cited by 32 publications

(16 citation statements)

References 35 publications

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“…The process of neointimal growth in the presence of leukocyte infiltration has also been observed in other experimental animal models. 20,21 One advantage of the carotid ligation model is that an SMC-rich neointima consistently forms by 28 days. 12,13 Carotid ligation consistently induced a local inflammatory response manifested by leukocyte recruitment in the vessel wall and upregulation of adhesion molecules.…”

Section: Discussionmentioning

confidence: 99%

Adenosine A _2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model

McPherson

Barringhaus

Bishop

et al. 2001

ATVB

114

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Abstract-Endothelial activation and leukocyte recruitment are early events in atherosclerosis and the vascular response to injury. Adenosine has anti-inflammatory effects on leukocytes and endothelial cells mediated through its A 2A receptor. We tested the hypothesis that A 2A activation would reduce inflammation and neointimal formation in a murine carotid ligation model. Before injury, mice were randomized to a 7-day subcutaneous infusion of a specific A 2A receptor agonist (ATL-146e, 0.004 g/kg per minute), vehicle control, ATL-146e plus ZM241385 (a selective A 2A antagonist), or ZM241385 alone. Leukocyte recruitment and adhesion molecule expression were assessed at early time points, and the neointimal area was measured at 14 and 28 days after injury. Compared with control mice, ATL-146e-treated mice had significantly less neutrophil and macrophage recruitment and vascular cell adhesion molecule-1, intercellular adhesion molecule-1, and P-selectin expression in the first 7 days after injury. Neointimal area was markedly and persistently reduced by 80% at 14 and 28 days, despite termination of ATL infusion at 7 days. ATL-146eϩZM241385-treated and ZM241385-treated animals had neointimal areas similar to those of control animals, confirming that the observed effects of ATL-146e were mediated specifically by the A 2A receptor. These data demonstrate that novel stimulation of adenosine A 2A receptors can inhibit early inflammatory processes that are important in neointimal formation after vascular injury.

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Section: Discussionmentioning

confidence: 99%

Adenosine A _2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model

McPherson

Barringhaus

Bishop

et al. 2001

ATVB

114

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“…28,31,32 In vascular diseases, there is an enhanced infiltration of inflammatory cells containing high levels of NADPH oxidase and expression by vascular cells of not only neutrophil-like oxidases, but other oxidases as well (eg, 15-lipoxygenase, XO), all capable of mediating direct electron transfer to lucigenin. 9,[53][54][55][56][57][58][59][60] Within an intact cellular or tissue environment, it has not been determined with precision the enzyme(s) that are responsible for the observed "lucigenin reductase" activity. Thus, in conditions that have been associated with elevated lucigenin chemiluminescence, the apparent increase in rates of O 2…”

Section: Coelenterazine-dependent Chemiluminescencementioning

confidence: 99%

Chemiluminescent Detection of Oxidants in Vascular Tissue

Tarpey

White

Suarez

et al. 1999

Circulation Research

144

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Abstract-Lucigenin-amplified chemiluminescence has frequently been used to assess the formation of superoxide in vascular tissues. However, the ability of lucigenin to undergo redox cycling in purified enzyme-substrate mixtures has raised questions concerning the use of lucigenin as an appropriate probe for the measurement of superoxide production. Addition of lucigenin to reaction mixtures of xanthine oxidase plus NADH resulted in increased oxygen consumption, as well as superoxide dismutase-inhibitable reduction of cytochrome c, indicative of enhanced rates of superoxide formation. Additionally, it was revealed that lucigenin stimulated oxidant formation by both cultured bovine aortic endothelial cells and isolated rings from rat aorta. Lucigenin treatment resulted in enhanced hydrogen peroxide release from endothelial cells, whereas exposure to lucigenin resulted in inhibition of endothelium-dependent relaxation in isolated aortic rings that was superoxide dismutase inhibitable. In contrast, the chemiluminescent probe coelenterazine had no significant effect on xanthine oxidase-dependent oxygen consumption, endothelial cell hydrogen peroxide release, or endothelium-dependent relaxation. Study of enzyme and vascular systems indicated that coelenterazine chemiluminescence is a sensitive marker for detecting both superoxide and peroxynitrite.

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“…Activated neutrophils might produce oxygen free radicals and therefore modify LDL but they are found in small numbers in the atherosclerotic intima (53). However it has been shown in rabbits fed a high cholesterol diet that polymorphonuclear neutrophils were the most numerous cells at the beginning of the atheromateous process, and were soon replaced by monocytes and lymphocytes (54). Therefore it seems particularly interesting to study the interaction between polymorphonuclear neutrophils and lipoproteins during the early stages of atherogenesis in animal models.…”

Section: Discussionmentioning

confidence: 99%

Effects of Human Low-Density Lipoproteins on Superoxide Production by Formyl-Methionyl-Leucyl-Phenylalanine Activated Polymorphonuclear Leukocytes

Bonneau¹,

Couderc²,

Tissot³

et al. 1997

Clinical Chemistry and Laboratory Medicine

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Summary: Neutrophils play a major role in the host defence by producing reactive oxygen species. These products are liberated by activated cells and are known to cause endothelial cell injury and damage. The present study shows that low-density lipoproteins increase Superoxide anion production by twofold in polymorphonuclear leukocytes stimulated by formyl-Met-Leu-Phe in vitro. Moreover, LDL induced a large increase in phosphoinositides and cytosolic-free calcium. Data from experiments performed on neutrophils treated with pertussis toxin, staurosporine, propranolol or nifiumic acid suggest that modulation of phospholipase D and A 2 activities could be involved in the modification by LDL of leukocyte response to formyl-Met-Leu-Phe. LDL lipid moiety could play a key role in their action on polymorphonuclear functions because cholesterol was exchanged between lipoproteins and cells that can modify membrane fluidity and interact with the formyl-Met-Leu-Phe receptor.

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Recruitment and dynamics of leukocytes in the formation of arterial intimal thickening — A comparative study with normo- and hypercholesterolemic rabbits

Cited by 32 publications

References 35 publications

Adenosine A _2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model

Adenosine A _2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model

Chemiluminescent Detection of Oxidants in Vascular Tissue

Effects of Human Low-Density Lipoproteins on Superoxide Production by Formyl-Methionyl-Leucyl-Phenylalanine Activated Polymorphonuclear Leukocytes

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Recruitment and dynamics of leukocytes in the formation of arterial intimal thickening — A comparative study with normo- and hypercholesterolemic rabbits

Cited by 32 publications

References 35 publications

Adenosine A 2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model

Adenosine A 2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model

Chemiluminescent Detection of Oxidants in Vascular Tissue

Effects of Human Low-Density Lipoproteins on Superoxide Production by Formyl-Methionyl-Leucyl-Phenylalanine Activated Polymorphonuclear Leukocytes

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Adenosine A _2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model

Adenosine A _2A Receptor Stimulation Reduces Inflammation and Neointimal Growth in a Murine Carotid Ligation Model