Extracellular Matrix Modulates Macrophage Functions Characteristic to Atheroma

Wesley, Robert B.; Meng, Xiaoping; Godin, Denis; Galis, Zorina S.

doi:10.1161/01.atv.18.3.432

Cited by 139 publications

(36 citation statements)

References 49 publications

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“…Indeed, plaque instability strongly depends on the activation and recruitment of monocytes to the arterial wall, driven by chemoattractant cytokines (27,44). In parallel, COX-2 and PGE 2 promote the release and activation of matrix-degrading enzymes, such as matrix metalloproteinase 2 (MMP-2) and MMP-9 (24,44,45), which contribute to plaque rupture (24,46,47). In this regard, our data suggest that the presence of chronic arthritis in hyperlipemic rabbits results in a more vulnerable vessel wall at the site of the endothelial lesion.…”

Section: Discussionmentioning

confidence: 99%

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Largo

Sánchez‐Pernaute

Marcos

et al. 2008

Arthritis & Rheumatism

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Objective. To determine whether systemic inflammation induced by chronic antigen-induced arthritis (AIA) accelerates vascular lesions in rabbits with atherosclerosis.Methods. Two models of atherosclerosis and chronic AIA were combined. Atherosclerosis was induced by coupling a hyperlipemic diet with an endothelial lesion at the femoral arteries, while chronic AIA was induced by ovalbumin injection. Markers in sera and peripheral blood mononuclear cells (PBMCs) as well as vessels and synovial membranes from the rabbits with the double phenotype (both chronic AIA and atherosclerosis) were compared with those from rabbits with each disease alone.Results. Serum levels of interleukin-6, C-reactive protein, and prostaglandin E 2 increased in rabbits with both chronic AIA and atherosclerosis as compared with healthy animals or animals with either chronic AIA alone or atherosclerosis alone. NF-B binding and CCL2 and cyclooxygenase 2 (COX-2) expression were higher in PBMCs from rabbits with both chronic AIA and atherosclerosis than in PBMCs from healthy rabbits. The intima-media thickness ratio of femoral arteries was equally increased in rabbits with atherosclerosis alone and in rabbits with both chronic AIA and atherosclerosis, but the latter group showed a higher level of macrophage infiltration. Femoral CCL2 and COX-2 expression was increased in rabbits with both chronic AIA and atherosclerosis as compared with rabbits with atherosclerosis alone. In the aortas, vascular lesions were found in 27% of rabbits with atherosclerosis alone and in 60% of rabbits with both chronic AIA and atherosclerosis. Rabbits with both chronic AIA and atherosclerosis exhibited more severe synovitis and higher synovial expression of CCL2 than did rabbits with chronic AIA alone.Conclusion. The onset of chronic AIA in animals with atherosclerosis resulted in the local and systemic up-regulation of mediators of tissue inflammation and plaque instability associated with a higher incidence of aortic lesions. This model could represent a novel approach to the study of inflammation-associated atherosclerosis.

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Section: Discussionmentioning

confidence: 99%

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Largo

Sánchez‐Pernaute

Marcos

et al. 2008

Arthritis & Rheumatism

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“…Plating human peripheral blood mononuclear cells (PBMCs) on a type I collagen matrix resulted in increased differentiation and activation, as evidenced by increased cell spreading, and changes in cell surface marker expression, including decreased CD14 expression (part of the lipopolysaccharide receptor complex) and increased CD71 expression (the transferrin receptor). 49 Furthermore, adhesion to type I collagen increased macrophage phagocytic activity, 50 leading to the increased uptake of acetylated low-density lipoprotein (LDL). 49 Collagen stimulation also enhanced phorbol myristate acetate (PMA)-induced superoxide production by macrophages, and primed the secretion of arachidonic acid metabolites such as prostaglandin E2 and thromboxane B2.…”

Section: Collagen Regulation Of Inflammatory Cells In Atherosclerosismentioning

confidence: 99%

“…49 Furthermore, adhesion to type I collagen increased macrophage phagocytic activity, 50 leading to the increased uptake of acetylated low-density lipoprotein (LDL). 49 Collagen stimulation also enhanced phorbol myristate acetate (PMA)-induced superoxide production by macrophages, and primed the secretion of arachidonic acid metabolites such as prostaglandin E2 and thromboxane B2. 51 Finally, type I collagen stimulated MMP-9 expression by PBMCs 49 and MMP-1 expression by alveolar macrophages in vitro.…”

Section: Collagen Regulation Of Inflammatory Cells In Atherosclerosismentioning

confidence: 99%

“…49 Collagen stimulation also enhanced phorbol myristate acetate (PMA)-induced superoxide production by macrophages, and primed the secretion of arachidonic acid metabolites such as prostaglandin E2 and thromboxane B2. 51 Finally, type I collagen stimulated MMP-9 expression by PBMCs 49 and MMP-1 expression by alveolar macrophages in vitro. 52 Akin to the differences described above for SMCs, polymeric and monomeric type I collagen elicit different responses in macrophages.…”

Section: Collagen Regulation Of Inflammatory Cells In Atherosclerosismentioning

confidence: 99%

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Collagens in the progression and complications of atherosclerosis

et al. 2009

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Collagens constitute a major portion of the extracellular matrix in the atherosclerotic plaque, where they contribute to the strength and integrity of the fibrous cap, and also modulate cellular responses via specific receptors and signaling pathways. This review focuses on the diverse roles that collagens play in atherosclerosis; regulating the infiltration and differentiation of smooth muscle cells and macrophages; controlling matrix remodeling through feedback signaling to proteinases; and influencing the development of atherosclerotic complications such as plaque rupture, aneurysm formation and calcification. Expanding our understanding of the pathways involved in cell-matrix interactions will provide new therapeutic targets and strategies for the diagnosis and treatment of atherosclerosis.

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“…For example, PGE 2 has been shown to induce production of the inflammatory cytokine interleukin-6. 15 Matrix metalloproteinases (MMPs) have been implicated in macrophage migration, 16 and COX-2 expression and PGE 2 have been shown to promote the release and activation of MMPs. 17 Therefore, COX-2 inhibition might interfere with macrophage migration by reducing release and activation of MMPs.…”

mentioning

confidence: 99%

Cyclooxygenase-2 Promotes Early Atherosclerotic Lesion Formation in LDL Receptor–Deficient Mice

Burleigh¹,

Babaev²,

Oates³

et al. 2002

Circulation

273

192

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Background — Atherosclerosis has features of an inflammatory disease. Because cyclooxygenase (COX)-2 is expressed in atherosclerotic lesions and promotes inflammation, we tested the hypotheses that selective COX-2 inhibition would reduce early lesion formation in LDL receptor–deficient (LDLR −/− ) mice and that macrophage COX-2 expression contributes to atherogenesis in LDLR −/− mice. Methods and Results — Treatment of male LDLR −/− mice fed the Western diet with rofecoxib or indomethacin for 6 weeks resulted in significant reductions in atherosclerosis in the proximal aorta (25% and 37%) and in the aorta en face (58% and 57%), respectively. Rofecoxib treatment did not inhibit platelet thromboxane production, a COX-1–mediated process, but it significantly reduced the urinary prostacyclin metabolite 2,3-dinor-6-keto-PGF 1α . Fetal liver cell transplantation was used to generate LDLR −/− mice null for expression of the COX-2 gene by macrophages. After 8 weeks on the Western diet, COX-2 −/− →LDLR −/− mice developed significantly less (33% to 39%) atherosclerosis than control COX-2 +/+ →LDLR −/− mice. In both the inhibitor studies and the transplant studies, serum lipids did not differ significantly between groups. Conclusions — The present studies provide strong pharmacological and genetic evidence that COX-2 promotes early atherosclerotic lesion formation in LDLR −/− mice in vivo. These results support the potential of anti-inflammatory approaches to the prevention of atherosclerosis. (Circulation. 2002;105:1816-1823.)

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Extracellular Matrix Modulates Macrophage Functions Characteristic to Atheroma

Cited by 139 publications

References 49 publications

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Chronic arthritis aggravates vascular lesions in rabbits with atherosclerosis: A novel model of atherosclerosis associated with chronic inflammation

Collagens in the progression and complications of atherosclerosis

Cyclooxygenase-2 Promotes Early Atherosclerotic Lesion Formation in LDL Receptor–Deficient Mice

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