Aortic intimal monocyte recruitment in the normo and hypercholesterolemic baboon (Papio cynocephalus)

Schwartz, Colin J.; Sprague, Eugene A.; Kelley, Jim; Valente, Anthony J.; Suenram, C. Alan

doi:10.1007/bf00704370

Cited by 60 publications

(20 citation statements)

References 29 publications

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“…This may result in the local accumulation of monocytes within the vessel wall. Such a process would have direct relevance for the increased incidence of atherosclerosis in diabetes, as intimal monocyte recruitment is thought to be an important early step in the pathogenesis of atherosclerosis [25]. The adhesion of activated monocytes to AGE-proteins within the vessel wall may result in the remodelling of vessel structure following protease secretion [4,5].…”

Section: Discussionmentioning

confidence: 99%

Activated human monocytes exhibit receptor-mediated adhesion to a non-enzymatically glycosylated protein substrate

Gilcrease

Hoover

1990

Diabetologia

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Summary.Non-enzymatic glycosylation of proteins is thought to play an important role in the development of diabetic vascular disease. Advanced glycosylation end products have been shown to accumulate on basement membranes and collagen in diabetes, and receptors for such adducts have recently been found on murine macrophages. We have observed that human monocytes activated by endotoxin express receptors for advanced glycosylation end products of similar affinity and number as has been previously reported for murine macrophages. In addition, there is an increased adherence of activated human monocytes to a nonenzymatically glycosylated albumin substrate, and such adhesion can be competitively inhibited up to 50% by soluble, non-enzymatically glycosylated albumin. We suggest that increased adherence of activated monocytes to non-enzymatically glycosylated proteins in the vessel wall may result in monocyte stimulation and/or local monocyte accumulation and thereby contribute to vascular disease in diabetes.

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Section: Discussionmentioning

confidence: 99%

Activated human monocytes exhibit receptor-mediated adhesion to a non-enzymatically glycosylated protein substrate

Gilcrease

Hoover

1990

Diabetologia

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“…Restoration of migratory capacity was accompanied by alterations in the cytoskeleton system, especially in actin arrangement are a major constituent of the atherosclerotic plaque and play an important role in the development of the lesion. 1 " 4 In vitro studies have shown that modified forms of low density Lipoprotein (LDL) cause accumulation of cholesterol esters in cultured macrophages, 5 " 9 whereas normal LDL does not result in significant lipid accumulation within these cells. 5 Steinberg et al 10 have reported that LDL is converted by endothelial cells or chemical oxidation with Cu 2+ into a negatively charged form, which is avidly taken up by macrophages via the scavenger receptor.…”

Section: A Mechanism For Atherosclerosis Regression?mentioning

confidence: 99%

Endocytosis of oxidized LDL and reversibility of migration inhibition in macrophage-derived foam cells in vitro. A mechanism for atherosclerosis regression?

Pataki

Lusztig

Robenek

1992

Arterioscler Thromb

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The ability of macrophage-derived foam cells to migrate from atherosclerotic lesions represents one potential mechanism for the regression of atherosclerosis. It is, however, generally recognized that the transformation of macrophages into foam cells results in greatly reduced migrational ability. In the present study, we set out to investigate the factors affecting migratory capability in foam cell-like cells with the use of an in vitro assay. Foam cell-like cells were prepared by incubating macrophages in the presence of oxidized low density lipoprotein (LDL). The transformation to a typical foam cell morphology was demonstrated by Nile red staining (light microscopy), and the mechanisms of binding, uptake, and intracellular processing of oxidized LDL were established by colloidal gold labeling on the ultrastructural level. With the in vitro assay, the migration of these foam cell-like cells was found to be markedly inhibited compared with untreated, control macrophages. However, zymosan-activated mouse serum restored migration in oxidized LDL-treated cells to levels similar to those of control cells. Restoration of migratory capacity was accompanied by alterations in the cytoskeleton system, especially in actin arrangement.

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“…The role of monocytes in the pathogenesis of atherosclerosis is well recognized and the adhesion of blood-borne monocytes to the endothelium of lesion-prone regions of the vasculature is one of the earliest documented events in numerous animal mod-els of atherosclerosis (1)(2)(3)(4)(5)(6)(7). Altered or dysfunctional endothelium expresses a number of cytokines, adhesion molecules, vasoactive compounds, and growth factors, which in turn attract, activate, and cause the transendothelial migration of monocytes (8)(9)(10)(11)(12).…”

Section: Introductionmentioning

confidence: 99%

Alpha-tocopherol inhibits agonist-induced monocytic cell adhesion to cultured human endothelial cells.

Faruqi¹,

Motte²,

DiCorleto³

1994

J. Clin. Invest.

210

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Antioxidants have been proposed to be anti-atherosclerotic agents; however, the mechanisms underlying their beneficial effects are poorly understood. We have examined the effect of a-tocopherol (a-tcp) on one cellular event in atherosclerotic plaque development, monocyte adhesion to stimulated endothelial cells (ECs). Human umbilical vein ECs were pretreated with a-tcp before stimulation with known agonists of monocyte adhesion: IL-1 (10 ng/ml), LPS (10 ng/ ml), thrombin (30 U/ml), or PMA (10 nM). Agonist-induced monocytic cell adhesion, but not basal adhesion, was inhibited in a time-and concentration-dependent manner by atcp. The IC50 of a-tcp on an IL-i-induced response was 45 jpM. The inhibition correlated with a decrease in steady state levels of E-selectin mRNA and cell surface expression of E-selectin which is consistent with the ability of a monoclonal antibody to E-selectin to inhibit monocytic cell adhesion in this system. Probucol (50 ,uM) and N-acetylcysteine (20 mM) also inhibited agonist-induced monocytic cell adhesion; whereas, several other antioxidants had no significant effect. Protein kinase C (PKC) does not appear to play a role in the a-tcp effect since no suppression of phosphorylation of PKC substrates was observed. Activation of the transcription factor NF-cB is reported to be necessary but not sufficient for E-selectin expression in EC. Electrophoretic mobility shift assays failed to show an cr-tcp-induced decrease in activation of this transcription factor after cytokine stimulation. It has been hypothesized that ca-tcp acts as an anti-atherosclerotic molecule by inhibiting generation of oxidized LDL-a putative triggering molecule in the atherosclerotic process. Our results point to a novel alternative mechanism of action of a-tcp. (J. Clin. Invest. 1994. 94:592-600.)

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Aortic intimal monocyte recruitment in the normo and hypercholesterolemic baboon (Papio cynocephalus)

Cited by 60 publications

References 29 publications

Activated human monocytes exhibit receptor-mediated adhesion to a non-enzymatically glycosylated protein substrate

Activated human monocytes exhibit receptor-mediated adhesion to a non-enzymatically glycosylated protein substrate

Endocytosis of oxidized LDL and reversibility of migration inhibition in macrophage-derived foam cells in vitro. A mechanism for atherosclerosis regression?

Alpha-tocopherol inhibits agonist-induced monocytic cell adhesion to cultured human endothelial cells.

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