Activated Platelets Induce Monocyte Chemotactic Protein-1 Secretion and Surface Expression of Intercellular Adhesion Molecule-1 on Endothelial Cells

Gawaz, Meinrad; Neumann, Franz Josef; Dickfeld, Timm; Koch, Werner; Laugwitz, Karl Ludwig; Adelsberger, Helmut; Langenbrink, Kirsten; Page, Sharon; Neumeier, D.; Schömig, Albert; Brand, Korbinian

doi:10.1161/01.cir.98.12.1164

Cited by 271 publications

(205 citation statements)

References 47 publications

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“…Accordingly in our previous study, which examined the interaction between monocytes and MC, both cell-to-cell contact and soluble factors were required for the maximum activation of the latter (18). Other studies have shown that platelet contact induces chemokine or adhesion molecule expression by endothelial cells or leukocytes through NF-B activation (10,12). NF-B plays a critical role in inflammatory response through induction of a variety of proinflammatory genes.…”

Section: Discussionmentioning

confidence: 99%

Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Tanaka

Kuroiwa²,

Ikeuchi³

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Platelets are thought to play an important role in the initiation and the progression of a variety of glomerulonephritides. This study examined whether platelets induce production of monocyte chemoattractant protein-1 (MCP-1), a chemokine involved in leukocyte recruitment and glomerular injury, by cultured human mesangial cells (MC). To this end, platelets isolated from normal human donors were cocultured with MC at various ratios. MCP-1 synthesis was evaluated by quantitative real-time PCR and enzyme-linked immunosorbent assay. Platelets at 1:100 ratio (MC to platelets) induced an approximately 20-fold increase in mesangial MCP-1 mRNA and protein expression through an obligatory cell-to-cell contact-dependent mechanism. Importantly, blockade of the CD40/CD40 ligand (CD40L) pathway with neutralizing antibodies decreased MCP-1 production by approximately 60%. It was confirmed that CD40 was functionally expressed on MC. Gelshift assays and inhibitors of phosphorylation were used to demonstrate that activation of p38 mitogen-activated protein kinase, protein tyrosine kinases, and nuclear factor-B activation were essential for MCP-1 production. These data indicate that platelet/MC contact stimulates the production of MCP-1 and may contribute to glomerular inflammatory responses by recruiting leukocytes from the peripheral blood.

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Section: Discussionmentioning

confidence: 99%

Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Tanaka

Kuroiwa²,

Ikeuchi³

et al. 2002

Journal of the American Society of Nephrology

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“…32,33 Blocking nuclear factor-B activity in endothelial cells by anti-sense oligonucleotides will affect not only ICAM-1 upregulation but also MCP-1 production and, ultimately, the homing of monocytes. 34 Adhesion and transmigration, mediated by several interacting molecular mechanisms, appear to be essential for monocyte traffic in atherosclerosis. Some of these factors, such as nuclear factor-b, MCP-1, interleukin-8/neutrophil-activating peptide, plateletactivating factor, and RANTES, may be activated or upregulated at an early stage in apoE Ϫ/Ϫ but not wild-type mice.…”

Section: Discussionmentioning

confidence: 99%

Modulation of Expression of Endothelial Intercellular Adhesion Molecule-1, Platelet–Endothelial Cell Adhesion Molecule-1, and Vascular Cell Adhesion Molecule-1 in Aortic Arch Lesions of Apolipoprotein E–Deficient Compared With Wild-Type Mice

Zibara

Chignier

Covacho

et al. 2000

ATVB

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Abstract-Human vascular adhesion molecules, such as intercellular adhesion molecule-1 (ICAM-1), platelet-endothelial cell adhesion molecule-1 (PECAM-1), and vascular cell adhesion molecule-1 (VCAM-1), are thought to play a critical role in the homing of leukocytes to sites of atherosclerotic lesions. However, very little is known about the expression of adhesion molecules in the vasculature of mice models, such as apolipoprotein E knockout (apoE Ϫ/Ϫ ) mice, the lesions of which closely mimic human atherosclerotic lesions. This study has first quantitatively characterized the mean expression of endothelial adhesion molecules, lining the whole vessel intimal circumference, over a period of time (0 to 20 weeks of diet) in aortic arch lesions of male apoE-deficient compared with wild-type (C57BL/6) mice. These animals were fed a chow or a cholesterol-rich diet. ApoE Ϫ/Ϫ animals showed first an increase (at 6 weeks) and then a reduction (at 16 weeks) in the mean expression of ICAM-1 (PϽ0.05) and PECAM-1 (PϽ0.05) but not VCAM-1 levels. Such modulation of the mean expression of adhesion molecules was not observed in wild-type mice. Confirmation of immunohistochemistry results on ICAM-1 was obtained by Northern blots performed on the aortic arch of apoE and C57BL6 chow-fed mice over a period of 20 weeks. Moreover, the presence of VCAM-1 was also confirmed at the RNA level, on aortas of control and apoE mice, by reverse transcription-polymerase chain reaction. In the second part of the study, we assayed the levels of adhesion molecules, in different types of histologically defined atherosclerotic lesions, in apoE Ϫ/Ϫ animals fed for 20 weeks. All 3 adhesion molecules (ICAM-1, PECAM-1, and VCAM-1) were observed to be reduced in fibrofatty and complex lesions but not in fatty streaks or in areas without lesions. These results indicate that the expression of these adhesion molecules in apoE-deficient animals varies with the evolution of the plaque from a fatty to a fibrous stage. (Arterioscler Thromb Vasc

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“…20,21 The endothelial cells seem a likely candidate, because they first receive the impact of acute hyperglycemia, which may reduce NO availability. 19 Further support for this hypothesis comes from the results of a recent study that shows that ADP-activated platelets induce surface expression of ICAM-1 in cultured endothelial cells 22 : an additional effect of acute hyperglycemia in humans is to increase platelet aggregation in response to stimulants such as ADP, which, according to Grawaz et al, 22 may contribute to the elevation of plasma sICAM-1 levels. Last, the increased plasma sICAM-1 levels seen after an oral glucose challenge in humans is completely prevented by the administration of the antioxidant glutathione, 13 pointing to an important role for oxidative stress in mediation of the effects of hyperglycemia on sICAM-1 levels.…”

Section: Marfella Et Al Circulating Adhesion Molecules In Humansmentioning

confidence: 97%

Circulating Adhesion Molecules in Humans

et al. 2000

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Background-We assessed the role of glucose and insulin in the regulation of circulating levels of soluble intercellular adhesion molecule-1 (sICAM-1) and vascular adhesion molecule-1 (sVCAM-1) in normal subjects and in patients with type 2 diabetes. Methods and Results-Plasma glucose concentrations were acutely raised in 10 normal subjects and 10 newly diagnosed, complication-free type 2 diabetic patients and maintained at 15 mmol/L for 2 hours. In normal subjects, plasma sICAM-1, but not sVCAM-1, levels rose significantly (PϽ0.01) at 1 hour and returned to basal values at 2 hours. In another study, octreotide was infused during the hyperglycemic clamp to block the release of endogenous insulin; this prevented the late fall of plasma sICAM-l levels observed in under control clamp conditions. The diabetic patients had plasma sICAM-1 levels significantly higher (PϽ0.01) than those of the control subjects; plasma sVCAM-1 levels were similar. Both sICAM-l and sVCAM-1 concentrations did not change significantly during the control hyperglycemic clamp; however, octreotide infusion increased plasma sICAM-1 levels, which remained significantly (PϽ0.05) above baseline during the whole clamp. In an additional 10 type 2 diabetic patients, overnight euglycemia (plasma glucose 5.5 mmol/L) obtained with the aid of an artificial pancreas or supplementation with L-arginine (10 g PO for 30 days), the natural precursor of NO, normalized the increased plasma sICAM-1 levels. Conclusions-Acute hyperglycemia increases circulating sICAM-1 levels in normal subjects, whereas the correction of hyperglycemia with insulin or L-arginine supplementation restored to normal levels the increased plasma sICAM-1 levels of type 2 diabetic patients.

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Activated Platelets Induce Monocyte Chemotactic Protein-1 Secretion and Surface Expression of Intercellular Adhesion Molecule-1 on Endothelial Cells

Abstract: The present study indicates that activated platelets modulate chemotactic (MCP-1) and adhesive (ICAM-1) properties of endothelial cells via an NF-kappaB-dependent mechanism. Platelet-induced activation of the NF-kappaB system might contribute to early inflammatory events in atherogenesis.

Cited by 271 publications

References 47 publications

Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Human Platelets Stimulate Mesangial Cells to Produce Monocyte Chemoattractant Protein-1 via the CD40/CD40 Ligand Pathway and May Amplify Glomerular Injury

Modulation of Expression of Endothelial Intercellular Adhesion Molecule-1, Platelet–Endothelial Cell Adhesion Molecule-1, and Vascular Cell Adhesion Molecule-1 in Aortic Arch Lesions of Apolipoprotein E–Deficient Compared With Wild-Type Mice

Circulating Adhesion Molecules in Humans

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