Monocyte–platelet complexes on CD14/CD16 monocyte subsets: relationship with ApoA-I levels. A preliminary study

Boudjeltia, Karim Zouaoui; Brohée, Dany; Piro, P.; Nuyens, Vincent; Ducobu, Jean; Kherkofs, Myriam; Antwerpen, Pierre Van; Cauchie, Philippe; Remacle, Claude; Vanhaeverbeek, Michael

doi:10.1016/j.carpath.2007.10.004

Cited by 5 publications

(5 citation statements)

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“…Increasing evidence indicates that interactions between platelets and oxidized lipoproteins play a major role in the initiation, development and progression of atherosclerosis3–5. Apolipoprotein A-I (ApoA-I)6, apoA-I Milano 7 or high-density lipoprotein (HDL)8 have been shown to inhibit platelet hyper-reactivity and reverse the pro-thrombotic effects of hyperlipidemia. The atheroprotective and antithrombotic activity of HDL is generally attributed to the ability of HDL to promote reverse cholesterol transport and to the antioxidant, antiinflammatory properties of the lipids and proteins associated with HDL9.…”

mentioning

confidence: 99%

L-4F Alters Hyperlipidemic (But Not Healthy) Mouse Plasma to Reduce Platelet Aggregation

Buga

Navab

Imaizumi

et al. 2010

ATVB

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Background and Purpose-Hyperlipidemia is associated with platelet hyperreactivity. We hypothesized that L-4F, an apolipoprotein A-I mimetic peptide, would inhibit platelet aggregation in hyperlipidemic mice. Methods and Results-Injecting L-4F into apolipoprotein E (apoE)-null and low-density lipoprotein receptor-null mice resulted in a significant reduction in platelet aggregation in response to agonists; however, there was no reduction in platelet aggregation after injection of L-4F into wild-type (WT) mice. Consistent with these results, injection of L-4F into apoE-null mice prolonged bleeding time; the same result was not found in WT mice. Incubating L-4F in vitro with apoE-null platelet-rich plasma also resulted in decreased platelet aggregation. However, incubating washed platelets from either apoE-null or WT mice with L-4F did not alter aggregation.Compared with WT mice, unstimulated platelets from apoE-null mice contained significantly more 12-hydroxy 5,8,10,14-eicosatetraenoic acid, thromboxane A 2 , and prostaglandins D 2 and E 2 . In response to agonists, platelets from L-4F-treated apoE-null mice formed significantly less thromboxane A 2 , prostaglandins D 2 and E 2 , and 12-hydroxy 5,8,10,14-eicosatetraenoic acid. Conclusion-By

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confidence: 99%

L-4F Alters Hyperlipidemic (But Not Healthy) Mouse Plasma to Reduce Platelet Aggregation

Buga

Navab

Imaizumi

et al. 2010

ATVB

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“…This could contribute to the role of monocytes in atherogenesis, although so far in human monocyte subsets, no difference in PSGL-1 expression has been detected [66,67]. Reports about this matter are only few, and contradicting data have also been presented [68,69]. The link between human monocyte subsets and formation of PMC therefore still needs further clarification.…”

Section: Pmc-formation and Functional Consequencesmentioning

confidence: 99%

Molecular and functional interactions among monocytes, platelets, and endothelial cells and their relevance for cardiovascular diseases

Gils

Zwaginga

Hordijk

2008

Journal of Leukocyte Biology

259

211

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Platelets, monocytes, and endothelial cells are instrumental in the development and progression of cardiovascular diseases. Inflammation, a key process underlying cardiovascular disorders, is accompanied and amplified by activation of platelets and consequent binding of such platelets to the endothelium. There, platelet-derived chemokines, in conjunction with increased expression of adhesion molecules, promote the recruitment of circulating monocytes that will eventually migrate across the endothelial lining of the vessel into the tissues. Additionally, platelets may already become activated in the circulation and may form platelet-monocyte complexes, which show increased adhesive and migratory capacities themselves but also facilitate recruitment of noncomplexed leukocytes. They should therefore be considered as important mediators of inflammation. In molecular terms, these events are additionally governed by chemokines released and presented by the endothelium as well as the different classes of endothelial adhesion molecules that regulate the interactions among the various cell types. Most important in this respect are the selectins and their ligands, such as P-selectin glycoprotein (GP) ligand 1, and the integrins binding to Ig-like cell adhesion molecules as well as to GP, such as von Willebrand factor, present in the extracellular matrix or on activated endothelium. This review aims to provide an overview of these complex interactions and of their functional implications for inflammation and development of cardiovascular disease.

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“…16e20 Investigations into the platelet-binding capacity of each subset have so far presented contradictory results, with our group showing that there are similar levels of platelet binding to both classical and nonclassical monocytes. 13 In contrast, Boudjeltia et al 21 reported that platelet binding was much higher to CD14 þ CD16 þ monocytes than CD14 þþ CD16 -monocytes. It is possible that the differences in these results may reflect variations in the methodologies used.…”

Section: Introductionmentioning

confidence: 94%

“…It is possible that the differences in these results may reflect variations in the methodologies used. 13,21 Monocyte-platelet complexes have been identified as being present in a number of chronic inflammatory diseases, including atherosclerosis, 22,23 type I diabetes, 24 rheumatoid arthritis, and systemic erythematosus. 25 Interactions between monocytes and platelets were initially suggested to represent a surrogate measure of platelet activation; 26 however, there is growing evidence that the cross talk between monocytes and activated platelets promotes the activation and modulation of monocyte behavior, and that these interactions at sites of injury and infection may function to further promote the inflammatory response.…”

Section: Introductionmentioning

confidence: 99%

The Pathophysiological Relevance of Monocyte-platelet Interactions in Inflammatory Disease

Stephen

Dransfield

2010

Journal of Experimental & Clinical Medicine

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Monocyte–platelet complexes on CD14/CD16 monocyte subsets: relationship with ApoA-I levels. A preliminary study

Cited by 5 publications

References 14 publications

L-4F Alters Hyperlipidemic (But Not Healthy) Mouse Plasma to Reduce Platelet Aggregation

L-4F Alters Hyperlipidemic (But Not Healthy) Mouse Plasma to Reduce Platelet Aggregation

Molecular and functional interactions among monocytes, platelets, and endothelial cells and their relevance for cardiovascular diseases

The Pathophysiological Relevance of Monocyte-platelet Interactions in Inflammatory Disease

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