Risk stratification of patients with acute myocardial infarction by quantification of circulating monocyte-platelet aggregates

“…Moreover, markers of inflammation predict cardiovascular events in several disease states [4][5][6]. Increased platelet activation [7,8] and sympathovagal imbalance of cardiac autonomic nervous system (ANS) activity [9][10][11][12] are also well-known predictors of acute coronary events.…”

Section: Introductionmentioning

confidence: 99%

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

Lanza

Barone

Scalone

et al. 2010

Journal of Internal Medicine

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“…Increased levels of platelet-monocyte aggregates are found in patients with acute myocardial infarction and can therefore been seen as an early marker of acute myocardial infarction. 45 Selectively blocking platelet-monocyte interactions is currently under evaluation in clinical trials. Inclacumab, an anti-P-selectin antibody, hinders the formation of platelet-monocyte aggregates and thereby prevents the inflammatory burst of these interactions.…”

Section: Discussionmentioning

confidence: 99%

Platelet CD40 Exacerbates Atherosclerosis by Transcellular Activation of Endothelial Cells and Leukocytes

Gerdes

Seijkens

Lievens

et al. 2016

ATVB

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Objective— Beyond their eminent role in hemostasis and thrombosis, platelets are recognized as mediators of inflammation. Platelet cluster of differentiation 40 (CD40) ligand (CD40L and CD154) plays a key role in mediating platelet-induced inflammation in atherosclerosis. CD40, the receptor for CD40L, is present on platelets; however, the role of CD40 on this cell type is until now undefined. Approach and Results— We found that in both mice and humans, platelet CD40 mediates the formation of platelet–leukocyte aggregates and the release of chemokine (C-X-C motif) ligand 4. Leukocytes were also less prone to adhere to CD40-deficient thrombi. However, platelet CD40 was not involved in platelet aggregation. Activated platelets isolated from Cd40 −/− Apoe −/− mice adhered less to the endothelium upon injection into Apoe −/− mice when compared with CD40-sufficient platelets. Furthermore, lack of CD40 on injected platelets led to reduced leukocyte recruitment to the carotid artery as assayed by intravital microscopy. This was accompanied by a decrease in endothelial vascular cell adhesion molecule-1, platelet endothelial cell adhesion molecule, VE-cadherin, and P-selectin expression. To investigate the effect of platelet CD40 in atherosclerosis, Apoe −/− mice received thrombin-activated Apoe −/− or Cd40 −/− Apoe −/− platelets every 5 days for 12 weeks, starting at the age of 17 weeks, when atherosclerotic plaques had already formed. When compared with mice that received Apoe −/− platelets, those receiving Cd40 −/− Apoe −/− platelets exhibited a >2-fold reduction in atherosclerosis. Plaques of mice receiving CD40-deficient platelets were less advanced, contained less macrophages, neutrophils, and collagen, and displayed smaller lipid cores. Conclusions— Platelet CD40 plays a crucial role in inflammation by stimulating leukocyte activation and recruitment and activation of endothelial cells, thereby promoting atherosclerosis.

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“…[26][27][28] In addition, PLAs have been observed in prethrombotic or prothrombotic clinical conditions, and may provide a suitable predictor of acute myocardial infarction. 29,30 It was demonstrated that repeated injection of thrombinactivated platelets into Apoe Ϫ/Ϫ mice resulted in acceleration of atherosclerosis, which was caused by platelet-mediated activation of the endothelium and P-selectin-dependent formation of PLAs. 23 Considering the role of platelet CD40L in both thrombosis and inflammation, we investigated the atherogenic contribution of platelet CD40L.…”

Section: Introductionmentioning

confidence: 99%

Platelet CD40L mediates thrombotic and inflammatory processes in atherosclerosis

Lievens

Zernecke

Seijkens

et al. 2010

Blood

255

221

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CD40 ligand (CD40L), identified as a costimulatory molecule expressed on T cells, is also expressed and functional on platelets. We investigated the thrombotic and inflammatory contributions of platelet CD40L in atherosclerosis. Although CD40L-deficient (Cd40l ؊/؊ ) platelets exhibited impaired platelet aggregation and thrombus stability, the effects of platelet CD40L on inflammatory processes in atherosclerosis were more remarkable. Repeated injections of activated Cd40l ؊/؊ platelets into Apoe ؊/؊ mice strongly decreased both platelet and leukocyte adhesion to the endothelium and decreased plasma CCL2 levels compared with wildtype platelets. Moreover, Cd40l ؊/؊ platelets failed to form proinflammatory plateletleukocyte aggregates. Expression of CD40L on platelets was required for plateletinduced atherosclerosis as injection of Cd40l ؊/؊ platelets in contrast to Cd40l ؉/؉ platelets did not promote lesion formation. Remarkably, injection of Cd40l ؉/؉ , but not Cd40l ؊/؊ , platelets transiently decreased the amount of regulatory T cells

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Risk stratification of patients with acute myocardial infarction by quantification of circulating monocyte-platelet aggregates

Cited by 17 publications

References 7 publications

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

Inflammation-related effects of adjuvant influenza A vaccination on platelet activation and cardiac autonomic function

Platelet CD40 Exacerbates Atherosclerosis by Transcellular Activation of Endothelial Cells and Leukocytes

Platelet CD40L mediates thrombotic and inflammatory processes in atherosclerosis

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