The Uncoupling of Monocyte–Platelet Interactions from the Induction of Proinflammatory Signaling in Monocytes

Stephen, Jillian; Emerson, Barry; Fox, Keith A.A.; Dransfield, Ian

doi:10.4049/jimmunol.1301250

Cited by 54 publications

(46 citation statements)

References 52 publications

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“…The present study revealed that HCN1 expression was not detectable in the atrial muscle of dogs in the AF or sham control groups, which may have been due to very low expression levels. The results were consistent with the findings of previous studies, including the study by Stephen et al (14). It is widely accepted that HCN3 is expressed primarily in the central nervous system and not in the heart; however, the present study did not include the detection of HCN3.…”

Section: Discussionsupporting

confidence: 93%

Expression of hyperpolarization-activated cyclic nucleotide-gated channel isoforms in a canine model of atrial fibrillation

Zhang

Gan

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to analyze the mRNA and protein expression levels of atrial hyperpolarization-activated cyclic nucleotide-gated (HCN) channel isoforms in the left atrial muscle of dogs with multiple organ failure. A total of 14 beagle dogs with multiple organ failure, including seven cases with sinus rhythm and seven cases with atrial fibrillation (AF), underwent surgery to remove a sample of left atrial appendage tissue. The expression levels of a number of HCN channel subtypes were subsequently measured using quantitative polymerase chain reaction and western blot analysis. The mRNA and protein expression levels of HCN2 and HCN4 increased significantly in the AF group when compared with the sinus rhythm group. However, expression of the HCN1 isoform was not detected. Therefore, increased expression levels of HCN2 and HCN4 may be important molecular mechanisms in the pathogenesis of AF, which were associated with differences in patients with valvular heart disease.

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Section: Discussionsupporting

confidence: 93%

Expression of hyperpolarization-activated cyclic nucleotide-gated channel isoforms in a canine model of atrial fibrillation

Zhang

Gan

et al. 2016

Experimental and Therapeutic Medicine

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“…During in vitro platelet stimulation experiments using thrombin, however, monocyte interaction with activated platelets resulted in increased cytokine production [30]. Induction of pro-inflammatory signaling in monocytes by platelets was dependent on secreted platelet products, not on direct platelet-monocyte interaction as reported in another study [31]. Although cytokine production is indispensable for an adequate host response to invading pathogens, excessive cytokine production might have detrimental effects during severe infection [32].…”

Section: Discussionmentioning

confidence: 88%

Platelet and endothelial cell P-selectin are required for host defense against Klebsiella pneumoniae-induced pneumosepsis

Stoppelaar

Veer

Roelofs

et al. 2015

Journal of Thrombosis and Haemostasis

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To cite this article: de Stoppelaar SF, van't Veer C, Roelofs JJTH, Claushuis TAM, de Boer OJ, Tanck MWT, Hoogendijk AJ, van der Poll T.Platelet and endothelial cell P-selectin are required for host defense against Klebsiella pneumoniae-induced pneumosepsis. J Thromb Haemost 2015; 13: 1128-38.Summary. Background: Sepsis is associated with activation of platelets and endothelial cells accompanied by enhanced P-selectin surface expression. Both platelet-and endothelial P-selectin have been associated with leukocyte recruitment and induction of inflammatory alterations. Klebsiella (K.) pneumoniae is a common human sepsis pathogen, particularly in the context of pneumonia. Methods: Wild-type (WT) and P-selectin-deficient (Selp À/ À ) mice or bone marrow chimeric mice were infected with K. pneumoniae via the airways to induce pneumosepsis. Mice were sacrificed during early (12 h after infection) or late-stage (44 h) sepsis for analyses, or followed in a survival study. Results: Selp À/À mice displayed 10-1000-fold higher bacterial burdens in the lungs, blood and distant organs during late-stage sepsis. P-selectin deficiency did not influence leukocyte recruitment to the lungs, but was associated with decreased platelet-monocyte complexes and increased cytokine release. Bone marrow transfer studies revealed a role for both platelet and endothelial cell P-selectin as mice deficient in platelet or endothelial cell P-selectin displayed an intermediate phenotype in bacterial loads and survival compared with full wild-type or full knockout control mice. Conclusion: Both platelet and endothelial cell P-selectin contribute to host defense during Klebsiella pneumosepsis.

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“…These observations are in line with results from a recent study, showing that in response to thrombin activated platelets, not thrombin itself, trigger early signaling events (such as intracellular Ca ++ flux) in monocytes on platelet-monocyte interaction. 39 Platelet interaction with monocytes via P-selectin-PSGL-1 further increased the rate and quantity of OxLDL uptake by monocytes in a dose-dependent manner. Scavenger receptor CD36, the major receptor for OxLDL on platelets, 23,24 was mainly responsible for the platelet-mediated effects on OxLDL uptake by monocytes.…”

Section: Discussionmentioning

confidence: 95%

Platelets Mediate Oxidized Low-Density Lipoprotein–Induced Monocyte Extravasation and Foam Cell Formation

Badrnya

Schrottmaier

Kral

et al. 2014

ATVB

143

115

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Objective-A growing body of evidence indicates that platelets contribute to the onset and progression of atherosclerosis by modulating immune responses. We aimed to elucidate the effects of oxidized low-density lipoprotein (OxLDL) on platelet-monocyte interactions and the consequences of these interactions on platelet phagocytosis, chemokine release, monocyte extravasation, and foam cell formation. Approach and Results-Confocal microscopy and flow cytometric analysis revealed that in vitro and in vivo stimulation with OxLDL resulted in rapid formation of platelet-monocyte aggregates, with a preference for CD16+ monocyte subsets. This platelet-monocyte interaction facilitated OxLDL uptake by monocytes, in a process that involved platelet CD36-OxLDL interaction, release of chemokines, such as CXC motif ligand 4, direct platelet-monocyte interaction, and phagocytosis of platelets. Inhibition of cyclooxygenase with acetylsalicylic acid and antagonists of ADP receptors, P2Y1 and P2Y12, partly abrogated OxLDL-induced platelet-monocyte aggregates and platelet-mediated lipid uptake in monocytes. Platelets also enhanced OxLDL-induced monocyte transmigration across an endothelial monolayer via direct interaction with monocytes in a transwell assay. Importantly, in LDLR −/− mice, platelet depletion resulted in a significant decrease of peritoneal macrophage recruitment and foam cell formation in a thioglycollate-elicited peritonitis model. In platelet-depleted wild-type mice, transfusion of ex vivo OxLDL-stimulated platelets induced monocyte extravasation to a higher extent when compared with resting platelets. Conclusions-Our results on OxLDL-mediated platelet-monocyte aggregate formation, which promoted phenotypic changes in monocytes, monocyte extravasation and enhanced foam cell formation in vitro and in vivo, provide a novel mechanism for how platelets potentiate key steps of atherosclerotic plaque development and plaque destabilization.

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The Uncoupling of Monocyte–Platelet Interactions from the Induction of Proinflammatory Signaling in Monocytes

Cited by 54 publications

References 52 publications

Expression of hyperpolarization-activated cyclic nucleotide-gated channel isoforms in a canine model of atrial fibrillation

Expression of hyperpolarization-activated cyclic nucleotide-gated channel isoforms in a canine model of atrial fibrillation

Platelet and endothelial cell P-selectin are required for host defense against Klebsiella pneumoniae-induced pneumosepsis

Platelets Mediate Oxidized Low-Density Lipoprotein–Induced Monocyte Extravasation and Foam Cell Formation

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