Transfer of tissue factor from leukocytes to platelets is mediated by CD15 and tissue factor

Rauch, Ursula; Bonderman, Diana; Bohrmann, Bernd; Badimón, Juan J.; Himber, Jacques; Riederer, Markus A.; Nemerson, Yale

doi:10.1182/blood.v96.1.170

Cited by 315 publications

(58 citation statements)

References 35 publications

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“…However, leukocyte-derived MV were associated with platelets which subsequently altered the reactivity status of the platelets (Figure 1). These data provide evidence as have other studies that MV generated by one cell type in response to LPS alter reactivity of other cell types within the circulation (69,(73)(74)(75)(76). Although existing data provide evidence that LPS induces MV release from isolated cell or cells in vitro, more studies are needed to understand how other bacterial proteins affect MV production from host cells in vivo.…”

Section: Host Processes Triggered By Bacterial Infection Direct Resposupporting

confidence: 54%

“…Pro-inflammatory agents-Release of cytokines provoked in the host cells by invading micro-organisms may in turn stimulate release of MV from non-infected cells (9). For example, pro-inflammatory cytokines such as TNFα or interleukin-1 (IL-1) stimulate MV production from endothelial cells and monocytes which contain tissue factor (TF) and have high procoagulant activity (75)(76)(77). Activated complement component (C5a) also increases the release of cellular MV from endothelia and platelets (78).…”

Section: Indirect Response Of Mammalian Cells To Infection-associatedmentioning

confidence: 99%

“…MV also represent a reservoir of blood borne tissue factor (TF) activity (109,110). Monocytes and polymorphonuclear leukocytes are one source of TF-bearing MV, which when transferred or in association with platelets, trigger and propagate thrombosis (76). Whether platelets produce TF is controversial (109).…”

Section: In the Initiation And Amplification Of Coagulation And Thmentioning

confidence: 99%

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Microvesicles at the Crossroads Between Infection and Cardiovascular Diseases

Xiong

Miller

et al. 2012

Journal of Cardiovascular Pharmacology

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Observational and experimental studies continue to support the association of infection and infection-stimulated inflammation with development of cardiovascular disease (CVD) including atherosclerosis and thrombosis. Microvesicles (MV) are heterogeneous populations of sealed membrane-derived vesicles shed into circulation by activated mammalian cells and/or pathogenic microbes that may represent an interface between bacterial/microbial infection and increased risk of CVD. This review evaluates how MV act to modulate and intersect immunological and inflammatory responses to infection with particular attention to progression of CVD. While infection-related stimuli provoke release of MV from blood and vascular cells, MV express phosphatidylserine (PS) and other procoagulant factors on their surface which initiate and amplify blood coagulation. In addition, MV mediate cell-cell adhesion which may stimulate production of pro-inflammatory cytokines in vascular cells, which in turn aggravate progression of CVD and propagate atherothrombosis. MV transfer membrane receptors, RNA and proteins among cells, and present auto-antigens from their cells of origin to proximal or remote target cells. Because MV harbor cell surface proteins and contain cytoplasmic components of the parent cell, they mediate biological messages and play a pivotal role in the crossroad between infection-stimulated inflammation and cardiovascular diseases.

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Section: Host Processes Triggered By Bacterial Infection Direct Resposupporting

confidence: 54%

Section: Indirect Response Of Mammalian Cells To Infection-associatedmentioning

confidence: 99%

Section: In the Initiation And Amplification Of Coagulation And Thmentioning

confidence: 99%

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Microvesicles at the Crossroads Between Infection and Cardiovascular Diseases

Xiong

Miller

et al. 2012

Journal of Cardiovascular Pharmacology

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“…Two isoforms of TF are expressed in human vascular cells, membrane bound human "full length" TF-flTF [12,14] and the soluble alternatively spliced human (asH)TF doi: 10.1111/j.1755-5922.2011.00305.x [15,16]. FlTF and soluble asTF circulate in blood and contribute to thrombogenesis [17][18][19][20][21][22].…”

Section: Introductionmentioning

confidence: 99%

Bivalirudin Inhibits Periprocedural Platelet Function and Tissue Factor Expression of Human Smooth Muscle Cells

Pepke¹,

Eisenreich²,

Jaster³

et al. 2011

Cardiovascular Therapeutics

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SUMMARYAim: A major concern of stent implantation after percutaneous coronary intervention (PCI) is acute stent thrombosis. Effective inhibition of periprocedural platelet function in patients with coronary artery disease (CAD) leads to an improved outcome. In this study, we examined the periprocedural platelet reactivity after administrating bivalirudin during PCI compared to unfractionated heparin (UFH) administration. Further, the effect of bivalirudin on induced tissue factor (TF) expression in smooth muscle cells (SMC) was determined. Methods: Patients with CAD (n = 58) and double antithrombotic medication were treated intraprocedural with UFH (n = 30) or bivalirudin (n = 28). Platelet activation markers were flow cytometrically measured before and after stenting. The expression of TF in SMC was determined by real-time PCR and Western blotting. The thrombogenicity of platelet-derived microparticles and SMC was assessed via a TF activity assay. Results: Bivalirudin significantly diminished the agonist-induced platelet reactivity post-PCI. Compared to UFH treatment, the adenosine diphosphate (ADP) and thrombin receptor-activating peptide (TRAP)-induced thrombospondin expression post-PCI was reduced when bivalirudin was administrated during intervention. In contrast to UFH, bivalirudin reduced the P-selectin expression of unstimulated and ADP-induced platelets post-PCI. Moreover, bivalirudin inhibited the thrombin-, but not FVIIa-or FVIIa/FX-induced TF expression and pro-coagulant TF activity of SMC. Moreover, bivalirudin reduced the TF activity of platelet-derived microparticles postinduction with TRAP or ADP. Conclusions: Bivalirudin is better than UFH in reducing periprocedural platelet activation. Moreover, thrombin-induced TF expression is inhibited by bivalirudin. Thus, bivalirudin seems to be a better anticoagulant during PCI than UFH.

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“…Blood coagulation components are not simply bystanders but can either amplify or inhibit the inflammatory response. Blood clotting can be initiated when inflammatory cytokines and endotoxin induce the de novo synthesis of tissue factor on leukocytes [3]. Exposure of tissue factor to the blood then triggers the coagulation cascade.…”

mentioning

confidence: 99%

Interactions between the innate immune and blood coagulation systems

Esmon

2004

Trends in Immunology

160

121

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Blood coagulation and inflammation are universal responses to infection and there is crosstalk between inflammation and coagulation that can either amplify or dampen the responses. Loss of appropriate interactions between these systems probably contributes to morbidity and mortality in infectious diseases. For instance, inflammatory cytokines and leukocyte elastase can downregulate natural anticoagulant proteins that help to maintain endothelial-cell integrity, control clotting, inhibit vasoactive peptides and dampen leukocyte infiltration into the vessel wall. This Review will summarize our current understanding of the mechanisms involved in the crosstalk between these two important systems.

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Transfer of tissue factor from leukocytes to platelets is mediated by CD15 and tissue factor

Cited by 315 publications

References 35 publications

Microvesicles at the Crossroads Between Infection and Cardiovascular Diseases

Microvesicles at the Crossroads Between Infection and Cardiovascular Diseases

Bivalirudin Inhibits Periprocedural Platelet Function and Tissue Factor Expression of Human Smooth Muscle Cells

Interactions between the innate immune and blood coagulation systems

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