Platelet-Associated Tissue Factor Contributes to the Collagen-Triggered Activation of Blood Coagulation

Zillmann, Andreas; Luther, Thomas; Müller, Ingrid; Kotzsch, Matthias; Spannagl, Michael; Kauke, Teresa; Oelschlägel, Uta; Zahler, Stefan; Engelmann, Bernd

doi:10.1006/bbrc.2001.4399

Cited by 165 publications

(141 citation statements)

References 25 publications

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“…While some authors neither detected TF antigen nor activity in resting as well as calcium ionophore-or collagen-stimulated platelets, 52 others described functional TF in platelets. [53][54][55][56][57] Indeed, different mechanisms of TF expression in platelets have been described, underscoring a potential role of platelet TF. Translocation and activation of existing TF protein from intracellular compartments to the platelet surface, uptake of TF from other sources, mainly via MPs, and de novo TF mRNA and protein synthesis have been proposed (Figure 4).…”

Section: Granulocytesmentioning

confidence: 99%

Tissue Factor and Cardiovascular Disease: Quo Vadis?

Berndt

Tanner

Lüscher

2010

Circ J

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The coagulation cascade represents a system of proteases responsible to maintain vascular integrity and to induce rapid clot formation after vessel injury. Tissue factor (TF), the key initiator of the coagulation cascade, binds to factor VIIa and thereby activates factor IX and factor X, resulting in thrombus formation. Different stimuli enhance TF gene expression in endothelial and vascular smooth muscle cells. In addition to these vascular cells, TF has recently been detected in the bloodstream in circulating cells such as leukocytes and platelets, as a component of microparticles, and as a soluble, alternatively spliced form of TF. Various cardiovascular risk factors like hypertension, diabetes, and dyslipidemia, increase levels of TF. In line with this observation, enhanced vascular TF expression occurs during atherogenesis, particularly in patients with acute coronary syndromes. (Circ J 2010; 74: 3 - 12)

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Section: Granulocytesmentioning

confidence: 99%

Tissue Factor and Cardiovascular Disease: Quo Vadis?

Berndt

Tanner

Lüscher

2010

Circ J

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“…Recent evidence suggests that tissue factor antigen may form on the surface of platelets adhering to neutrophils or monocytes (196). The authors suggest that the release of elastase by the leukocytes may inactivate the tissue factor pathway inhibitor.…”

Section: Interactions With Leukocytesmentioning

confidence: 99%

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Sercombe

Dinh

Gomis

2002

Japanese Journal of Pharmacology

182

140

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ABSTRACT-Aneurysmal subarachnoid hemorrhage frequently results in complications including intracranial hypertension, rebleeding and vasospasm. The extravasated blood is responsible for a cascade of reactions involving release of various vasoactive and pro-inflammatory factors (several of which are purported to induce vasospasm) from blood and vascular components in the subarachnoid space. The authors review the available evidence linking these factors to the development of inflammatory lesions of the cerebral vasculature, emphasizing: 1) neurogenic inflammation due to massive release of sensory nerve neuropeptides; 2) hemoglobin from lysed erythrocytes, which creates functional lesions of endothelial and smooth muscle cells; 3) activity, expression and metabolites of lipoxygenases cyclooxygenases and nitric oxide synthases; 4) the possible role of endothelin-1 as a pro-inflammatory agent; 5) serotonin, histamine and bradykinin which are especially involved in blood-brain barrier disruption; 6) the prothrombotic and pro-inflammatory action of complement and thrombin towards endothelium; 7) the multiple actions of activated platelets, including platelet-derived growth factor production; 8) the presence of perivascular and intramural macrophages and granulocytes and their interaction with adhesion molecules; 9) the evolution, origins, and effects of pro-inflammatory cytokines, especially IL-1, TNF-a and IL-6. Human and animal studies on the use of anti-inflammatory agents in subarachnoid hemorrhage include superoxide and other radical scavengers, lipid peroxidation inhibitors, iron chelators, NSAIDs, glucocorticoids, and serine protease inhibitors. Many animal studies claim reduced vasospasm, but these effects are not always confirmed in human trials, where symptomatic vasospasm and outcome are the major endpoints. Despite recent work on penetrating vessel constriction, there is a paucity of studies on inflammatory markers in the microcirculation.

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“…6 It has been recently reported that platelets, under well-controlled experimental conditions, contain functionally active TF, which might derive from leukocytes through a particle transfer mechanism. 7,8 In the present study, we report for the first time that activation of human platelets by the agonists ADP, thrombin receptor-activating peptide (TRAP), and epinephrine induces TF expression on the cell membrane in a time-and concentration-dependent manner, thereby making TF capable of interacting with plasma factor VIIa (FVIIa) and generating FXa. Moreover, we show that this expression is modulated by some, but not all, antiplatelet agents.…”

mentioning

confidence: 91%

Platelet Activation Induces Cell-Surface Immunoreactive Tissue Factor Expression, Which Is Modulated Differently by Antiplatelet Drugs

Camera

Frigerio

Toschi

et al. 2003

ATVB

129

108

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Objective-Tissue factor (TF) is the main activator of the coagulation cascade occurring in physiologic and pathologic conditions. Recent data suggest that human platelets might contain TF that is possibly derived from leukocytes. In this study, we investigated whether intraplatelet TF can be exposed on the membrane by platelet agonists. The modulation of this process by antiplatelet drugs has been evaluated as well. Methods and Results-Flow cytometric analysis of unstimulated platelets showed a small amount of membrane-associated immunoreactive TF (irTF) in whole blood, platelet-rich plasma, and washed platelets isolated from healthy subjects. ADP, thrombin receptor-activating peptide, and epinephrine significantly increased functionally active, membraneassociated irTF. ADP induced irTF exposure in a concentration-and time-dependent fashion. Agonist-induced irTF expression was completely inhibited by iloprost but not by aspirin. Interestingly, glycoprotein IIb/IIIa antagonists did not inhibit but rather potentiated the stimulatory effect of ADP on platelet irTF expression. Real-time polymerase chain reaction experiments showed detectable amounts of TF mRNA in unstimulated platelets. Conclusions-These findings indicate that platelet agonists and antiplatelet drugs might modulate platelet-associated irTF expression. Regulated TF expression establishes the potential for a previously unrecognized role for platelets in sustaining thrombus formation and growth via coagulation-mediated mechanisms. (Arterioscler Thromb Vasc Biol. 2003;23:1690-1696.)Key Words: platelets Ⅲ tissue factor Ⅲ coagulation Ⅲ thrombosis Ⅲ antiplatelet agents C linical and experimental evidence indicates that tissue factor (TF), a 47-kDa glycoprotein, triggers activation of the coagulation cascade that occurs in several human diseases, such as sepsis and other systemic conditions. 1 In addition, TF has been shown to be present in atherosclerotic plaques. 2,3 In particular, TF protein and activity have been found to be increased in coronary plaques, thus playing a crucial role in human coronary syndromes. 4 Vessel wallassociated TF, however, does not entirely explain the thrombogenic potential of vascular lesions when they are exposed to flowing blood. It has been proposed that thrombus growth might be promoted by circulating (ie, microparticle or platelet-associated) TF. 5 Indeed, to interact with plasma coagulation proteins and thus sustain thrombus growth, TF might diffuse from its source to the initial platelet layer. Because the time to capture any diffusing species increases as the square of distance, the shortened distance resulting from TF associated with circulating platelets might have very significant effects on subsequent reaction velocities.Considerable data now support the hypothesis that platelets actively modulate the propagation of coagulation by expressing specific, high-affinity receptors for coagulation proteases, zymogens, and cofactors that contribute to localize thrombin generation at the site of vascular injury. 6 It has be...

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Platelet-Associated Tissue Factor Contributes to the Collagen-Triggered Activation of Blood Coagulation

Cited by 165 publications

References 25 publications

Tissue Factor and Cardiovascular Disease: Quo Vadis?

Tissue Factor and Cardiovascular Disease: Quo Vadis?

Cerebrovascular Inflammation Following Subarachnoid Hemorrhage

Platelet Activation Induces Cell-Surface Immunoreactive Tissue Factor Expression, Which Is Modulated Differently by Antiplatelet Drugs

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