Tissue factor in blood cells and endothelial cells

Østerud, Bjarne

doi:10.2741/e376

Cited by 56 publications

(41 citation statements)

References 65 publications

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“…C3 should also be able to participate in the cross‐talk between platelets, leukocytes, and ECs during thrombotic reactions, by facilitating platelet‐PMN complex formation. Moreover, PMP formation should increase thrombotic reactions, since PMNs have been suggested to acquire TF by binding platelet‐ and monocyte‐derived TF‐containing microparticles . Elevated levels of plasma C3 are associated with thrombotic events, and we can speculate that in the context of the present study, increased plasma levels of C3 would increase the transfer of TF‐bearing PMPs to leukocytes, resulting in an increased procoagulatory state in patients at risk.…”

Section: Interaction Between Activated Platelets Leukocytes and Ecsmentioning

confidence: 60%

Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross‐talk act as a linchpin in the events leading to thromboinflammation

Ekdahl

Teramura

Hamad

et al. 2016

Immunological Reviews

130

127

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Innate immunity is fundamental to our defense against microorganisms. Physiologically, the intravascular innate immune system acts as a purging system that identifies and removes foreign substances leading to thromboinflammatory responses, tissue remodeling, and repair. It is also a key contributor to the adverse effects observed in many diseases and therapies involving biomaterials and therapeutic cells/organs. The intravascular innate immune system consists of the cascade systems of the blood (the complement, contact, coagulation, and fibrinolytic systems), the blood cells (polymorphonuclear cells, monocytes, platelets), and the endothelial cell lining of the vessels. Activation of the intravascular innate immune system in vivo leads to thromboinflammation that can be activated by several of the system's pathways and that initiates repair after tissue damage and leads to adverse reactions in several disorders and treatment modalities. In this review, we summarize the current knowledge in the field and discuss the obstacles that exist in order to study the cross-talk between the components of the intravascular innate immune system. These include the use of purified in vitro systems, animal models and various types of anticoagulants. In order to avoid some of these obstacles we have developed specialized human whole blood models that allow investigation of the cross-talk between the various cascade systems and the blood cells. We in particular stress that platelets are involved in these interactions and that the lectin pathway of the complement system is an emerging part of innate immunity that interacts with the contact/coagulation system. Understanding the resulting thromboinflammation will allow development of new therapeutic modalities.

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Section: Interaction Between Activated Platelets Leukocytes and Ecsmentioning

confidence: 60%

Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross‐talk act as a linchpin in the events leading to thromboinflammation

Ekdahl

Teramura

Hamad

et al. 2016

Immunological Reviews

130

127

View full text Add to dashboard Cite

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“…B and A). After cancer activation of blood cells (e.g., monocytes and platelets), TF may derive from both its expression at their membranes and its release from the microparticles (MPs) produced by these cells . In particular, monocytes are considered a major source of the so‐called blood‐borne TF circulating in the blood, their TF production is triggered by IL‐1β and TNF directly secreted by tumor cells.…”

Section: Coagulation‐related Proteins and Cancermentioning

confidence: 99%

Coagulation and fibrinolysis in gastric cancer

Repetto

2017

Annals of the New York Academy of Sciences

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Coagulation is a highly conserved process occurring after an injury to a blood vessel and resulting in hemostasis. In the thrombus microenvironment, finely orchestrated events restore vessel integrity through platelet activation, adhesion, and aggregation (primary hemostasis), followed by the coagulation cascades, thrombin generation, and fibrin clot deposition (secondary hemostasis). Several studies on cancer have provided insight into dramatic changes to coagulation-related events (i.e., fibrin clot deposition, fibrinolysis) during tumor pathogenesis, progression, and metastasis, in addition to a tumor-driven systemic activation of hemostasis and thrombosis (Trousseau's syndrome). Diverse molecular and cellular effectors participate in the cross talk between hemostasis and tumors. Here, we focus on some aspects of the interconnection between cancer biology and hemostatic components, with particular attention to some key coagulation-related proteins (e.g., tissue factor, thrombin, fibrinogen, and D-dimers) in the particular case of gastric cancer (GC). Recent advances in deciphering the complex molecular link between GC and the coagulation system are described, showing their important roles in better management of patients affected by GC.

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“…To date, RMPs have been shown to initiate and propagate coagulation by activation of Factor XI or XII, independent of tissue factor (TF) . Although controversial, it has been suggested that MPs may be a reservoir of blood‐borne TF, and clinical studies have indicated that the presence of TF‐exposing MPs was associated with a high incidence of venous thromboembolism in patients with cancer . Jy and coworkers observed that RMPs can enhance coagulation independent of the intrinsic pathway, because the effects of RMPs on clotting time were not completely abolished by blocking the intrinsic pathway with corn trypsin inhibitor .…”

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confidence: 99%

Microparticles from stored red blood cells enhance procoagulant and proinflammatory activity

et al. 2017

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BACKGROUND:The pathomechanisms of morbidity due to blood transfusions are not yet entirely understood. Elevated levels of red blood cell-derived microparticles (RMPs) are found in coagulation-related pathologies and also in stored blood. Previous research has shown that RMPs mediate transfusion-related complications by the intrinsic pathway. We hypothesized that RMPs might play a role in post-transfusion thrombotic complications by enhancing procoagulant activity also through the extrinsic pathway of coagulation. STUDY DESIGN AND METHODS:In this laboratory study, blood from 18 healthy volunteers was stimulated with microparticles from expired stored red blood cells. Various clotting parameters were recorded. Flow cytometry, enzyme-linked immunosorbent assays, and real-time polymerase chain reaction were used to investigate possible mediating mechanisms. RESULTS:The addition of RMPs shortened the clotting time from 194 to 161 seconds (p < 0.001). After incubation with RMPs, there was increased expression of tissue factor (TF) on monocytes and in plasma. TF messenger RNA expression increased in a timedependent and concentration-dependent manner. There was a significant induction of interleukin-1b and interleukin-6. After stimulation with RMPs, there was a significant increase in the number of activated platelets, an increased percentage of PAC-1/CD62P (procaspase activating compound-1/platelet surface P-selectin) double-positive platelets, and an increased number of platelet-neutrophil duplets and platelet-monocyte duplets, indicating enhanced interaction of platelets with neutrophils and monocytes. Levels of CXCL-8 (C-X-C motif chemokine ligand 1) and interleukin-6 were significantly higher after treatment with RMPs. CONCLUSION:Our results suggest that RMPs trigger coagulation through TF signaling, induce the secretion of proinflammatory cytokines, and induce cell-cell interaction between platelets and neutrophils. Thus, under certain conditions, RMPs could play a role in posttransfusion complications through these mechanisms. C ell-derived microparticles (MPs) are membrane vesicles smaller than 1 lm in diameter that are released by various types of cells during cell activation, injury, and apoptosis.1 Release ofMPs is also an integral part of red blood cell (RBC) aging and a prominent feature of the RBC storage lesion. It has been demonstrated that MPs are involved in a broad range of (patho-)physiological processes, such as angiogenesis, inflammation, and coagulation. Therefore, the biological effects and possible clinical relevance of RBCderived MPs (RMPs) need to be clarified. 2-5ABBREVIATION: CXCL-8 5 chemokine C-X-C motif ligand 8; Clinical studies have revealed that elevated levels of circulating RMPs are related to the hypercoagulable state in sickle-cell crisis, venous thromboembolism, and other conditions known to affect coagulation, such as diabetes, cardiovascular disease, and sepsis. [6][7][8][9][10] In addition, it has been observed that patients receiving RBCs are at risk for thrombotic events in a...

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Tissue factor in blood cells and endothelial cells

Cited by 56 publications

References 65 publications

Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross‐talk act as a linchpin in the events leading to thromboinflammation

Dangerous liaisons: complement, coagulation, and kallikrein/kinin cross‐talk act as a linchpin in the events leading to thromboinflammation

Coagulation and fibrinolysis in gastric cancer

Microparticles from stored red blood cells enhance procoagulant and proinflammatory activity

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