Tissue factor-positive neutrophils bind to injured endothelial wall and initiate thrombus formation.

@article{Darbousset2012TissueFN,
  title={Tissue factor-positive neutrophils bind to injured endothelial wall and initiate thrombus formation.},
  author={Roxane Darbousset and Grace M. Thomas and Soraya Mezouar and Corinne Fr{\`e}re and R{\'e}nat{\'e} Bonier and Nigel Mackman and Thomas Renn{\'e} and Françoise Dignat-George and Christophe Dubois and Laurence Panicot-Dubois},
  journal={Blood},
  year={2012},
  volume={120 10},
  pages={
          2133-43
        }
}
For a long time, blood coagulation and innate immunity have been viewed as interrelated responses. Recently, the presence of leukocytes at the sites of vessel injury has been described. Here we analyzed interaction of neutrophils, monocytes, and platelets in thrombus formation after a laser-induced injury in vivo. Neutrophils immediately adhered to injured vessels, preceding platelets, by binding to the activated endothelium via leukocyte function antigen-1-ICAM-1 interactions. Monocytes rolled… 
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References

SHOWING 1-10 OF 50 REFERENCES
Blood-borne tissue factor: another view of thrombosis.
  • P. Giesen, U. Rauch, +7 authors Y. Nemerson
  • Medicine, Biology
    Proceedings of the National Academy of Sciences of the United States of America
  • 1999
TLDR
It is suggested that blood-borne TF is inherently thrombogenic and may be involved in thrombus propagation at the site of vascular injury.
Leukocyte accumulation promoting fibrin deposition is mediated in vivo by P-selectin on adherent platelets
TLDR
Results indicate that P-selectin is an important adhesion molecule on platelets, mediating platelet–leukocyte binding in vivo, that the presence of leukocytes in thrombi is mediated by P- selectin, and that these leukocyte promote fibrin deposition.
Par4 is required for platelet thrombus propagation but not fibrin generation in a mouse model of thrombosis
TLDR
It is suggested that platelet activation by thrombin is necessary for normal propagation of a platelet thrombus at a distance from the injured vessel wall and hence for normalThrombus growth.
Reciprocal coupling of coagulation and innate immunity via neutrophil serine proteases
TLDR
The ability of coagulation to suppress pathogen dissemination indicates that microvessel thrombosis represents a physiological tool of host defense, although the molecular determinants and in vivo significance of this association remain unclear.
Tissue factor expression in blood cells.
Hematopoietic cell-derived microparticle tissue factor contributes to fibrin formation during thrombus propagation.
TLDR
It is demonstrated that blood-borne TF associated with hematopoietic cell-derived microparticles contributes to thrombus propagation.
Neutrophil extracellular traps promote deep vein thrombosis in mice
TLDR
Extracellular chromatin, likely originating from neutrophils, is a structural part of a venous thrombus and both the DNA scaffold and histones appear to contribute to the pathogenesis of DVT in mice.
Thrombin-initiated platelet activation in vivo is vWF independent during thrombus formation in a laser injury model.
TLDR
The results indicate that the tissue factor-mediated pathway of thrombin generation, but not the collagen-induced GPVI- mediated pathway, is the major pathway leading to platelet activation after laser-induced injury under the conditions employed.
Laser-induced endothelial cell activation supports fibrin formation.
TLDR
Laser-induced vessel wall injury leads to rapid thrombus formation in an animal thrombosis model and laser activated endothelial cells can support formation of tenase and prothrombinase and may be a source of activated tissue factor as well.
Defective thrombus formation in mice lacking coagulation factor XII
TLDR
These unexpected findings change the long-standing concept that the FXII-induced intrinsic coagulation pathway is not important for clotting in vivo and identify FXII as a novel target for antithrombotic therapy.
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