scholarly journals Tissue Factor Activity Is Increased in Neutrophils from JAK2 V617F ‐mutated Essential Thrombocythemia and Polycythemia Vera Patients

Author(s):  
Brandi N. Reeves ◽  
Soo Jin Kim ◽  
Jihyun Song ◽  
Kathryn J. Wilson ◽  
Michael W. Henderson ◽  
...  
2009 ◽  
Vol 7 (1) ◽  
pp. 121-131 ◽  
Author(s):  
H. KOTHARI ◽  
G. KAUR ◽  
S. SAHOO ◽  
S. IDELL ◽  
L. V. M. RAO ◽  
...  

2016 ◽  
Vol 12 (5) ◽  
pp. 3273-3277 ◽  
Author(s):  
Antonio Angelini ◽  
Sebastiano Miscia ◽  
Maria Antonietta Centurione ◽  
Roberta Di Pietro ◽  
Lucia Centurione

Blood ◽  
1989 ◽  
Vol 73 (4) ◽  
pp. 968-975
Author(s):  
HJ Weiss ◽  
VT Turitto ◽  
HR Baumgartner ◽  
Y Nemerson ◽  
T Hoffmann

By a variety of methods, tissue factor activity was demonstrated in the subendothelium of rabbit aorta and human umbilical artery. In one method, everted segments of de-endothelialized vessels were mounted in an annular perfusion chamber and the subendothelial surface was exposed to nonanticoagulated human blood under controlled flow. Procoagulant activity was assessed by measuring fibrin deposition on subendothelium and fibrinopeptide A (FPA) levels in post chamber blood. Both fibrin deposition and FPA were decreased with rabbit vessel segments exposed (at a shear rate of 650 seconds-1) to blood from patients with factor VII deficiency and with umbilical artery segments (at shear rates of 90 to 180 seconds-1) that had been pretreated with a monoclonal antibody to human tissue factor. In a second method, everted umbilical artery segments were mounted on a stir bar and the subendothelial surface was exposed, with stirring, to plasma or purified coagulation factors. The capacity of the surface to clot plasma on addition of calcium was inhibited by the antibody to tissue factor. The surface also activated purified 3H-factor X in the presence of factor VIIa, but not in its absence, and this surface property was almost entirely eliminated by pretreating the vessel segments with antitissue factor. Tissue factor activity in subendothelium could play a role in both the arrest of bleeding and in promoting the formation of thrombi at sites of vascular injury.


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