Download PDF
Thromb Haemost 2001; 85(06): 1055-1059
DOI: 10.1055/s-0037-1615963
Review Article
Schattauer GmbH

The Role of Factor XI in a Dilute Thromboplastin Assay of Extrinsic Coagulation Pathway

Rong He
1   Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China
,
Shilong Xiong
1   Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China
,
Xiaofan He
1   Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China
,
Fayi Liu
1   Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China
,
Jianzhong Han
1   Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China
,
Juncheng Li
1   Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China
,
Shilin He
1   Thrombosis and Hemostasis Laboratory, Department of Physiology, Hunan Medical University, Changsha, Hunan, P. R. China
› Author Affiliations
Further Information

Publication History

Received 27 March 2000

Accepted after resubmission 22 January 2001

Publication Date:
12 December 2017 (online)

    Permissions and Reprints

Summary

Blood coagulation has been thought to be composed of both intrinsic and extrinsic pathways. Recent evidence strongly supports the critical role of the extrinsic pathway in the initiation of blood coagulation. This investigation established an assay that examines the role of FXI in the thromboplastin-initiated (extrinsic) coagulation based on this new concept. Plasma clotting times were measured at different concentrations of thromboplastin with activated FXII inhibited (FXIIa-inhibited Diluted Thromboplastin Time, FXIIaiDTT). Only at low concentrations of thromboplastin was FXIIaiDTT of FXI-deficient plasma significantly prolonged than that of normal plasma. Depletion of FXI from normal plasma prolonged its FXIIaiDTT and replenishment of FXI shortened it. FXIIaiDTTs of both FVIII-deficient and FIX-deficient plasma were remarkably prolonged, and addition of normal plasma dose-dependently shortened it. Furthermore, earlier α-thrombin inhibition was directly correlated with decreasing FXa generation. The amount of FXa production was: platelet-rich plasma > platelet-poor plasma > FXI-deficient plasma. Therefore, our findings from the FXIIaiDTT assays not only support the critical role of extrinsic pathway in blood coagulation initiation, but also demonstrate the importance of FXI as an amplifier of thrombin generation in thromboplastin-initiated coagulation.

Key words

Blood coagulation - thromboplastin - factor VIII - factor IX - factor XI
 

  • References

  • 1 Davie EW, Fujikawa K, Kisiel W. The coagulation cascade: initiation, maintenance and regulation. Biochemistry 1991; 30: 10363-70.
    CrossrefPubMedGoogle Scholar
  • 2 Pixley RA, de la Cadona R, Page JD, Kaufman N, Wyshock EG, Chang A, Taylor Jr FB, Colman RW. The contact system contributes to hypotension but not disseminated intravascular coagulation in lethal bacteremia. In vivo use of a monoclonal anti-factor XII antibody to block contact activation in baboons. J Clin Invest 1993; 91: 61-8.
    CrossrefPubMedGoogle Scholar
  • 3 Broze Jr GJ. Tissue factor pathway inhibitor and the revised theory of coagulation. Annu Rev Med 1995; 46: 103-12.
    CrossrefPubMedGoogle Scholar
  • 4 Rapaport SI, Rao LVM. The tissue factor pathway: how it has become a “prima ballerina”. Thromb Haemost 1995; 74: 7-17.
    PubMedGoogle Scholar
  • 5 Camerer E, Kolstø AB, Prydz H. Cell biology of tissue factor: the principal initiator of blood coagulation. Thromb Res 1996; 81: 1-41.
    CrossrefPubMedGoogle Scholar
  • 6 Gailani D, Broze Jr GJ. Factor XI activation in a revised model of blood coagulation. Science 1991; 253: 909-12.
    CrossrefPubMedGoogle Scholar
  • 7 Brunnee T, La Porta C, Reddigan SR, Salerno VM, Kaplan AP, Silverberg M. Activation of Factor XI in plasma is dependent on Factor XII. Blood 1993; 81: 580-6.
    PubMedGoogle Scholar
  • 8 Hoffman M, Monroe DM, Roberts HR. Cellular interaction in hemostasis. Haemostasis 1996; 26 (Suppl. 01) 12-6.
    PubMedGoogle Scholar
  • 9 Rand MD, Lock JB, van’t Veer C, Gaffney DP, Mann KG. Blood clotting in minimally altered whole blood. Blood 1996; 88: 3432-45.
    PubMedGoogle Scholar
  • 10 Lawson JH, Kalafatis M, Stram S, Mann KG. A model for the tissue factor pathway to thrombin. J Biol Chem 1994; 269: 23357-66.
    PubMedGoogle Scholar
  • 11 Cawthern KM, van’t Veer C, Lock JB, DiLorenzo ME, Branda RF, Mann KG. Blood coagulation in hemophilia A and hemophilia C. Blood 1998; 91: 4581-92.
    PubMedGoogle Scholar
  • 12 Naito K, Fujikawa K. Activation of human blood coagulation factor XI independent of factor XII. J Biol Chem 1991; 266: 7353-8.
    PubMedGoogle Scholar
  • 13 Von dem Borne PAK, Koppelman SJ, Bouma BN, Meijers JCM. Surface independent factor XI activation by thrombin in the presence of high molecular weight kininogen. Thromb Haemost 1994; 72: 397-402.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 14 Rydel TJ, Ravichandran KG, Tulinsky A, Bode W, Huber R, Roitsch C, Fenton JW. The structure of a complex of recombinant hirudin and human α-thrombin. Science 1990; 249: 277-80.
    CrossrefPubMedGoogle Scholar
  • 15 Markwardt F. Hirudin and derivatives as anticoagulant agents. Thromb Haemost 1991; 66: 141-52.
    Article in Thieme ConnectPubMedGoogle Scholar
  • 16 Baglia FA, Walsh PN. Prothrombin is a cofactor for the binding of factor XI to The platelet surface and for platelet-mediated factor XI activation by thrombin. Biochemistry 1998; 37: 2271-81.
    CrossrefPubMedGoogle Scholar
  • 17 Oliver JA, Monroe DM, Roberts HR, Hoffman M. Thrombin activates factor XI on activated platelets in the absence of factor XII. Arterioscler Thromb Vasc Biol 1999; 19: 170-7.
    CrossrefPubMedGoogle Scholar