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Contributions of contact activation pathways of coagulation factor XII in plasma
Author(s) -
Chatterjee Kaushik,
Guo Zhe,
Vogler Erwin A.,
Siedlecki Christopher A.
Publication year - 2009
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.32076
Subject(s) - factor xii , prekallikrein , kallikrein , zymogen , coagulation , wetting , materials science , biophysics , chemistry , biochemistry , medicine , biology , enzyme , composite material
Activation of human blood plasma coagulation by contact with hydrophilic or hydrophobic surfaces (procoagulants) is dominated by kallikrein (Kal)‐mediated activation of the blood zymogen FXII (Hageman Factor). Mathematical modeling of prekallikrein (PK)‐deficient platelet‐poor plasma (d PK PPP) and PK‐reconstituted d PK PPP (Rd PK PPP) coagulation shows that autoactivation of FXII ( $ {\rm{FXII}}\mathop {-\!\!\!-\!\!\!-\!\!\!-\!\!\!\rightarrow}\limits^{{\rm{surface}}} {\rm{FXIIa}}$ ) produces no more than about 25% of the total FXIIa produced by the intrinsic pathway. Autoactivation and reciprocal‐activation increase in the same proportion with procoagulant surface energy (water‐wettability), whereas total amount of FXIIa produced per‐unit‐area procoagulant remains roughly constant for any particular procoagulant. These results suggest that procoagulant surfaces initiate the intrinsic cascade by producing a bolus of FXIIa in proportion to surface energy or surface area but play no additional role in subsequent molecular events in the cascade. Results further suggest that reciprocal‐activation occurs in proportion to the amount of FXIIa produced by the initiating autoactivation step. © 2008 Wiley Periodicals, Inc. J Biomed Mater Res, 2009