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Evidence against Collagen Activation of Platelet‐Associated Factor XI as a Mechanism for Initiating Intrinsic Clotting
Author(s) -
ØSterud Bjarne,
Harper Elvin,
Rapaport Samuel I.,
Lavine Kathrine K.
Publication year - 1979
Publication title -
scandinavian journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.904
H-Index - 84
eISSN - 1600-0609
pISSN - 0036-553X
DOI - 10.1111/j.1600-0609.1979.tb02798.x
Subject(s) - factor ixa , chemistry , platelet , clotting time , factor ix , calcium , clotting factor , incubation , platelet factor 4 , sodium dodecyl sulfate , factor x , polyacrylamide gel electrophoresis , factor xii , coagulation , biochemistry , medicine , heparin , thrombin , enzyme , organic chemistry
Collagen activation of platelet‐associated Factor XI has been proposed as a mechanism for initiating intrinsic clotting independent of Factor XII. Since this could explain the lack of bleeding in patients with hereditary Factor XII deficiency, pre‐kallikrein deficiency and high molecular weight kininogen deficiency, we subjected the hypothesis to rigorous testing. Incubation of isolated platelets with collagen and calcium ions failed to generate activity shortening the clotting time of an acivated Factor XI (XI a ) assay that had been modified to eliminate effects due to platelet‐associated activated Factor V. Nor could generation of traces of Factor XI a in such mixtures be detected by incubation with purified Factor IX and testing for the generation of activated Factor IX (IX a ) in clotting and amidolytic assays. Moreover, when blood or platelet‐rich plasma containing added 125 I‐Factor IX was incubated with calcium ions and collagen and then subjected to reduced sodium.dodecyl sulfate poly‐acrylamide gel electrophoresis, the radioactivity profiles revealed only native 125 I‐Factor IX without evidence of the polypeptide chains of Factor IX a . The negative results of this study mitigate against the hypothesis that collagen activation of platelet‐associated Factor XI represents a physiologically significant mechanism for initiating clotting independent of Factor XII.