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The human complement system in thrombin-mediated platelet function.

M J Polley, R Nachman

    The Journal of Experimental Medicine
    |June 1, 1978
    PubMed
    Summary
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    Thrombin binding to platelets triggers complement uptake and enhances serotonin release. This novel complement activation pathway involves thrombin forming a C3 convertase on the platelet surface, boosting platelet aggregation.

    Area of Science:

    • Immunology
    • Hematology
    • Biochemistry

    Background:

    • Complement system activation plays a role in inflammatory and immune responses.
    • Platelets are key participants in hemostasis and thrombosis, and their function can be modulated by complement.
    • Thrombin is a critical enzyme in coagulation and also influences platelet activation.

    Purpose of the Study:

    • To investigate the role of the complement system in thrombin-induced platelet activation.
    • To elucidate the mechanism of complement activation on platelet surfaces mediated by thrombin.
    • To determine the effect of complement on platelet aggregation and serotonin release.

    Main Methods:

    • Utilized radiolabeled complement components (C3 and C5) to demonstrate membrane-specific uptake by platelets.

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  • Employed electron microscopy with ferritin-conjugated antibodies for visualization of component uptake.
  • Assessed platelet aggregation and serotonin release in the presence and absence of complement.
  • Measured lactic dehydrogenase release to confirm nonlytic serotonin release.

    • Main Results:

    • Thrombin induced membrane-specific uptake of C3 and C5 by platelets.
    • Complement was not essential but significantly enhanced thrombin-induced platelet aggregation and serotonin release.
    • Serotonin release was confirmed as a nonlytic process.
    • A novel mechanism of complement activation was proposed, involving thrombin forming a platelet-associated C3 convertase.

    Conclusions:

    • Thrombin binding to platelets initiates a novel complement activation cascade.
    • Complement enhances thrombin-mediated platelet functions, including aggregation and serotonin release.
    • This interaction highlights a new pathway linking coagulation and complement systems in platelet biology.