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Platelet activation and blood coagulation.

Johan W M Heemskerk1, Edouard M Bevers, Theo Lindhout

  • 1Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University, The Netherlands. jwm.heemskerk@bioch.unimaas.nl

Thrombosis and Haemostasis
|August 28, 2002
PubMed
Summary

Platelet activation and blood coagulation are intertwined processes crucial for hemostasis. Activated platelets expose phosphatidylserine, promoting coagulation and taking on initiating roles in the process.

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Area of Science:

  • Hematology
  • Biochemistry
  • Cell Biology

Background:

  • Platelet activation and blood coagulation are interdependent processes in hemostasis and thrombosis.
  • Thrombin, a product of coagulation, is a potent agonist for platelet activation.
  • Activated platelets adopt a procoagulant state, particularly after elevated cytosolic calcium levels.

Purpose of the Study:

  • To elucidate the mechanisms by which activated platelets promote blood coagulation.
  • To detail the role of phosphatidylserine exposure in supporting coagulation complex assembly.
  • To investigate the contribution of platelets to the initiation phase of coagulation.

Main Methods:

  • Investigated platelet activation via glycoprotein VI interaction with collagen.
  • Analyzed the role of cytosolic calcium ([Ca2+]i) in inducing a procoagulant platelet state.

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  • Examined the mechanisms of phosphatidylserine (PS) exposure, including aminophospholipid translocase inhibition and phospholipid scramblase activation.
  • Studied calpain-mediated protein cleavage in membrane blebbing and vesiculation.
  • Assessed the support of tenase and prothrombinase complex assembly and activation on PS-exposing platelets.
  • Evaluated platelet provision of binding sites for prothrombin and factor XI.

    • Main Results:

    • Platelet activation, particularly via collagen-induced pathways, leads to elevated cytosolic calcium.
    • This elevation triggers phosphatidylserine (PS) exposure on the outer platelet surface, forming membrane blebs and microvesicles.
    • PS exposure significantly enhances coagulation by facilitating tenase and prothrombinase complex formation, supported by factors IXa and Va.
    • Platelets provide essential binding sites for prothrombin and factor XI, contributing to coagulation initiation.
    • Platelets can assume the initiating role typically played by tissue factor and factor VIIa.

    Conclusions:

    • Activated platelets are critical accelerators and initiators of blood coagulation.
    • Phosphatidylserine exposure on activated platelets is a key mechanism for promoting coagulation complex formation.
    • Platelets play a multifaceted role in hemostasis, bridging platelet activation and the coagulation cascade.