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Related Experiment Videos

Tissue factor expression by monocytes: regulation and pathophysiological roles

B Osterud1

  • 1Department of Biochemistry, Institute of Medical Biology, University of Tromsø, Norway. bjarne@fagmed.uit.no

Blood Coagulation & Fibrinolysis : an International Journal in Haemostasis and Thrombosis
|November 18, 1998
PubMed
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Tissue factor (TF) expression on monocytes drives thrombin generation, impacting wound repair and diseases like sepsis and cancer. Phosphatidylserine exposure on viable monocytes enhances this pro-coagulant activity.

Area of Science:

  • Hematology
  • Immunology
  • Molecular Biology

Background:

  • Tissue factor (TF) expressed by monocytes/macrophages is central to thrombin generation.
  • TF plays roles in physiological processes like wound repair and pathophysiological conditions including sepsis, thrombosis, and cancer.
  • Monocyte TF expression is regulated by transcription factors NF-kappaB and AP-1, influenced by the phospholipase A2 pathway in whole blood.

Purpose of the Study:

  • To investigate the mechanisms regulating tissue factor catalytic activity on monocytes.
  • To understand the role of phosphatidylserine exposure in TF-mediated thrombin generation.
  • To elucidate the interplay between monocytes, platelets, and granulocytes in TF expression.

Main Methods:

  • Analysis of tissue factor expression and activity in monocytes.

Related Experiment Videos

  • Investigation of the role of phospholipase A2 pathway in TF regulation.
  • Assessment of platelet and granulocyte involvement in TF activity via P-selectin.
  • Evaluation of phosphatidylserine exposure on monocyte surface.

    • Main Results:

    • TF expression on viable monocytes has significantly lower catalytic activity (approx. 10%) compared to lysed cells.
    • This difference is attributed to the increased availability of anionic phospholipid (phosphatidylserine) upon cell lysis.
    • Pathophysiological exposure of phosphatidylserine on viable monocyte surfaces can strongly stimulate thrombin generation, mimicking platelet membrane activity.

    Conclusions:

    • Monocyte TF catalytic activity is modulated by phospholipid distribution, particularly phosphatidylserine exposure.
    • Phosphatidylserine on the outer monocyte surface is a key factor in TF-driven thrombin generation, relevant in pathological states.
    • Platelets and granulocytes, through P-selectin-dependent mechanisms, influence monocyte TF activity, highlighting a complex cellular crosstalk.