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Updated: Jan 10, 2026

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Tissue factor expression by endothelial cells in sickle cell anemia

A Solovey1, L Gui, N S Key

  • 1Department of Medicine, University of Minnesota, Minneapolis, Minnesota 55455, USA.

The Journal of Clinical Investigation
|June 13, 1998
PubMed
Summary

Circulating endothelial cells in sickle cell anemia patients express tissue factor (TF), a key coagulation trigger. This finding suggests the endothelium plays a significant role in activating blood clotting, especially during disease episodes.

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Area of Science:

  • Hematology
  • Vascular Biology
  • Coagulation Science

Background:

  • The role of vascular endothelium in coagulation system activation is unclear.
  • Limited evidence exists for in vivo endothelial cell expression of tissue factor (TF), the coagulation system's trigger.
  • Sickle cell anemia is associated with coagulation activation.

Purpose of the Study:

  • To investigate tissue factor (TF) expression on circulating endothelial cells (CECs) in normal individuals and sickle cell anemia patients.
  • To determine if TF expressed on CECs is functional and correlates with disease state.

Main Methods:

  • Analysis of TF antigen and mRNA expression on CECs from normal controls and sickle cell patients.
  • Functional assays including Factor VIIa binding and Factor Xa generation.
  • Comparison of TF expression in steady-state versus acute vaso-occlusive episodes in sickle cell patients.

Main Results:

  • Sickle cell CECs abnormally express TF antigen, with significantly higher percentages in steady-state (66+/-13%) and acute episodes (83+/-19%) compared to normal controls (10+/-13%).
  • TF expression on sickle CECs was confirmed at both the mRNA and protein levels.
  • The expressed TF was functional, supporting Factor VIIa binding and Factor Xa generation.

Conclusions:

  • Endothelial cells in vivo can express functional tissue factor (TF).
  • The vascular endothelium, via TF expression on CECs, likely contributes significantly to coagulation activation in sickle cell disease.
  • These findings implicate the endothelium as a critical pathophysiological trigger for coagulation.