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Serum amyloid A induces monocyte tissue factor.

Hong Cai1, Changjie Song, Ikuko Endoh

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Serum amyloid A (SAA) rapidly induces human monocyte tissue factor (TF) production, a key factor in inflammation-associated thrombosis. This contrasts with C-reactive protein (CRP) and highlights SAA

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Area of Science:

  • Immunology
  • Molecular Biology
  • Hematology

Background:

  • Inflammatory conditions elevate C-reactive protein (CRP) and serum amyloid A (SAA) levels.
  • CRP-induced monocyte tissue factor (TF) is implicated in inflammation-associated thrombosis.
  • The specific role of SAA in inducing TF and its contribution to thrombosis require further elucidation.

Purpose of the Study:

  • To investigate the capacity of serum amyloid A (SAA) to induce tissue factor (TF) in human monocytes.
  • To compare the TF-inducing potency and kinetics of SAA with C-reactive protein (CRP).
  • To elucidate the molecular pathways and receptors involved in SAA-mediated TF induction.

Main Methods:

  • Measurement of TF mRNA and procoagulant activity in peripheral blood mononuclear cells (PBMCs) stimulated with SAA and CRP.
  • Assessment of TF dependency on coagulation factors VII and X, and TF antigen levels on CD14+ monocytes.
  • Inhibitor studies targeting NF-kappaB, MAPK pathways, cyclo-oxygenase, and RAGE.
  • Analysis of SAA binding to RAGE and the effect of RAGE competitors.

Main Results:

  • SAA rapidly induced TF mRNA and procoagulant activity in human monocytes, significantly faster and more potently than CRP.
  • TF induction by SAA involved NF-kappaB activation via ERK1/2 and p38 MAPK pathways, independent of cyclo-oxygenase.
  • SAA-induced TF generation was partially inhibited by high-density lipoprotein and significantly suppressed by RAGE blockade.
  • PBMCs from rheumatoid arthritis patients showed heightened sensitivity to SAA-induced TF compared to healthy individuals.

Conclusions:

  • SAA is a potent and rapid inducer of human monocyte tissue factor, suggesting a significant role in inflammation-associated thrombosis.
  • The SAA-RAGE axis is crucial for TF induction, offering potential therapeutic targets.
  • Increased SAA sensitivity in rheumatoid arthritis patients links inflammation directly to thrombotic risk via TF induction.