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C-reactive protein promotes monocyte-platelet aggregation: an additional link to the inflammatory-thrombotic

Haim D Danenberg1, Neelesh Kantak, Etty Grad

  • 1Heart Institute, Hadassah Hebrew University Medical Center, Jerusalem, Israel. danen@md.huji.ac.il

European Journal of Haematology
|January 27, 2007
PubMed

Insights

C-reactive protein (CRP) promotes monocyte-platelet aggregate formation, linking inflammation and thrombosis. This process is calcium-dependent and mediated via P-selectin glycoprotein ligand-1, offering a potential therapeutic target.

Area of Science:

  • Cardiovascular Science
  • Immunology
  • Hematology

Background:

  • C-reactive protein (CRP) is a known risk marker for cardiovascular events.
  • Monocyte-platelet aggregate (MPA) formation is linked to acute cardiovascular disease and inflammation.
  • The pro-thrombotic activities of CRP warrant investigation into its role in MPA formation.

Purpose of the Study:

  • To investigate the effect of CRP on monocyte-platelet aggregate (MPA) formation ex vivo and in vivo.
  • To elucidate the mechanisms underlying CRP-induced MPA formation.
  • To explore the inflammatory-thrombotic link regulated by CRP.

Main Methods:

  • Flow cytometry with dual-labeling for monocytes and platelets was used to examine MPA formation.
  • Human blood was incubated with recombinant human CRP (rhCRP).
  • Experiments were conducted in transgenic mice expressing the human CRP gene (CRPtg) and wild-type mice, with and without lipopolysaccharide (LPS) challenge.

Main Results:

  • Incubation of human blood with rhCRP doubled MPA formation.
  • CRP-induced MPA formation is calcium-dependent and mediated via P-selectin glycoprotein ligand-1 (PSGL-1) binding.
  • In CRPtg mice, LPS injection preferentially increased MPA formation compared to wild-type mice, indicating an in vivo effect.

Conclusions:

  • CRP actively promotes MPA formation both ex vivo and in vivo.
  • The aggregation process is calcium-dependent and involves PSGL-1.
  • These findings suggest a critical inflammatory-thrombotic link regulated by CRP, highlighting a potential therapeutic target for thrombotic disorders.
Abstract

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