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C-reactive protein isoforms differ in their effects on thrombus growth

Blanca Molins1, Esther Peña, Gemma Vilahur

  • 1Cardiovascular Research Center, CSIC-ICCC, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain.

Arteriosclerosis, Thrombosis, and Vascular Biology
|September 13, 2008
PubMed

Insights

Modified C-reactive protein (mCRP) significantly enhances platelet adhesion and thrombus growth under arterial flow. Native C-reactive protein (natCRP) showed no effect, suggesting mCRP has a prothrombotic role.

Area of Science:

  • Cardiovascular Biology
  • Hemostasis and Thrombosis
  • Inflammation and Immunology

Background:

  • C-reactive protein (CRP) is an acute-phase protein involved in inflammation.
  • Distinct isoforms of CRP, native (natCRP) and modified (mCRP), may have different biological functions.
  • Understanding CRP's role in thrombosis is crucial for cardiovascular disease management.

Purpose of the Study:

  • To investigate the differential impact of natCRP and mCRP on platelet adhesion and thrombus formation.
  • To determine the prothrombotic potential of mCRP compared to natCRP under arterial flow conditions.

Main Methods:

  • Perfusing blood over type I collagen at high shear rates (1500 s(-1)).
  • Evaluating platelet deposition and thrombus growth using confocal microscopy.
  • Assessing platelet activation markers (P-selectin, CD36, CD63) via flow cytometry and immunohistochemistry.

Main Results:

  • mCRP significantly increased platelet adhesion and thrombus growth, both when incubated with blood and when immobilized.
  • natCRP did not affect platelet adhesion or thrombus growth.
  • mCRP upregulated P-selectin and CD36 on platelets, indicating enhanced activation, without affecting CD63 or PAC-1 binding.

Conclusions:

  • Modified CRP (mCRP) exhibits a prothrombotic phenotype, promoting platelet deposition and thrombus growth under arterial flow.
  • Native CRP (natCRP) does not appear to influence thrombus formation under these conditions.
  • These findings highlight the distinct roles of CRP isoforms in thrombosis.
Abstract

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