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C-reactive protein decreases expression of thrombomodulin and endothelial protein C receptor in human endothelial

Bicheng Nan1, Hui Yang, Shaoyu Yan

  • 1Molecular Surgeon Research Center, Division of Vascular Surgery and Endovascular Therapy, Michael E. DeBakey Department of Surgery, Baylor College of Medicine, Houston, TX 77030, USA.

Surgery
|September 13, 2005
PubMed

Insights

C-reactive protein (CRP) reduces thrombomodulin (TM) and EPCR expression in endothelial cells, promoting thrombosis. Curcumin blocks this effect, suggesting a therapeutic target for thrombotic conditions.

Area of Science:

  • Vascular Biology
  • Inflammation and Thrombosis

Background:

  • C-reactive protein (CRP) is linked to atherosclerosis and thrombosis.
  • The direct impact of CRP on endothelial cell antithrombotic properties remains unclear.

Purpose of the Study:

  • To investigate the effect of CRP on thrombomodulin (TM) and endothelial protein C receptor (EPCR) expression in human endothelial cells.

Main Methods:

  • Human coronary artery endothelial cells (HCAECs) were treated with varying concentrations and durations of CRP.
  • Messenger RNA (mRNA) levels of TM and EPCR were quantified using real-time polymerase chain reaction.
  • Anti-CD32 antibody and curcumin were employed to investigate potential blocking mechanisms.

Main Results:

  • CRP significantly downregulated TM mRNA levels in HCAECs by up to 30% and EPCR mRNA levels by up to 34%.
  • These effects were observed in multiple human endothelial cell types.
  • Anti-CD32 partially inhibited CRP's downregulation of TM and EPCR, while curcumin completely reversed these effects.

Conclusions:

  • CRP diminishes TM and EPCR expression in human endothelial cells, contributing to pro-thrombotic states.
  • The CRP-mediated downregulation is partially mediated through CD32.
  • Curcumin effectively counteracts CRP-induced suppression of TM and EPCR expression.
Abstract

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