Modulation of C-reactive protein-mediated monocyte chemoattractant protein-1 induction in human endothelial cells by anti-atherosclerosis drugs

Circulation. 2001 May 29;103(21):2531-4. doi: 10.1161/01.cir.103.21.2531.

Abstract

Background: C-reactive protein (CRP) induces adhesion molecule expression by endothelial cells. However, the effects of CRP on chemokine expression by endothelial cells are not known.

Methods and results: We tested the effects of CRP on the production of the chemokines monocyte chemoattractant protein-1 (MCP-1) and RANTES in cultured human umbilical vein endothelial cells. The secretion of chemokines was assessed by ELISA. Incubation with 100 microgram/mL recombinant human CRP induced a 7-fold increase in MCP-1 but no change in RANTES secretion. We showed that the effect of CRP on MCP-1 was present even at 5 microgram/mL CRP, with stepwise increases as the CRP concentration was increased to 10, 50, and 100 microgram/mL. The effect of CRP on MCP-1 induction was not influenced by aspirin (at concentrations up to 1 mmol/L), but it was significantly inhibited by 5 micromol/L simvastatin. The peroxisome proliferator-activated receptor-alpha activators fenofibrate (100 micromol/L) and Wy-14649 (100 micromol/L) almost completely abolished the induction of MCP-1, but the peroxisome proliferator-activated receptor-gamma activator ciglitazone had only a moderate effect.

Conclusions: These results further strengthen the role of CRP in the pathogenesis of vascular inflammation and, likely, atherosclerosis and provide a crucial insight into a novel mechanism of action of anti-atherosclerosis drugs such as simvastatin and fenofibrate.

MeSH terms

  • C-Reactive Protein / pharmacology*
  • Cells, Cultured
  • Chemokine CCL2 / metabolism*
  • Chemokine CCL5 / metabolism
  • Dose-Response Relationship, Drug
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / drug effects*
  • Endothelium, Vascular / metabolism
  • Fenofibrate / pharmacology
  • Humans
  • Hypolipidemic Agents / pharmacology*
  • Receptors, Cytoplasmic and Nuclear / metabolism
  • Simvastatin / pharmacology
  • Time Factors
  • Transcription Factors / metabolism

Substances

  • Chemokine CCL2
  • Chemokine CCL5
  • Hypolipidemic Agents
  • Receptors, Cytoplasmic and Nuclear
  • Transcription Factors
  • C-Reactive Protein
  • Simvastatin
  • Fenofibrate