Modulatory effects of atorvastatin on endothelial cell-derived chemokines, cytokines, and angiogenic factors

Pharmacotherapy. 2006 Mar;26(3):333-40. doi: 10.1592/phco.26.3.333.

Abstract

Study objective: To investigate the immunomodulatory effects of 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins) by determining whether atorvastatin alters the production of specific endothelium-derived immunoactive proteins and whether its treatment effects depend on its concentration and/or inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase.

Design: In vitro study using a multiplexing method for protein measurement.

Setting: University laboratory.

Measurements and main results: Human umbilical vein endothelial cells were cultured to approximately 80% confluence and treated with atorvastatin 1-50 microM alone or with mevalonate for 24 hours. Untreated cells served as controls. Culture-conditioned media were removed and multiplex assayed for protein content of epithelial neutrophil-activating peptide-78, interleukin-8, monocyte chemotactic protein-1, interleukin-6, interleukin-10, fibroblast growth factor, and granulocyte colony stimulating factor. Atorvastatin significantly reduced the production of epithelial neutrophil-activating peptide-78, interleukin-6, interleukin-8, and monocyte chemotactic protein-1 (p<0.001 to p<0.05) in a concentration-dependent manner without affecting basal production of interleukin-10, fibroblast growth factor, and granulocyte colony stimulating factor. The treatment effects of atorvastatin were reversed with concurrent mevalonate therapy.

Conclusion: By inhibiting 3-hydroxy-3-methylglutaryl coenzyme A reductase, atorvastatin lowered concentrations of several inflammatory molecules derived from basal-state endothelial cells in a concentration-dependent manner. The in vivo importance of these immunomodulatory effects needs further investigation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Atorvastatin
  • Cells, Cultured
  • Chemokine CCL2 / metabolism
  • Chemokine CXCL5
  • Chemokines, CXC / metabolism
  • Endothelial Cells / drug effects*
  • Endothelial Cells / metabolism
  • Fibroblast Growth Factors / metabolism
  • Granulocyte Colony-Stimulating Factor / metabolism
  • Heptanoic Acids / pharmacology*
  • Humans
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors / pharmacology*
  • Immunologic Factors / pharmacology*
  • Interleukin-6 / metabolism
  • Interleukin-8 / metabolism
  • Mevalonic Acid / pharmacology
  • Pyrroles / pharmacology*

Substances

  • CXCL5 protein, human
  • Chemokine CCL2
  • Chemokine CXCL5
  • Chemokines, CXC
  • Heptanoic Acids
  • Hydroxymethylglutaryl-CoA Reductase Inhibitors
  • Immunologic Factors
  • Interleukin-6
  • Interleukin-8
  • Pyrroles
  • Granulocyte Colony-Stimulating Factor
  • Fibroblast Growth Factors
  • Atorvastatin
  • Mevalonic Acid