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Related Experiment Videos

PPAR activators inhibit endothelial cell migration by targeting Akt.

Stephan Goetze1, Friedrich Eilers, Anne Bungenstock

  • 1Department of Medicine/Cardiology, German Heart Institute Berlin, Augustenburger Platz 1, 13353 Berlin, Germany. goetze@dhzb.be

Biochemical and Biophysical Research Communications
|June 11, 2002
PubMed
Summary

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Peroxisome proliferator-activated receptors (PPARs) activators inhibit endothelial cell migration, a key process in atherosclerosis. This suggests PPARs may protect blood vessels from metabolic disorder-related damage.

Area of Science:

  • Cardiovascular Biology
  • Metabolic Regulation
  • Cellular Signaling

Background:

  • Peroxisome proliferator-activated receptors (PPARs) are crucial regulators of lipid and glucose metabolism.
  • PPARs exhibit vascular effects, potentially benefiting metabolic disorders and atherosclerotic vascular disease.
  • Endothelial cell migration is a critical factor in atherosclerosis development.

Purpose of the Study:

  • To investigate the effects of PPARalpha- and PPARgamma-activators on endothelial cell migration.
  • To determine the signaling pathways involved in PPAR-mediated inhibition of endothelial cell migration.

Main Methods:

  • Utilized PPARalpha-activators (fenofibrate, WY14643) and PPARgamma-activators (troglitazone, ciglitazone).
  • Assessed the impact on VEGF-induced migration of human umbilical vein endothelial cells (EC).

Related Experiment Videos

  • Employed pharmacological inhibitors (wortmannin for PI3K, PD98059 for ERK MAPK) to probe signaling pathways.
  • Analyzed Akt and ERK MAPK phosphorylation levels.

    • Main Results:

    • Both PPARalpha- and PPARgamma-activators significantly inhibited VEGF-induced EC migration in a concentration-dependent manner.
    • VEGF-induced Akt phosphorylation was suppressed by both PPARalpha- and gamma-activators.
    • VEGF-stimulated ERK MAPK activation remained unaffected by PPAR-activators, suggesting inhibition occurs downstream or independently of this pathway.

    Conclusions:

    • PPAR-activators demonstrate significant antimigratory effects on endothelial cells.
    • By inhibiting EC migration, PPAR-activators may offer protection against vascular pathologies linked to metabolic disorders.
    • These findings highlight a potential therapeutic role for PPAR-activators in managing atherosclerotic vascular disease in metabolic conditions.