PPARbeta/delta selectively induces differentiation and inhibits cell proliferation

Cell Death Differ. 2006 Jan;13(1):53-60. doi: 10.1038/sj.cdd.4401713.

Abstract

Peroxisome proliferator-activated receptor (PPAR) beta-null mice exhibit exacerbated epithelial cell proliferation and enhanced sensitivity to skin carcinogenesis, suggesting that ligand activation of PPARbeta will inhibit keratinocyte proliferation. By using of a highly specific ligand (GW0742) and the PPARbeta-null mouse model, activation of PPARbeta was found to selectively induce keratinocyte terminal differentiation and inhibit keratinocyte proliferation. Additionally, GW0742 was found to be anti-inflammatory due to inhibition of myeloperoxidase activity, independent of PPARbeta. These data suggest that ligand activation of PPARbeta could be a novel approach to selectively induce differentiation and inhibit cell proliferation, thus representing a new molecular target for the treatment of skin disorders resulting from altered cell proliferation such as psoriasis and cancer.

Publication types

  • Research Support, N.I.H., Extramural

MeSH terms

  • Animals
  • Calcium / pharmacology
  • Calcium Signaling
  • Cell Differentiation / drug effects
  • Cell Proliferation / drug effects
  • Cells, Cultured
  • Enzyme Inhibitors / pharmacology
  • In Vitro Techniques
  • Keratinocytes / cytology*
  • Keratinocytes / drug effects
  • Keratinocytes / metabolism*
  • Ligands
  • Mice
  • Mice, Knockout
  • Models, Biological
  • PPAR-beta / deficiency
  • PPAR-beta / genetics
  • PPAR-beta / metabolism*
  • Peroxidase / antagonists & inhibitors
  • Tetradecanoylphorbol Acetate / pharmacology
  • Thiazoles / metabolism
  • Thiazoles / pharmacology

Substances

  • Enzyme Inhibitors
  • Ligands
  • PPAR-beta
  • Thiazoles
  • (4-(((2-(3-fluoro-4-(trifluoromethyl)phenyl)-4-methyl-1,3-thiazol-5-yl)methyl)sulfanyl)-2-methylphenoxy)acetic acid
  • Peroxidase
  • Tetradecanoylphorbol Acetate
  • Calcium