Anti-apoptotic role of EGF in HaCaT keratinocytes via a PPARbeta-dependent mechanism

Wound Repair Regen. 2008 Sep-Oct;16(5):691-8. doi: 10.1111/j.1524-475X.2008.00419.x.

Abstract

Epidermal growth factor (EGF) plays an important role in epithelial cell proliferation and apoptosis. Our recent studies found that EGF-attenuated tumor necrosis factor-alpha induced HaCaT keratinocyte apoptosis, and this effect was accompanied by up-regulation of the expression of peroxisome proliferator-activated receptor beta (PPARbeta). However, little is known about whether PPARbeta is functionally involved in the inhibition of keratinocyte apoptosis by EGF. Here, we showed that EGF up-regulated the DNA-binding and transcriptional regulation activities of PPARbeta. Antisense phosphorothioate oligonucleotides against PPARbeta markedly inhibited de novo synthesis of PPARbeta and attenuated the protective effect of EGF on tumor necrosis factor-alpha-induced apoptosis. L165041, a specific PPARbeta ligand, significantly enhanced the transcriptional regulation activity of PPARbeta and increased the protective effect of EGF. These results suggest a molecular mechanism by which EGF protects HaCaT keratinocytes against apoptosis in a PPARbeta-dependent manner.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Apoptosis / physiology*
  • Cell Line
  • Epidermal Growth Factor / physiology*
  • Humans
  • Keratinocytes / physiology*
  • PPAR-beta / antagonists & inhibitors
  • PPAR-beta / physiology*
  • Tumor Necrosis Factor-alpha / physiology
  • Up-Regulation

Substances

  • PPAR-beta
  • Tumor Necrosis Factor-alpha
  • Epidermal Growth Factor