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Anti-apoptotic role of EGF in HaCaT keratinocytes via a PPARβ-dependent mechanism.
- Source :
-
Wound Repair & Regeneration . Sep/Oct2008, Vol. 16 Issue 5, p691-698. 8p. 1 Black and White Photograph, 4 Graphs. - Publication Year :
- 2008
-
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-α induced HaCaT keratinocyte apoptosis, and this effect was accompanied by up-regulation of the expression of peroxisome proliferator-activated receptor β (PPARβ). However, little is known about whether PPARβ 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 PPARβ. Antisense phosphorothioate oligonucleotides against PPARβ markedly inhibited de novo synthesis of PPARβ and attenuated the protective effect of EGF on tumor necrosis factor-α–induced apoptosis. L165041, a specific PPARβ ligand, significantly enhanced the transcriptional regulation activity of PPARβ and increased the protective effect of EGF. These results suggest a molecular mechanism by which EGF protects HaCaT keratinocytes against apoptosis in a PPARβ-dependent manner. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 10671927
- Volume :
- 16
- Issue :
- 5
- Database :
- Academic Search Index
- Journal :
- Wound Repair & Regeneration
- Publication Type :
- Academic Journal
- Accession number :
- 34137873
- Full Text :
- https://doi.org/10.1111/j.1524-475X.2008.00419.x