| First Author | Tan NS | Year | 2001 |
| Journal | Genes Dev | Volume | 15 |
| Issue | 24 | Pages | 3263-77 |
| PubMed ID | 11751632 | Mgi Jnum | J:73469 |
| Mgi Id | MGI:2155525 | Doi | 10.1101/gad.207501 |
| Citation | Tan NS, et al. (2001) Critical roles of PPARbeta/delta in keratinocyte response to inflammation. Genes Dev 15(24):3263-77 |
| abstractText | The immediate response to skin injury is the release of inflammatory signals. It is shown here, by use of cultures of primary keratinocytes from wild-type and PPARbeta/delta(-/-) mice, that such signals including TNF-alpha and IFN-gamma, induce keratinocyte differentiation. This cytokine-dependent cell differentiation pathway requires up-regulation of the PPARbeta/delta gene via the stress-associated kinase cascade, which targets an AP-1 site in the PPARbeta/delta promoter. In addition, the pro-inflammatory cytokines also initiate the production of endogenous PPARbeta/delta ligands, which are essential for PPARbeta/delta activation and action. Activated PPARbeta/delta regulates the expression of genes associated with apoptosis resulting in an increased resistance of cultured keratinocytes to cell death. This effect is also observed in vivo during wound healing after an injury, as shown in dorsal skin of PPARbeta/delta(+/+) and PPARbeta/delta(+/-) mice. |
