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. 2001 Dec 15;15(24):3263–3277. doi: 10.1101/gad.207501

Figure 6.

Figure 6

Inflammation-induced PPARβ expression protects keratinocytes from apoptosis. (A) Elevated PPARβ expression inhibits TNFα-induced apoptosis. Keratinocytes prepared from PPARβ+/+,PPARβ+/−, and PPARβ−/− mice were either transfected with expression vectors harboring the wtPPARβ and/or cultured in the absence or presence of TNF-α and L165041 (LD, 5 μM) as indicated. The level of TNFα-induced apoptosis was monitored by caspase 8 activity. Keratinocytes expressing wtPPARβ were more resistant to apoptosis signals, whereas PPARβ+/− cells showed an increase susceptibility. PPARβ−/− keratinocytes exhibited higher basal caspase 8 activity and were more sensitive to TNFα-induced apoptosis, but could be rescued by transfection with the vector expressing wtPPARβ. Values are means of three independent experiments. (B) PPARβ−/− keratinocytes are more susceptible to TNFα-induced apoptosis. Culture of primary keratinocytes from wild-type and from PPARβ−/− mice were exposed to TNF-α. Apoptosis was measured by radioactive DNA fragmentation assay over indicated periods of time. Values are means of three independent experiments.