Abstract
TCDD stimulated IL-1β gene expression in differentiating human keratinocyte cell lines in a time- and dose-dependent manner. Increases in prointerleukin-1β (pIL-1β) protein and IL-1β steady state mRNA levels were observed in both SCC-12F and HaCaT cells following TCDD treatment. When pretreated with α-naphthoflavone, an AhR antagonist, TCDD-mediated increases in IL-1β gene expression were attenuated, demonstrating for the first time that the environmental toxin, TCDD, can stimulate cytokine (IL-1β) gene expression in an AhR-dependent manner. Nuclear run-on experiments were performed in SCC-12 cells to determine if the AhR-dependent increases in IL-1β expression were due to transcriptional activation of the IL-1β gene. Results showed high constitutive levels of IL-1β transcriptional activity, however, TCDD treatment, which stimulated IL-1β steady state mRNA levels, failed to potentiate IL-1β transcription. Taken together, these results demonstrate that AhR-mediated IL-1β regulation is occurring posttranscriptionally.
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