Figure 1.

Loss of IKKβ upregulates TGFβ expression and activity. The IKKβ-competent, i.e. wild type and Ikkβ ^−/−/Ad-IKKβ, and IKKβ-deficient, i.e. Ikkβ ^−/− and Ikkβ ^−/− /Ad-GFP, fibroblasts were examined for Tgfβ2 and 3 (A) mRNA expression and (B) promoter activity, and for (C) basal (un-treated) and TGFβ1-induced SMAD activity (SBE-luc) and (D) SMAD phosphorylation, and IKKβ, α-SMA and β-actin expression. (E) The Ikkβ ^−/− cells, either uninfected or infected with Ad-IKKβ and Ad-SMAD7, were examined for the expression of SMAD-target genes, i.e. Acta2, Smad6 and Ctgf. Results represent the mean values ± SD from at least three independent experiments. *P < 0.05, **P < 0.01 and ***P < 0.001 were considered significantly different from the wild type or control samples