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. 2016 Mar 5;7(5):338–350. doi: 10.1007/s13238-015-0241-6

Figure 5.

Figure 5

Activation of ROS-TGFβ-NOX amplification loop in the IKKβ-null cells. The intracellular GSH in wild type, TGFβ1 treated wild type and Ikkβ −/− cells, (A) in the presence or absence of the TGFβ receptor inhibitor SB505124, or (C) in the presence or absence of the NOX inhibitor DPI. (B) The mRNA of genes coding for components of the NADH complexes in IKKβ-competent, i.e. wild type and Ikkβ −/−/Ad-IKKβ, and IKKβ-deficient, i.e. Ikkβ −/− and Ikkβ −/−/Ad-β-Gal, cells. (D) The mRNA for oxidative stress marker Hmox-1 in wild type, Ikkβ −/− and in Ikkβ F/F fibroblasts infected with Ad-Cre for 0 to 180 days with or without Ad-IKKβ. 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