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. 2010 Dec 3;300(2):L295–L304. doi: 10.1152/ajplung.00134.2010

Fig. 4.

Fig. 4.

Role of Smad-dependent signaling in the regulation of Nox4, MnSOD, catalase expression, and IL-6 release by TGF-β. A: effect of TGF-β on Smad3 phosphorylation over time. ASMCs were treated with TGF-β (1 ng/ml) for different times over a 24-h period. Phosphorylated and total Smad3 protein expression was determined in whole cell lysates by Western blotting. The blot is representative of experiments on 4 ASMC donors. B–D: ASMCs were infected with null virus (Null), wt-Smad2 (S2), wt-Smad3 (S3), wt-Smad7 (S7), or dn-Smad3 (dn-S3) adenoviral constructs for 72 h and stimulated with TGF-β (1 ng/ml) for the last 24 h of the infection period. Data are expressed as fold change in Nox4 (B), catalase (C), MnSOD (D) mRNA expression, and IL-6 release (E) with respect to null virus control. Bars represent means ± SE of 3 ASMC donors. *P < 0.05, **P < 0.01, ***P < 0.001 compared with null; #P < 0.05 and ##P < 0.01 compared with null, TGF-β-stimulated cells.