Research Paper Volume 16, Issue 7 pp 6588—6612
TGF-β downstream of Smad3 and MAPK signaling antagonistically regulate the viability and partial epithelial–mesenchymal transition of liver progenitor cells
Figure 5. TGF-β activated Erk, JNK and p38 MAPK signaling and inhibited TGFβ-Smad3 signaling in LPCs. (A–C) LPCs were treated with TGF-β and/or kinase inhibitors as indicated, and the levels of phospho-Smad2 and Smad3 at the C-terminus and related total Smad2 and 3 proteins in the cells were analyzed via Western blotting. GAPDH was used as a loading control. (D–F) LPCs were cotransfected with pRL-TK and SBE4-luc and treated with TGF-β and/or kinase inhibitors as indicated. Luciferase activity was normalized to Renilla luciferase activity and is expressed as the means ± SEMs of triplicate measurements. The following comparisons of the bars were made: a, P < 0.01, second with first; b, P < 0.001, third with first; c, P < 0.01, third with second; d, P < 0.01, fourth with second; e, P < 0. 001, fourth with third; f, P < 0.05, third with second. The experiments were repeated three times. One-way ANOVA was used for statistical analysis. The data are presented as the mean ± S.E.M.