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

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Figure 4. Inhibition of TGF-β-induced Erk, JNK or p38 MAPK signaling augmented TGF-β-mediated EMT and motility in LPCs. (AC) Liver progenitor cell lines (WB-F344 and LE/6) were treated with TGF-β and/or kinase inhibitors as indicated for 3 days and then subjected to phalloidin staining for F-actin (red). DAPI (blue) was used to stain the cell nuclei. The white arrows indicate F-actin rearrangements. Scale bar, 25 μm. (DF) WB-F344 and LE/6 cells were treated with TGF-β and/or kinase inhibitors as indicated for three days, and Western blot analyses were carried out with antibodies against E-cadherin and vimentin. Representative bands of three independent experiments are shown, and GAPDH was used as a loading control. (G) Cell motility analyses of LPCs treated with TGF-β and/or kinase inhibitors as indicated (for WB-F344 cells, TGF-β and/or kinase inhibitors were added for seven hrs, and for LE/6 cells, TGF-β and/or kinase inhibitors were added for 24 hrs). The average number of migrated cells per field in three independent experiments is shown. One-way ANOVA was used for statistical analysis. The data are presented as the mean ± S.E.M. *p < 0.05; **p < 0.01; and ***p < 0.001.