Figure 1

Trichostatin A inhibits α-SMA up-regulation and JNK activation, but not the activation of Smad, p38 and ERK in TGF-β1-treated fibroblasts. (a) Western blot analysis of α-SMA expression in NRK-49F cells that were treated with TGF-β1 (5 ng/ml) in combination with different concentrations of TSA or the solvent control (Dimethyl sulfoxide; DMSO) for 48 hr. Relative expression levels of α-SMA, normalized to β-actin, in the treated cells were quantified by densitometry (n = 6, bottom panel). Symbol # indicates significant difference vs. the control or vehicle group (P < 0.05). (b) Effects of TSA on cell viability of TGF-β1-treated NRK-49F cells. MTT assays were used to determine the cell viability and results were presented as means ± SEM calculated from at least three independent experiments. Symbol # indicates significant difference vs. the control group (P < 0.05). (c) Effects of TSA on the TGF-β1-mediated activation of Smad2, Smad3 and different MAP kinases. NRK-49F cells were treated with TGF-β1 in the presence or absence of TSA (200 or 500 nM), and the expression levels of phospho-Smad2 (at 30 min), phospho-Smad3 (at 60 min), phospho-p38 (at 90 min), phospho-ERK (at 90 min) and phospho-JNK (at 90 min) were examined in cell samples (n = 6). ^#P < 0.05 vs. control group; *P < 0.05 vs. TGF-β1 group and ^@P < 0.05 vs. the group treated with TGF-β1 plus TSA (200 nM).