Fig. 4

Effects of TGF-β2 on phosphorylation of STAT3 or SAPK/JNK in hTM cells. A Enzyme-linked immunosorbent analysis revealed significant downregulation of phospho-STAT3/total STAT3 ratio in hTM cells after treatment with TGF-β2 at the concentration of 10 ng/ml, compared with control or concentrations of 0.1 and 1 ng/ml. The ratio was also significantly downregulated after treatment with TGF-β2 at the concentration of 1 ng/ml, compared with 0.1 ng/ml (n = 4). B–D Western blotting of stress-activated protein kinase (SAPK)/Jun amino terminal kinase (JNK) and STAT3 in TGF-β2 treated hTM cells (n = 3). Representative bands for SAPK/JNK and STAT3 are shown in (B), while the relative expression levels of STAT3 (C) and SAPK/JNK (D) are shown compared with the loading control (β-tubulin) (n = 3). Phospho-STAT3 was significantly upregulated when hTM cells were treated with 0.1 ng/ml TGF-β2 compared with control, and downregulated compared with 10 ng/ml TGF-β2 (C). Phospho-SAPK/JNK was significantly upregulated when hTM cells were treated with 1 ng/ml TGF-β2. Quantitative analysis also revealed significant differences (D). ^*P < 0.05, ^**P < 0.01, ^***P < 0.01. (E–G) Western blotting of stress-activated protein kinase (SAPK)/Jun amino terminal kinase (JNK) and STAT3 in TGF-β2 treated CMV-infected hTM cells (n = 3). Representative bands for SAPK/JNK and STAT3 are shown in E, while the relative expression levels of STAT3 (F) and SAPK/JNK (G) are shown compared with the loading control (β-tubulin) (n = 3). Phospho-STAT3 was significantly upregulated when hTM cells were infected with CMV compared with control, and this change was attenuated by treatment with 1 ng or 10 ng/ml TGF-β2 (F). Phospho-SAPK/JNK was significantly upregulated when hTM cells were infected with CMV compared with control, and this change was attenuated by treatment with 1 ng or 10 ng/ml TGF-β2 (F). Quantitative analysis also revealed significant differences. ^*P < 0.05, ^**P < 0.01, ^***P < 0.001