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. 2020 Nov 29;21(23):9084. doi: 10.3390/ijms21239084

Figure 6.

Figure 6

ERK, ADAM17, and RSK1 mediate TGF-β-induced C/EBPβ in human lung epithelial A549 cells. (A) A549 cells were processed with the ERK inhibitor U0126 (10 μM) for 20 min. After 20 min, the cells were treated with TGF-β (10 ng/mL) for an additional 20 min. C/EBPβ phosphorylation and C/EBPβ levels in cell lysates were immunodetected with specific antibodies. Data are expressed as mean ± SEM of three independent experiments. * p < 0.05, compared the TGF-β group without U0126 treatment. (B) A549 cells were transfected with control siRNA (con siRNA) and ADAM17 siRNA (25 nM). After 24 h, the cells were stimulated with TGF-β (10 ng/mL) for an additional 20 min. Cell lysates were prepared, and specific antibodies for C/EBPβ phosphorylation and C/EBPβ were immunodetected. Data are expressed as mean ± SEM of three independent experiments. * p < 0.05, compared with TGF-β plus the control siRNA group. (C) Cells were transfected with control siRNA (con siRNA) and RSK1 siRNA (50 nM) for 24 h before they were processed with TGF-β (10 ng/mL) for an additional 20 min. C/EBPβ phosphorylation and C/EBPβ were detected in cell lysates through Western blotting. Data are expressed as mean ± SEM of three independent experiments. * p < 0.05, compared with TGF-β plus the control siRNA group.