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

Figure 4.

Figure 4

Involvement of RSK1 activation in TGF-β-induced CTGF expression through the ERK/ADAM17 pathway in human lung epithelial A549 cells. (A) Cells were transfected with 25 nM control siRNA (con siRNA) and 25 nM RSK1 siRNA for 48 h before they were stimulated with TGF-β (10 ng/mL) for an additional 6 h. Cell lysates were prepared, and specific antibodies for CTGF and α-tubulin were detected through Western blotting. Results are expressed as mean ± SEM of three independent experiments. * p < 0.05, compared with TGF-β plus the control siRNA group. (B) Cells were stimulated with TGF-β (10 ng/mL) for 0–30 min, and then the levels of RSK1 phosphorylation and RSK1 in cell lysates were immunodetected with specific antibodies. Results are presented as mean ± SEM of three independent experiments. * p < 0.05, compared with the control group without TGF-β treatment. (C) Cells were treated with the ADAM17 inhibitor TAPI-0 (10 μM) for 20 min before they were stimulated with TGF-β (10 ng/mL) for an additional 10 min. RSK1 phosphorylation and RSK1 in cell lysates were immunodetected with specific antibodies. Results are expressed as mean ± SEM of four independent experiments. * p < 0.05, compared with the TGF-β group without TAPI-0 treatment. (D) Cells were pretreated with U0126 (10 μM) for 20 min before they were stimulated with TGF-β (10 ng/mL) for an additional 10 min. RSK1 phosphorylation and RSK1 in cell lysates were immunodetected with specific antibodies. Results are presented as mean ± SEM of three independent experiments. * p < 0.05, compared with the TGF-β group without U0126 treatment.