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. 2023 Apr 9;24(8):6972. doi: 10.3390/ijms24086972

Figure 3.

Figure 3

ET-1 is a downstream effector of TGF-β1, and blockade of either Smad or ERK1/2 activities attenuates profibrotic effects of TGF-β1. (A–C) Serum-starved adult HCFs were pretreated with LY2109761 (TGF-β inh; 5 µM), bosentan (1 µM), or valsartan (valsar; 1 µM) for 1 h before treatment with 1 ng/mL TGF-β1 for 6 h (A) or 24 h (B,C). (D–F) Serum-starved adult HCFs were pretreated with 1 µM Smad inhibitor (Smad inh), 1 µM FR180204 (ERK inhibitor; ERK inh), 1 µM SB203580 (p38 MAPK inhibitor; p38 inh), or Smad inh plus ERK inh for 1 h before treatment with 1 ng/mL TGF-β1 for 6 h (D) or 24 h (E,F). (A,D) Relative mRNA levels of fibrotic markers, α-SMA and collagen I, were analyzed by qRT-PCR. Data are expressed as the mean ± SEM (n = 4). After treatment, immunofluorescence staining was used to determine α-SMA expression (green) (B,E) and stress fiber formation (red) (C,F). Nuclei were stained with DAPI (blue). Scale bar, 10 μm. Data are expressed as the mean ± SEM (n = 3). * p < 0.05 vs. vehicle; # p < 0.05 vs. TGF-β1.