Smad2/3 Antibody - #AF6367

Figure 4 FOXC2 driving EMT changes in PMCs may be achieved through the TGF-β1-Smad2/3 signaling feedback loop. A,B) Western blot analyses of FOXC2, Smad2/3, and p-Smad2/3 protein levels among different groups. n = 3 per group. Compared with the vector group, **p < 0.01, *p < 0.05. Compared with the vector group in the presence of TGF-β1, #p < 0.05. C,D) Western blot analyses of Smad2/3 and p-Smad2/3 protein levels among different groups. n = 3 per group. Compared with the vehicle group, **p < 0.01. Compared with the FOXC2-KD group, ##p < 0.01. E) Immunofluorescence staining images of nuclear accumulation of TGF-β1-induced Smad2/3 (red) in FOXC2-KD PMCs. Scale bar = 10 µm. F,G) Western blot analyses of Smad2/3 protein abundance in the cytoplasm and nucleus among different groups. n = 3 per group. Compared with the vehicle group, **p < 0.01. Compared with the TGF-β1, ##p < 0.01. H) The cell viability of PMCs treated with different concentrations of DGM (5, 10, 20, 40, 80, and 160 µM) for 24 h by CCK8 assay. n = 12 per group. Compared with the vehicle group, **p < 0.01. I) The cell viability of PMCs treated with TGF-β1 and different concentrations of DGM (10, 20, and 40 µM) for 24 h by CCK8 assay. n = 10 per group. Compared with the vehicle group, **p < 0.01. Compared with the TGF-β1 group, ##p < 0.01. J) Western blot analyses of the protein abundance of FOXC2, α-SMA, E-cadherin, Smad2/3, and p-Smad2/3 in PMCs treated with TGF-β1 and different concentrations of DGM (10, 20, and 40 µM) for 24 h. K–M) qRT-PCR analysis of mRNA expressions of FOXC2, α-SMA, and E-cadherin in PMCs treated with TGF-β1 and different concentrations of DGM (10, 20, and 40 µM) for 24 h. n = 6 per group. Compared with the vehicle group, **p < 0.01. Compared with the TGF-β1 group, ##p < 0.01, #p < 0.05.