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. 2024 Sep 12;15:7638. doi: 10.1038/s41467-024-52068-0

Fig. 6. PKN1/2 knockdown significantly reduced TGF-β-mediated p38 phosphorylation.

Fig. 6

a Western blot analysis for TGF-β-mediated phosphorylation of Smad2 (Ser465/467) and p38 (Thr180/182) in cardiac fibroblasts. The results represent three independent experiments. Western blot analysis (b) and quantification for TGF-β-mediated phosphorylation of endogenous Smad2 (c) and p38 (d) in cardiac fibroblasts after siRNA-mediated PKN1/2 knockdown (n = 4, biological replicates per group). ns, not significant; *p = 0.0169; ***p = 0.0005; ****p < 0.0001. Immunofluorescent images (e) and quantification of the number (f) of cardiac fibroblasts with phosphorylated Smad3 (Ser423/425; red) after siRNA-mediated PKN1/2 knockdown and TGF-β treatment (n = 4, biological replicates per group). ns, not significant; ****p < 0.0001. Immunofluorescent images (g) and quantification of the number (h) of cardiac fibroblasts with phosphorylated p38 (green) after siRNA-mediated PKN1/2 knockdown and TGF-β treatment (n = 4, biological replicates per group). ns, not significant; ****p < 0.0001. Data are presented as the mean ± SEM and analyzed using two-way ANOVA followed by Tukey’s post hoc test (c, d, f, h). The data represent three independent experiments with similar results. Source data are provided as a Source Data file.