Fig. 2: Fibroblasts in PKN1/2-deficient mice. | Nature Communications

Fig. 2: Fibroblasts in PKN1/2-deficient mice.

From: Protein kinase N promotes cardiac fibrosis in heart failure by fibroblast-to-myofibroblast conversion

Fig. 2

a Animals were treated with intraperitoneal injections of tamoxifen for 5 consecutive days, and the efficiency of recombination was determined 10 days later. b Western blot analysis for PKN1 and PKN2 in cardiac fibroblasts isolated from the heart of Pdgfra-PKN1/2 WT or KO mice after tamoxifen induction. GAPDH is used for control. c, d Statistical evaluation of (b) (n = 3, biological replicates per group). ns, not significant; ***p = 0.0002; ****p < 0.0001. e Physiological function in Pdgfra-PKN1/2 WT or KO male mice (n = 6, biological replicates per group). ns, not significant. f Left ventricular fractional shortening assessed using echocardiography (n = 8, biological replicates per group) and (g) fibrotic changes in left ventricles assessed using Picrosirius red staining (n = 6, biological replicates per group) after 4 weeks of sustained AngII infusion (100 ng·g−1·d−1) in Pdgfra-PKN1/2 WT or KO male mice. ns, not significant; ****p < 0.0001. Data are presented as the mean ± SEM and analyzed using a two-sided unpaired Student t test (e) and two-way ANOVA followed by Tukey’s post hoc test (c, d, f, g). The data represent three independent experiments with similar results. Source data are provided as a Source Data file.

Back to article page