Figure 4.
(a), Expression of PKN1, PKN2 and PKN3 in human hearts. Data were mined from an RNASeq database of patients with dilated cardiomyopathy (DCM; n = 97) and normal controls (Con; n = 108). Data for individual samples are shown with false discovery rates (FDR). (b and c) Immunoblotting of phospho-PKN1/2, total PKN1, total PKN2 and GAPDH in hearts from wild-type (WT) or Pkn2Het mice treated for 7 days with vehicle (Veh, V) or 0.8 mg/kg/d angiotensin II (AngII, A). Immunoblots are shown on the left with densitometric analysis on the right (normalised to the mean of vehicle-treated controls). Individual data points are provided with means ± SEM. Analysis used two-way ANOVA with Holm–Sidak's post-test. (d–h), Echocardiography of hearts from WT and Pkn2Het mice at baseline (d and e) or treated with vehicle or AngII for 7 days (f–h). Representative short-axis M-mode images used for assessment of cardiac dimensions are shown at baseline (d) and after treatment (f) (the same animals are shown). (g), Representative long-axis B-mode images used for speckle-tracking and strain analysis to assess cardiac function are shown after 7 days treatment. (e and h), Echocardiograms were analysed. Individual data points are provided with means ± SEM. Additional data are provided in Supplementary Table S1 and histology in S2. Analysis used unpaired, two-tailed t-tests (e) or two-way ANOVA with Holm–Sidak's post-test (g). LV, Left ventricle; ID, internal diameter; AW, anterior wall; PW, posterior wall; EDLVM, end diastolic LV mass.
PKN2 is associated with human heart failure and required for cardiac adaptation to hypertension in mice.

(a), Expression of PKN1, PKN2 and PKN3 in human hearts. Data were mined from an RNASeq database of patients with dilated cardiomyopathy (DCM; n = 97) and normal controls (Con; n = 108). Data for individual samples are shown with false discovery rates (FDR). (b and c) Immunoblotting of phospho-PKN1/2, total PKN1, total PKN2 and GAPDH in hearts from wild-type (WT) or Pkn2Het mice treated for 7 days with vehicle (Veh, V) or 0.8 mg/kg/d angiotensin II (AngII, A). Immunoblots are shown on the left with densitometric analysis on the right (normalised to the mean of vehicle-treated controls). Individual data points are provided with means ± SEM. Analysis used two-way ANOVA with Holm–Sidak's post-test. (dh), Echocardiography of hearts from WT and Pkn2Het mice at baseline (d and e) or treated with vehicle or AngII for 7 days (fh). Representative short-axis M-mode images used for assessment of cardiac dimensions are shown at baseline (d) and after treatment (f) (the same animals are shown). (g), Representative long-axis B-mode images used for speckle-tracking and strain analysis to assess cardiac function are shown after 7 days treatment. (e and h), Echocardiograms were analysed. Individual data points are provided with means ± SEM. Additional data are provided in Supplementary Table S1 and histology in S2. Analysis used unpaired, two-tailed t-tests (e) or two-way ANOVA with Holm–Sidak's post-test (g). LV, Left ventricle; ID, internal diameter; AW, anterior wall; PW, posterior wall; EDLVM, end diastolic LV mass.

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