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. 2020 Oct 20;11:5237. doi: 10.1038/s41467-020-18980-x

Fig. 4. Suppressed myocyte PKG activity in vivo worsens infarct remodeling.

Fig. 4

a PDE5A and PKG enzyme activity in peri-infarct region at baseline and after myocardial infarction in mice with myocyte-specific PDE5A overexpression (mPDE5oe) versus littermate controls (CON). 2WANOVA, Tukey Post mct: Upper: *10−5, †3 × 10−5, ‡8 × 10−4, §2.6 × 10−3; Lower: *2 × 10−8, †0.025, ‡9 × 10−7. b Example of M-mode echocardiograms in mPDE5/oe versus littermate controls 1-week following myocardial infarction (MI). c Summary data for left ventricular ejection fraction (EF, n = 7–8 mice/group) and for fibrosis (n = 3–8 biological replicates/group) for same study. For EF: Repeated measures mixed effects model, Holm-Sidak mct: *p < 2 × 10−8; †p = 0.03; for fibrosis: biological replicates: 3–5 – sham, 7–8 MI; Brown-Forsythe Welch ANOVA, Dunnetts mct: *p = 0.02, †0.008, ‡0.003. d Heart and Lung weight normalized to tibia length for same study (HW/TL, LW/TL respectively). N = 7–8 biological replicates; 2WANOVA, Sidaks mct: for HW/TL: *p = 0.04, †2 × 10−5, ‡0.01; LW/TL: *0.003, †8 × 10−9, ‡2 × 10−5. e Ubiquitinated protein increase after MI in the peri-infarct zone is greater in mPDE5/oe hearts. N = 6 biological replicates, 2WANOVA, Tukey mct: *8.6 × 10−6, ‡<10−8, ‡1.5 × 10−7. Source data are provided as a Source Data file. Individual data and mean ± SEM shown in each summary panel.