FMOD-KO mice show mildly exacerbated hypertrophic remodeling compared to wild-type, associated with increased ERK signaling upon aortic banding.

<p>Cardiac phenotype assessed by serial echocardiography at 2–12 weeks (w) (A-B and D-E, n sham = 5–10, n AB = 5–24) and organ weights at 2w and 12w (C and F, n sham = 5–14, n AB = 9–14) post aortic banding (AB). (A) Interventricular septum thickness in diastole (IVSd), (B) left ventricular posterior wall thickness in diastole (LVPWd), (C) heart weight-to-body weight (HW/BW) ratio, (D) LV interior diameter in diastole (LVIDd), (E) fractional shortening (FS) and (F) lung weight-to-body weight (LW/BW) ratio in fibromodulin knock-out (FMOD-KO) and wild-type (WT) control mice subjected to AB. (G) Representative histology image of a whole heart section at low magnification(scale bar 1000μm) and insets showing representative histology images at high magnification (scale bar 50μm) of the different groups at 12w post operation, green (WGA staining) shows outline of cardiomyocyte cross sectional area (CSA) and blue (DAPI staining) shows nucleus. (H) Quantitative changes in cardiomyocyte (CM) cross-sectional area (CSA) respective to average sham controls, measured on midventricular sections of FMOD-KO and WT mice 2, 4, and 12w post-AB, n = 2191–14485 CMs from n sham = 1–4 mice, and n AB = 2–4 mice. (I) Representative immunoblots and (J) quantitative phosphorylated (p) and total levels of the extracellular signal–regulated kinase 1 and 2 (ERK1 and ERK2, respectively) in LVs of FMOD-KO and WT mice 4w post-AB (n sham = 2, n AB = 3–5). Coomassie staining was used as loading control. Data are shown as mean±SEM. Statistical differences were tested using an unpaired t-test vs. WT AB, #p≤0.05; ###p≤0.005 (A, B, D and E 4-10w, H and J), one-way ANOVA with Dunn's post-hoc test vs. WT sham, *p≤0.05; **p≤0.01; ***p≤0.005, or vs. WT AB (A-F 2w and 12w).