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. 2015 Jun 29;10(6):e0131411. doi: 10.1371/journal.pone.0131411

Fig 4. Executioner caspase-deficiency induces progressive cardiomyocyte hypertrophy without affecting heart function.

Fig 4

(A) Progressive increase of cardiomyocyte (CM) cross-sectional area in the septum and ventricular wall of wild type (WT) and caspase-3 and -7 double knockout (KO) mice. **, p<0.01 KO vs. WT. N = 6 per gender, age and genotype. Representative microscopy images of heart histological preparations stained with FITC-WGA of 7-months-old WT and KO mice, bar: 50µm. (B) Cardiac function of 3-month-old wild type (WT) and caspase-3 and -7 double knockout (KO) mice. BW, body weight; IVS, inter-ventricular septum thickness; LVPW, left ventricular posterior wall thickness; LVEDD, left ventricular end diastolic diameter; LVESD, left ventricular end systolic diameter; EF, ejection fraction; FS, left ventricular fractional shortening; HR, heart rate in beats per minute. N = 9 (WT) and 10 (KO). P, statistical analysis by Student’s-t test. (C) Beta-adrenergic agonist-induced cardiac hypertrophy in wild type (WT) and caspase-3 and -7 double knockout (KO) mice (N = 6/genotype). Isoproterenol (ISO) at 8.8mg/kg/day or saline vehicle was administered to five 20-week-old mice per genotype using subcutaneously implanted osmotic pumps. Seven days later, heart weight and tibia length were recorded. *, p<0.05 Student’s-t test ISO vs. saline for each genotype. NS = not statistically significant changes. Bars are means ± s.e.m.