Fig. 7: Cardiomyocyte-specific overexpression of USP13 ameliorates established cardiac dysfunction, and STAT1 suppresses myocardial dysfunction regardless of the presence or absence of USP13.
a Wildtype (WT) and USP13cKO mice were subjected to TAC for 6 weeks. AAV9 cardiomyocyte-specific overexpressing USP13 (USP13OE), STAT1 (STAT1OE), or vehicle (EV) were injected at the end of 2nd week after TAC (2E + 11 v.g.). Echocardiography was performed at different stages (0, 4, and 6 weeks) after TAC. Mice were harvested 6 weeks after TAC. b Ejection fraction (EF) and fractional shortening (FS) at TAC 0, 4, 6 weeks. c–e M-mode echocardiographic images of left ventricle, EF and FS at TAC 6 week. f Representative images of gross-heart at TAC 6 week. g The ratio of heart weight (HW) to tibial length (TL). h Representative images of heart sections stained with H&E at TAC 6 week. i, j Representative images of heart sections stained with WGA and corresponding quantitative analysis at TAC 6 week. k, l Representative Masson’s trichrome stained images of heart sections and corresponding quantitative analysis at TAC 6 week. n = 7 for each group; For (d, e, g, j, l), adjusted P values were determined by one-way ANOVA with Bonferroni’s correction and data are presented as mean ± s.e.m.
