Analysis of MuRF2−/− hearts by conscious echocardiograpy, morphometrics, and heart failure-associated gene expression. a MuRF2−/− exhibit an accelerated heart failure by 6 weeks after the initiation of the high fat diet. b Representative 2D echocardiographic images from MuRF2−/− hearts at baseline and high fat diet challenge. c Endogenous MuRF2 inhibits HFD-induced LV Mass and heart wet weights, as MuRF2−/− hearts have a significant increase in heart weight normalized to body weight and tibia length (N = 5/group). d Representative gross histological analysis of MuRF2−/− hearts, found to have wall thinning and increased LV diameters by echocardiological analysis (N = 11 MuRF2+/+, N = 12 MuRF2−/−, see Table 1 and panel
a above). e RT-qPCR analysis of heart failure associated fetal gene expression in MuRF2−/− mice at baseline and after 26 weeks high fat diet challenge. Values expressed as Mean ± SE. A One Way ANOVA was performed on echocardiographic studies between all groups, followed by Holm-Sidak (Multiple Comparisons vs. MuRF2 +/+ baseline only). A Student’s t test was then run to compare MuRF2−/− to wildtype control at the same time point. §p < 0.05 by One Way ANOVA, ¶p < 0.05 vs. MuRF2+/+ baseline by multiple comparisons. $p < 0.05 vs. time-matched MuRF2+/+ (Student’s t test). Statistical analysis of heart weight/body weight was performed using a Student’s t test. RT-qPCR analysis analyzed by a One Way ANOVA followed by Holm-Sidak Multiple Comparisons (all pairwise comparisons) *p < 0.001, **p < 0.01, #p < 0.05.