Figure 5.

Combined deletion of muscle‐specific RING‐finger (MuRF)2 and MuRF3 leads to decreased cardiac function. (A) Immunoblotting of proteins from the hearts of control and double knockout (DKO) mice using anti‐MuRF2 and anti‐MuRF3 antibody, as indicated, confirmed absence of MuRF2 and/or MuRF3 proteins in the respective single and DKO mice. Actin served as loading control. (B) Quantification of heart and lung weight of 7‐ to 22‐week‐old control (n = 30) and DKO (n = 26) mice. Organ weights were normalized to tibia length. Data are shown as mean ± SEM. (C) Haematoxyline and eosin stain of sections from whole hearts (scale bare, 300 µm) and cross‐sections (middle panel, scale bare, 50 µm), and Gomori's trichrome stain of cross‐sections (right panel, scale bare, 50 µm) of hearts from control and DKO mice. (D) Echocardiography was performed to measure left ventricular (LV) end‐diastolic (EDD) and end‐systolic dimension (ESD), thickness of the left ventricular posterior wall (LVPW) in diastole and systole, left ventricular ejection fraction (EF), and cardiac output in 8‐week‐old control (n = 7) and DKO (n = 5) mice. Data are presented as mean ± SEM. *P < 0.05. (E) Real‐time RT–PCR analysis of myosin heavy chain Myh6, Myh7, Nppa, and Nppb gene expression in the hearts of control (n = 7) and DKO (n = 5) mice. Hprt expression was used as reference. Data are presented as mean ± SEM. **P < 0.01.