Fig. 5: mtCaMKII hearts show decreased complex I and increased complex II activity.
From: Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
a Western blot of heart lysates from WT (n = 5) and mtCaMKII (n = 5) using OxPhos antibody. b Protein expression for complexes I–V normalized to GAPDH quantified from (a). c Blue Native gel with mitochondria from WT and mtCaMKII hearts stained with Coomassie blue and d in-gel activity assays for complex I. These experiments were repeated twice with similar results. e, f Mitochondrial respiration measured under state 2 (substrate alone) and state 3 (substrate plus ADP) conditions in isolated mitochondria from WT (n = 7) and mtCaMKII (n = 9) hearts. Substrates favored complex I (pyruvate/malate, e) or complex II (succinate/rotenone, f) activity. g Western blot with OxPhos antibody and (h) summary data for complex I normalized to CoxIV in heart lysates from WT (n = 4), CKmito (n = 4), mtCaMKII (n = 4), and mtCaMKII x CKmito (n = 3) hearts. i Complex I activity measured in mitochondria isolated from WT (n = 8), CKmito (n = 8), mtCaMKII (n = 9), and mtCaMKII x CKmito (n = 6) hearts. Data are represented as mean ± SEM, significance was determined using a two-tailed Student’s t test or one-way ANOVA with Tukey’s multiple comparisons test. ***P < 0.001, **P < 0.01, *P < 0.05. Source data, including exact p values, are provided as a Source data file.
