Fig. 2: mtCaMKII does not affect hypertrophy, MCU, mitochondrial Ca2+, ROS, nor ΔΨmito.
From: Mitochondrial CaMKII causes adverse metabolic reprogramming and dilated cardiomyopathy
a Western blot for flag-CaMKII, VDAC1, and GAPDH in cytoplasm and mitochondria fractions from WT (n = 4) and mtCaMKII hearts (n = 4). b Quantification AC3-I-GFP fusion protein expression in cytoplasm and mitochondria from WT and AC3-I mouse hearts (n = 3). c Summary data for echocardiographic measurements from WT (n = 16), AC3-I (n = 13), mtCaMKII (n = 18), and mtCaMKII x AC3-I (n = 12) mice. d Summarized echocardiographic measurement data from WT (n = 12), mtCaMKIIN (n = 8), mtCaMKII (n = 10), and mtCaMKII x mtCaMKIIN (n = 10) mice. e Western blot and f summary data for flag-CaMKII normalized to GAPDH in mtCaMKII (n = 4) and mtCaMKII x mtCaMKIIN (n = 4) hearts. g Western blot and h summary data for phosphorylated MCU normalized to total MCU in mitochondria from WT (n = 4) and mtCaMKII (n = 4) hearts. i Mitochondrial Ca2+ uptake assay with cell membrane permeabilized adult ventricular myocytes from WT (n = 3) and mtCaMKII (n = 3) mice; arrows indicate addition of Ca2+. j Rate of Ca2+ uptake in permeabilized myocytes calculated from the first 3 peaks of Ca2+ addition and total Ca2+ uptake before mPTP opening in WT (n = 3) and mtCaMKII (n = 3) mice. k Total mitochondrial Ca2+ content normalized to total protein in isolated mitochondria from WT (n = 10) and mtCaMKII (n = 10) hearts. l H2O2 production measured by Amplex Red in isolated mitochondria from WT (n = 8) and mtCaMKII (n = 8) hearts. m Quantification of TUNEL positive nuclei from heart sections of WT (5 sections from n = 4 hearts) and mtCaMKII (5 sections from n = 3 hearts) mice. n Quantification of fibrosis by Masson’s Trichrome staining from WT (6 sections from n = 3 hearts) and mtCaMKII (6 sections from n = 3 hearts) heart sections. o Mitochondrial membrane potential (ΔΨmito) measured with TMRM under state 2 (substrate alone) and state 3 (substrate plus ADP) respiration in isolated mitochondria from WT (n = 4) and mtCaMKII (n = 4) 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 < 0.0001, ***P < 0.001, **P < 0.01, *P < 0.05, NS = not significant. Source data, including exact p values, are provided as a Source data file.
