Fig. 2: Impaired cardiac energy metabolism and mitochondrial dysfunction are caused by PHB2 ablation.
From: Prohibitin 2 deficiency impairs cardiac fatty acid oxidation and causes heart failure
a Cardiac ATP levels measured with luciferin assay in 6-week-old WT and Phb2 cKO mouse hearts. n = 6 mice per group. b Measurement of oxygen consumption rate (OCR) in isolated cardiomyocytes from 6-week-old WT and Phb2 cKO mice. Arrowheads indicate the time points of adding Oligo (oligomycin, 1 μm), FCCP (carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone, 1 μm), Rot (rotenone, 1 μm) and AA (antimycin, 1 μm). n = 3 mice per group. c Electron micrographs of mitochondrial morphology in left ventricular tissues from 6-week-old WT and Phb2 cKO mice. Scale bar: 0.5 μm. d Statistics of mitochondrial membrane potential measured with TMRM staining in isolated cardiomyocytes from 6-week-old WT and Phb2 cKO mice. n = 80–100 cells from six mice per group. e Statistics of mitochondrial ROS levels measured with mitoSOX staining in isolated cardiomyocytes from 6-week-old WT and Phb2 cKO mice. n = 80–100 cells from six mice per group. f Statistics of cytosolic ROS levels measured with DCF staining in isolated cardiomyocytes from 6-week-old WT and Phb2 cKO mice. n = 80–100 cells from six mice per group. All Data represent mean ± SEM. Significance was determined by two-tailed, unpaired Student’s t test. *p < 0.05, **p < 0.01, ***p < 0.001 versus WT group.
