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. 2013 Apr 15;288(22):15947–15958. doi: 10.1074/jbc.M112.426791

FIGURE 3.

FIGURE 3.

Defective mitochondrial clearance in caspase 1-deficient cells during oxidative stress. A, OCR in hepatocytes cultured under normoxia or treated with 6 h of hypoxia/1 h of reoxygenation. The OCR was normalized to protein content and is shown as fold changes of normoxic control. Data are mean ± S.D., n = 3. #, p < 0.05, hypoxia-reoxygenation versus normoxia; ***, p < 0.001, WT versus caspase 1−/−. FCCP: Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone 2-DG: 2-deoxyglucose. B, mitochondrial volume in hepatocytes cultured under normoxia or treated with 6 h of hypoxia/1 h of reoxygenation. Data are shown as fold changes of normoxic levels (mean ± S.E.). #, p < 0.05, normoxia versus hypoxia-reoxygenation; **, p < 0.01, WT versus caspase 1−/− or siCtrl versus siCasp-1; *, p < 0.05, vector versus caspase 1. C, mitochondrial content in WT hepatocytes pretreated with dimethyl sulfoxide (DMSO) or caspase 1 inhibitor before normoxic culture or treated with hypoxia/reoxygenation. Data are shown as fold changes of normoxic levels (mean ± S.E.). #, p < 0.05, normoxia versus hypoxia-reoxygenation; **, p < 0.01, WT versus caspase 1 inhibitor. D, the mitochondrial DNA copy number is shown as fold changes of normoxic levels. H-R: hypoxia-reoxygenation. Data are mean ± S.E., n = 3. #, p < 0.05, normoxia versus hypoxia or hypoxia-reoxygenation; *, p < 0.05, WT versus caspase 1−/−. E, the expression (left panel) and quantification (right panel) of Tom20 was assessed in WT hepatocytes transfected with control siRNA (siCtrl) or caspase 1 siRNA (siC1) 24 h before they were treated with hypoxia. Data are mean ± S.E., n = 3). *, p < 0.05. F, the expression (left panel) and quantification (right panel) of Tom20 in WT, caspase 1−/− hepatocytes, and caspase 1−/− hepatocytes reconstituted with mouse caspase 1. Data are mean ± S.E., n = 3. *, p < 0.05; **, p < 0.01.