Fig. 2

CDDP-induced, Phb1-dependent Oma1 cleavage, L-Opa1 processing, mitochondrial fragmentation and apoptosis in chemosensitive CECA cells. A OV2008 cells were treated with Phb1 siRNA (0–100 nM, 24 h; scrambled siRNA as control), and subsequently treated with CDDP (0–10 μM, 24 h). The contents of Oma1, Phb1, Opa1, p-p53 (ser15), and GAPDH (loading control) were determined by WB (Left upper panel). Apoptosis was examined by Hoechst assay (Right bottom panel). B OV2008 cells were treated with control siRNA or Phb1 siRNA (0–100 nM, 24 h), followed by CDDP (0–10 μM, 6 h). Mitochondrial phenotypes were examined by immunofluorescence confocal microscopy. Knock-down of Phb1 inhibited CDDP-induced complete mitochondrial fragmentation. Results are expressed as mean ± SEM (n = 3) and analyzed by 2-way ANOVA and Bonferroni post-hoc test. [*p < 0.05, **p < 0.01, ***p < 0.001 (versus CDDP group in absence of Phb1 siRNA); n = 3]