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. 2016 Dec 7;6:37927. doi: 10.1038/srep37927

Figure 7. Cyclosporine A treatment of H9C2 cells transfected with either mitochondrial Omi/HtrA2 or cytosolic Omi/HtrA2 after hypoxia and reoxygenation (H/R).

Figure 7

(a) Cyclosporine A (CsA, 0.1μmol) completely blocked translocation of Omi/HtrA2 from mitochondria (42 kD, mitochondrial Omi/HtrA2) to cytoplasm (36 kD, cytosolic Omi/HtrA2) after H/R. (b) CsA inhibited mitochondrial Omi/HtrA2-induced activation of caspase-3 after H/R. Vector (V): Pc3.1 vector; F-Omi (F-O): Pc3.1 vector with mitochondrial Omi/HtrA2; S-Omi: Pc3.1 vector with cytosolic Omi/HtrA2. H9C2 cells were treated with vehicle (DMSO) and cyclosporine A (CsA), a mitochondrial permeability transition pore inhibitor. n = 10–12 each. **p < 0.01 versus Sham; ##p < 0.01 versus Vector + H/R; ∆∆p < 0.01 versus Vehicle.