FIG. 9.

Effect of TN on mitochondrial integrity using mitochondrial membrane potential and mitochondrial permeability transition pore opening (mPTP) in cardiomyocytes from adult WT and MyAkt mice. Murine cardiomyocytes were incubated with TN (3 μg/ml) for 5–6 h in vitro before assessment of mitochondrial function. A cohort of WT cardiomyocytes were coincubated with the mPTP inhibitor cyclosporin A (200 nM), the GSK3β inhibitor SB216763 (10 μM), or the ER stress inhibitor TUDCA (500 μM) along with TN exposure. (A) Representative JC-1 fluorochrome images depicting mitochondrial membrane potential in the above-mentioned cardiomyocyte groups. The mitochondrial uncoupler carbonyl cyanide m-chlorophenylhydrazone (CCCP) (10 μM) was used as a positive control; (B) pooled data of mitochondrial membrane potential (ratio of the red fluorescence obtained at 590 nm to the green fluorescence at 530 nm); and (C) mPTP opening evaluated by NAD⁺, a marker for mitochondrial permeability transition pore opening; Mean±SEM, n=6 isolations per group, *p<0.05 versus WT group; ^#p<0.05 versus WT-TN group. (To see this illustration in color the reader is referred to the web version of this article at www.liebertonline.com/ars).