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. Author manuscript; available in PMC: 2020 Feb 1.
Published in final edited form as: J Mol Cell Cardiol. 2018 Dec 11;127:125–133. doi: 10.1016/j.yjmcc.2018.12.004

Figure 2. Q73 expression in H9C2 cells induces defects in mitochondrial health, autophagy and apoptosis.

Figure 2.

Mitochondrial health was evaluated using A. MitoSOX for mitochondrial ROS measurement and B. TMRM as a surrogate for mitochondrial membrane potential in H9C2 cardiomyocytes transfected with either Q23 or Q73 repeats for 48 hours and then treated with P110 (1μM once) or Veh, for an additional 24 h in serum free- galactose medium C. Heat map of RNA transcripts in these H9C2 cardiomyocytes, treated as in (A). D. Caspase 3 and E. Caspase 9 activities were measured using kits, in cells treated as in (A). LDH release as a surrogate for cell death in H9C2 cardiomyocytes transfected with either Q23 or Q73 repeats for 48 hours and then treated with P110 (1μM once) or Veh, for an additional 48 h in serum free- galactose medium. Data were evaluated by one-way ANOVA and Holm-Sidak's multiple comparisons test for multiple testing between each treatment group. **** p-value <0.0001; *** p-value <0.001; ** p-value <0.01; * p-value <0.05. All graphs represent mean ± s.d. (n= 5 or 6, as indicated in each panel).

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