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. 2018 Aug 31;33(1):1209–1225. doi: 10.1096/fj.201800876R

Figure 4.

Figure 4

Atorvastatin (Ator) and pravastatin (Prava) treatment inhibited RhoA kinase activity in cardiac myocytes, but only Ator increased LDH release and reduced oxygen consumption rate. Cardiac myocytes were treated with vehicle, RhoA activator (RhoA+), Ator, or Prava at 1 and 10 μM. A) After 48 h, total RhoA and activated RhoA expression was assessed by pull-down with GST-RBD. B) Densitometric analysis of RhoA pulldown assay. **P < 0.001, ****P < 0.0001 (1-way ANOVA with Tukey’s post hoc comparison). C) Representative images of NMVMs 48 h after treatment with, Ator, Prava, or vehicle at 1, 5, and 10 μM for 48 h. D) LDH release was measured in the culture medium 48 h after Ator, Prava, or vehicle treatment (n = 3 wells/treatment, each experiment repeated 3 times). Means ± sem. *P < 0.0001, Ator vs. Vehicle; #P < 0.0001, Ator vs. Prava (2-way ANOVA, with Tukey’s post hoc comparison). E) Bioenergetic analysis of HL-1 cells treated with vehicle, Ator, or Prava at 10 μM for 48 h. The OCR was measured after addition of oligomycin, FCCP, rotenone, and antimycin A 45,000 cells/well, 8 wells/plate, and repeated 3 times). Means ± sem. *P < 0.05 (2-way ANOVA).