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. 2016 Mar 6;110(2):227–237. doi: 10.1093/cvr/cvw048

Figure 6.

Figure 6

Pharmacological inhibition of GSK-3β upon reperfusion mimics effects of Kcne2 deletion on GSK-3β phosphorylation. (A) Left: representative western blots of phosphorylated GSK-3β and total GSK-3β isolated from ventricles of Kcne2+/+ and Kcne2−/− mice in the presence (+) or absence (−) of pharmacological inhibitor SB216763 in baseline and post-IRI. Right: quantification of p-GSK-3β/GSK-3β protein band density; n = 6–9, each group. ***P < 0.0001 compared with Kcne2+/+ with SB216763 (by one-way ANOVA). (B) Left: representative western blots of phosphorylated ERK1/2 and total ERK1/2 isolated from ventricles of Kcne2+/+ and Kcne2−/− mice in the presence (+) or absence (−) of pharmacological inhibitor SB216763 in baseline and post-IRI. Right: quantification of p- ERK1/2/ERK1/2 protein band density; n = 4–6, each group. (C) Left: representative western blots of phosphorylated AKT and total AKT isolated from ventricles of Kcne2+/+ and Kcne2−/− mice in the presence (+) or absence (−) of pharmacological inhibitor SB216763 in baseline and post-IRI. Right: quantification of p-AKT/AKT protein band density; n = 4–7, each group.