FIG 3.

Attenuated PI3K activation and increased dephosphorylation of prohypertrophic signaling intermediates in CIRS1KO and CIRS2KO hearts following exercise training. Two-way ANOVA was performed to analyze differences by swim training and genotype followed by Fisher's PLSD post hoc analysis. (a) PI3 kinase enzymatic activity (P < 0.05 for genotype, P < 0.05 for the interaction between swim training and genotype); (b) densitometric quantification of PI3 kinase p85 subunit protein; (c) PI3 kinase enzymatic activity normalized to p85 protein (n = 6; P < 0.05 for the interaction between swim training and genotype). (d to k) Representative Western blots (d) and densitometric quantification of P AKT Thr308/Total AKT (P < 0.05 for genotype, P < 0.05 for the interaction between swim training and genotype) (e), P AKT Ser473/Total AKT (P < 0.05 for genotype, P < 0.05 for the interaction between swim training and genotype) (f), P GSK3b Ser9/Total GSK3b (P < 0.05 for swim training, P < 0.05 for the interaction between swim training and genotype) (g), 4E-BP1 γ/GAPDH (P < 0.05 for swim training, P < 0.05 for the interaction between swim training and genotype) (h), P PP2A Tyr307/Total PP2A (P < 0.05 for swim training, genotype, and their interaction) (i), P JAK2 Tyr221/Total JAK2 (P < 0.05 for swim training, P < 0.05 for the interaction between swim training and genotype) (j), and P STAT3 Tyr705/Total STAT3 (P < 0.05 for swim training, P < 0.05 for the interaction between swim training and genotype) (n = 8) (k). *, P < 0.05 versus WT (same treatment); †, P < 0.05 versus sedentary (same genotype); ‡, P < 0.05 versus CIRS1KO (same treatment). n.s., no significant difference observed.