Figure 6.

In vitro assessment of PRKAA2 involvement in AdipoRon-stimulated autophagic flux. Adult cardiomyocytes isolated from WT or Prkaa2 DN mice were subjected to 3 h of simulated ischemia and 6 h of simulated reperfusion. At the time of reperfusion, cells were treated with vehicle or AdipoRon. (A) AdipoRon caused significant phosphorylation of ACACA, PIK3C3 (Ser164) and BECN1 (T119), and increased LAMP2 expression in cardiomyocytes from WT mice. (B) AdipoRon-induced phosphorylation of ACACA, PIK3C3 (Ser164), and BECN1 (Thr119) was abolished in cardiomyocytes from Prkaa2 DN mice; however, ADIPOR-induced LAMP2 expression was unaffected. N = 14–16 dishes from at least 5 mice/group. Data were analyzed by one-way ANOVA followed by the Tukey post hoc test for pairwise comparisons. *P < 0.05, **P < 0.01 between vehicle and AdipoRon-treated cells.