Figure 4: Carvedilol Activates AKT, Prevents the Doxorubicin-dependent Loss of β
2019-06-11T07:09:17Z (GMT) by
(A) Lysates from β1AR-overexpressing cardiomyocytes treated for 24 h with vehicle, 10 μM doxorubicin alone, or 10 μM doxorubicin plus 1 μM carvedilol were probed for β1AR and β2AR expression, protein kinase B (AKT) and ERK phosphorylation, and caspase-3 cleavage (with β-actin immunoreactivity used as a loading control). Results are representative of data obtained in 4 separate experiments on separate culture preparations. (B) Lysates from cardiomyocytes treated with 0.1 μM isoproterenol or 1 μM carvedilol for the indicated intervals were probed for ERK and AKT phosphorylation, with immunoreactivity for the cognate protein serving as a loading control. A representative experiment is depicted on top, with maximal agonist-dependent phosphorylation responses for ERK (at 5 min, n = 5) or AKT (at 30 min, n = 3) quantified at the bottom, with the basal value in each individual experiment set to 100% as a reference (open bar) and agonist-dependent increases in immunoreactivity expressed relative to basal (shaded bars). Abbreviations as in Figures 1 and 3.