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. 2011 Nov 2;6(11):e27294. doi: 10.1371/journal.pone.0027294

Figure 7. β-AR blockers suppressed overactivation of Calmodulin Kinase II in rat failing hearts.

Figure 7

(A) Metoprolol alleviated ER stress and overactivation of CaMKII induced by tunicamycin (TM). Cells were pretreated with KN93 (KN, 0.5 µmol/L or 2 µmol/L), metoprolol (M, 10 µmol/L or 20 µmol/L) for 1 hour, and exposed to TM (5 µg/ml) for 24 hours. Cell lysates were then immunoblotted for phosphorylated CaMKII, phosphorylated PERK, GRP78 and CHOP, which were all normalized to β-actin. *P<0.05 vs. control, #P<0.05 vs. TM. (B) Metoprolol suppressed the overactivation of CaMKII in AAC rats. *P<0.05 vs. sham, #P<0.05 vs. AAC.