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  • Title: Protein kinase A-dependent phosphorylation of ryanodine receptors increases Ca2+ leak in mouse heart.
    Author: Morimoto S, O-Uchi J, Kawai M, Hoshina T, Kusakari Y, Komukai K, Sasaki H, Hongo K, Kurihara S.
    Journal: Biochem Biophys Res Commun; 2009 Dec 04; 390(1):87-92. PubMed ID: 19781523.
    Abstract:
    In heart failure, chronic catecholaminergic stimulation increases diastolic Ca(2+) leak from ryanodine receptors (RyRs) of sarcoplasmic reticulum (SR), possibly due to the phosphorylation of RyRs through the activation of protein kinase A (PKA) or Ca(2+)/calmodulin-dependent protein kinase II (CaMKII). In the present study, we attempted to identify which activated kinase is responsible for the enhanced Ca(2+) leak caused by beta-adrenergic stimulation. Trabeculae obtained from the hearts of adult male C57BL/6J mice were treated with isoproterenol and then permeabilized with saponin. To examine SR functions, Ca(2+) in SR was released with caffeine and measured with fluo-3. The Ca(2+) leak in isoproterenol-treated preparations was significantly increased when the PKA-dependent phosphorylation of RyR was increased without the involvement of CaMKII-dependent phosphorylation. Both the increase in Ca(2+) leak and the phosphorylation of RyR were blocked by a PKA inhibitor. Our results show that beta-adrenergic stimulation increases Ca(2+) leak from SR through PKA-dependent phosphorylation of RyR.
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