Cardiac protein kinase D1 ablation alters the myocytes β-adrenergic response
β-adrenergic (β-AR) signaling is essential for the adaptation of the heart to exercise and stress. Chronic stress leads to the activation of Ca2+/calmodulin-dependent kinase II (CaMKII) and protein kinase D (PKD). Unlike CaMKII, the effects of PKD on excitation-contraction coupling (ECC) remain un clear. To elucidate the mechanisms of PKD-dependent ECC regulation, we used hearts from cardiac-specific PKD1 knockout (PKD1 cKO) mice and wild-type (WT) littermates. We measured calcium transients (CaT), Ca2+ sparks, contraction and L-type Ca2+ current in paced cardiomyocytes under acute β-AR stim ulation with isoproterenol (ISO; 100 nM).
Source: Journal of Molecular and Cellular Cardiology - Category: Cytology Authors: Juliana Mira Hernandez, Christopher Y. Ko, Avery R. Mandel, Erin Y. Shen, Sonya Baidar, Ashley R. Christensen, Kim Hellgren, Stefano Morotti, Jody L. Martin, Bence Hegyi, Julie Bossuyt, Donald M. Bers Source Type: research