Cardiac Protein Kinase D1 ablation alters the myocytes β-adrenergic response.

ABSTRACT: 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 unclear. 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 stimulation with isoproterenol (ISO; 100 nM). Sarcoplasmic reticulum (SR) Ca²⁺ load was assessed by rapid caffeine (10 mM) induced Ca²⁺ release. Express

SUBMITTER: Mira Hernandez J 

PROVIDER: S-EPMC11186477 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature