Circulation Research. 2003;92:904-911
Published online before print April 3, 2003, doi: 10.1161/01.RES.0000069685.20258.F1
Published online before print April 3, 2003, doi: 10.1161/01.RES.0000069685.20258.F1
© 2003 American Heart Association, Inc.
Cellular Biology |
Transgenic CaMKII
C Overexpression Uniquely Alters Cardiac Myocyte Ca2+ Handling
Reduced SR Ca2+ Load and Activated SR Ca2+ Release
From the Department of Physiology (L.S.M., L.C., J.D., D.M.B.), Stritch School of Medicine, Loyola University Chicago, Ill; and the Department of Pharmacology (T.Z., J.H.B.), University of California San Diego, Calif. Present address for L.S.M. is the Department of Cardiology, Georg-August-University Goettingen, Germany.
Correspondence to Donald M. Bers, PhD, Department of Physiology, Stritch School of Medicine, Loyola University Chicago, 2160 South First Ave, Maywood, IL 60153. E-mail dbers{at}lumc.edu
Ca2+/calmodulin-dependent protein kinase II (CaMKII) 
is the predominant cardiac isoform, and the C splice variant is cytoplasmic. We overexpressed CaMKIIC in mouse heart and observed dilated heart failure and altered myocyte Ca2+ regulation in 3-month-old CaMKIIC transgenic mice (TG) versus wild-type littermates (WT). Heart/body weight ratio and cardiomyocyte size were increased about 2-fold in TG versus WT. At 1 Hz, twitch shortening, [Ca2+]i transient amplitude, and diastolic [Ca2+]i were all reduced by 
50% in TG versus WT. This is explained by >50% reduction in SR Ca2+ content in TG versus WT. Peak Ca2+ current (ICa) was slightly increased, and action potential duration was prolonged in TG versus WT. Despite lower SR Ca2+ load and diastolic [Ca2+]i, fractional SR Ca2+ release was increased and resting spontaneous SR Ca2+ release events (Ca2+ sparks) were doubled in frequency in TG versus WT (with prolonged width and duration, but lower amplitude). Enhanced Ca2+ spark frequency was also seen in TG at 4 weeks (before heart failure onset). Acute CaMKII inhibition normalized Ca2+ spark frequency and ICa, consistent with direct CaMKII activation of ryanodine receptors (and ICa) in TG. The rate of [Ca2+]i decline during caffeine exposure was faster in TG, indicating enhanced Na+-Ca2+ exchange function (consistent with protein expression measurements). Enhanced diastolic SR Ca2+ leak (via sparks), reduced SR Ca2+-ATPase expression, and increased Na+-Ca2+ exchanger explain the reduced diastolic [Ca2+]i and SR Ca2+ content in TG. We conclude that CaMKIIC overexpression causes acute modulation of excitation-contraction coupling, which contributes to heart failure.
Key Words: calcium • Ca2+/calmodulin-dependent protein kinase II • sarcoplasmic reticulum • ryanodine receptor • heart
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