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Am J Physiol Cell Physiol 280: C1114-C1120, 2001;
0363-6143/01 $5.00
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Vol. 280, Issue 5, C1114-C1120, May 2001

Increased contractility and altered Ca2+ transients of mouse heart myocytes conditionally expressing PKCbeta

Lin Huang1, Beata M. Wolska1,2, David E. Montgomery1, Eileen M. Burkart1, Peter M. Buttrick2, and R. John Solaro1

1 Department of Physiology and Biophysics and 2 Section of Cardiology, Department of Medicine, Program in Cardiovascular Sciences, College of Medicine, University of Illinois at Chicago, Chicago, Illinois 60612

Activation of protein kinase C (PKC) in heart muscle signals hypertrophy and may also directly affect contractile function. We tested this idea using a transgenic (TG) mouse model in which conditionally expressed PKCbeta was turned on at 10 wk of age and remained on for either 6 or 10 mo. Compared with controls, TG cardiac myocytes demonstrated an increase in the peak amplitude of the Ca2+ transient, an increase in the extent and rate of shortening, and an increase in the rate of relengthening at both 6 and 10 mo of age. Phospholamban phosphorylation and Ca2+-uptake rates of sarcoplasmic reticulum vesicles were the same in TG and control heart preparations. At 10 mo, TG skinned fiber bundles demonstrated the same sensitivity to Ca2+ as controls, but maximum tension was depressed and there was increased myofilament protein phosphorylation. Our results differ from studies in which PKCbeta was constitutively overexpressed in the heart and in studies that reported a depression of myocyte contraction with no change in the Ca2+ transient.

hypertrophy; signal transduction; myofilaments; conditional transgenic; protein kinase C


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