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Am J Physiol Heart Circ Physiol (June 27, 2002). doi:10.1152/ajpheart.00313.2002
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Articles in PresS, published online ahead of print June 27, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00313.2002
Submitted on April 8, 2002
Accepted on June 24, 2002

Defective intracellular Ca2+ signaling contributes to cardiomyopathy in type 1 diabetic rats

Kin M. Choi1, Yan Zhong1, Brian D. Hoit2, Ingrid L. Grupp1, Harvey Hahn1, Keith W. Dilly3, Silvia Guatimosim3, W. Jonathan Lederer3, and Mohammed A. Matlib1*

1 Pharmacology and Cell Biophysics, University of Cincinnati, Cincinnati, OH, USA
2 Medicine, Case Western Reserve Ubiversity, Cleveland, OH, USA
3 Physiology, University of Maryland, Baltimore, MD, USA

* To whom correspondence should be addressed. E-mail: matlibma{at}uc.edu.

The goal of the study is to determine whether defects in intracellular Ca2+ signaling contribute to cardiomyopathy in streptozotocin (STZ)-induced diabetic rats. Depression in cardiac systolic and diastolic function was traced from live diabetic rats to isolated individual myocytes. The depression in contraction and relaxation in myocytes was found in parallel with depression in the rise and decline of intracellular free Ca2+ concentration ([Ca2+]i). The sarcoplasmic reticulum (SR) Ca2+ store and rates of Ca2+ release and re-sequestration into SR were depressed in diabetic rat myocytes. The rate of Ca2+ efflux via sarcolemmal Na+ -Ca2+ exchanger (NCX) was also depressed. However, there was no change in the voltage-dependent L-type Ca2+ channel current (ICa) that triggers Ca2+ release from SR. The depression in SR function was associated with decreased SR Ca2+-ATPase (SERCA2) and ryanodine receptor (RyR) proteins and increased total and non-phosphorylated phospholamban (PLB) proteins. The depression of NCX activity was associated with a decrease in its protein level. Thus, it is concluded that defects in intracellular Ca2+ signaling caused by alteration of expression and function of the proteins that regulate [Ca2+]i contribute to cardiomyopathy in STZ-induced diabetic rats. The increase in PLB, decrease in NCX, and unchanged L-type [Ca2+]channel activity in this model of diabetic cardiomyopathy are distinct from other types of cardiomyopathy.




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