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1 Institut für Pharmakologie und Toxikologie, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany
2 Physiologisches Institut, Justus-Liebig-Universität Gießen, Gießen, Germany
3 Institut für Pharmakologie und Toxikologie, Westfälische Wilhelms-Universität Münster, Münster, Germany
4 Dept. of Medicine and Biochemistry, Krannert Institute of Cardiology, Indianapolis, Indiana, United States
* To whom correspondence should be addressed. E-mail: ulrich.gergs{at}medizin.uni-halle.de.
Junctin is a transmembrane protein located at the cardiac junctional sarcoplasmic reticulum and forms a quaternary complex with the Ca2+ release channel, triadin and calsequestrin. Impaired protein interactions within this complex may alter the Ca2+ sensitivity of the Ca2+ release channel and may lead to cardiac dysfunction including hypertrophy, depressed contractility, and abnormal Ca2+ transients. To study the expression of junctin and for comparison triadin in heart failure, we measured the levels of these proteins in SR from normal and failing human hearts. Junctin was below our level of detection in SR membranes from failing human hearts, and triadin was downregulated by 22%. To better understand the role of junctin in the regulation of Ca2+ homeostasis and contraction of cardiac myocytes, we used an adenoviral approach to overexpress junctin in isolated rat cardiac myocytes. A recombinant adenovirus encoding the green fluorescent protein served as control. Infection of myocytes with the junctin-expressing virus resulted in an increased RNA and protein expression of junctin. Ca2+ transients showed a decreased maximum Ca2+ amplitude and contractility of myocytes was depressed. Our results demonstrate that an increased expression of junctin is associated with an impaired Ca2+ homeostasis. Downregulation of junctin in human heart failure may thus be a compensatory mechanism.
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