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Am J Physiol Heart Circ Physiol 293: H728-H734, 2007. First published March 30, 2007; doi:10.1152/ajpheart.01187.2006
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On the role of junctin in cardiac Ca2+ handling, contractility, and heart failure

Ulrich Gergs,1 Tobias Berndt,3 Jan Buskase,2 Larry R. Jones,4 Uwe Kirchhefer,2 Frank U. Müller,2 Klaus-Dieter Schlüter,3 Wilhelm Schmitz,2 and Joachim Neumann1

1Institut für Pharmakologie und Toxikologie, Martin-Luther-Universität Halle-Wittenberg, Halle (Saale), Germany; 2Institut für Pharmakologie und Toxikologie, Westfälische Wilhelms-Universität, Münster, Germany; 3Physiologisches Institut, Justus-Liebig-Universität, Giebetaen, Germany; and 4Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana

Submitted 30 October 2006 ; accepted in final form 29 March 2007

Junctin is a transmembrane protein located at the cardiac junctional sarcoplasmic reticulum (SR) 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 a 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.

junctin; adenovirus; cardiac myocytes; calcium transient; sarcoplasmic reticulum


Address for reprint requests and other correspondence: U. Gergs, Institut für Pharmakologie und Toxikologie, Martin-Luther-Universität Halle-Wittenberg, Magdeburger Str. 4, 06112 Halle (Saale), Germany (e-mail: ulrich.gergs{at}medizin.uni-halle.de)




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