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Am J Physiol Heart Circ Physiol 283: H1334-H1343, 2002. First published May 30, 2002; doi:10.1152/ajpheart.00937.2001
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Vol. 283, Issue 4, H1334-H1343, October 2002

Altered function in atrium of transgenic mice overexpressing triadin 1

Uwe Kirchhefer1, Hideo A. Baba2, Yvonne M. Kobayashi3, Larry R. Jones3, Wilhelm Schmitz1, and Joachim Neumann1

1 Institut für Pharmakologie und Toxikologie, Westfälische Wilhelms-Universität, 48149 Münster; 2 Institut für Pathologie, Universität Essen, 45147 Essen, Germany; and 3 Krannert Institute of Cardiology, Department of Medicine, Indiana University School of Medicine, Indianapolis, Indiana 46202

Triadin 1 is a protein in the cardiac junctional sarcoplasmic reticulum (SR) that interacts with the ryanodine receptor, junctin, and calsequestrin, proteins that are important for Ca2+ release. To better understand the role of triadin 1 in SR-Ca2+ release, we studied the time-dependent expression of SR proteins and contractility in atria of 3-, 6-, and 18-wk-old transgenic mice overexpressing canine cardiac triadin 1 under control of the alpha -myosin heavy chain (MHC) promoter. Three-week-old transgenic atria exhibited mild hypertrophy. Finally, atrial weight was increased by 110% in 18-wk-old transgenic mice. Triadin 1 overexpression was accompanied by time-dependent changes in the protein expression of the ryanodine receptor, junctin, and cardiac/slow-twitch muscle SR Ca2+-ATPase isoform. Force of contraction was already decreased in 3-wk-old transgenic atria. The application of caffeine led to a positive inotropic effect in transgenic atria of 3-wk-old mice. Rest pauses resulted in an increased potentiation of force of contraction after restimulation in 3- and 6-wk-old mice and a reduced potentiation of force of contraction in 18-wk-old transgenic mice. Hence, triadin 1 overexpression triggered time-dependent alterations in SR protein expression, Ca2+ homeostasis, and contractility, indicating for the first time an inhibitory function of triadin 1 on SR-Ca2+ release in vivo.

protein expression; force of contraction; sarcoplasmic reticulum-calcium release


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