Altered function in atrium of transgenic mice overexpressing triadin 1. Am J Physiol Heart Circ Physiol. 2002;283:H1334–H1343. doi: 10.1152/ajpheart.00937.2001

10.1152/ajpheart.00937.2001.—Triadin 1 is a protein in the cardiac junctional sarcoplasmic reticulum (SR) that interacts with the ryanodine receptor, junctin, and calsequestrin, pro-teins that are important for Ca2 release. To better under-stand 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 -myosin heavy chain (MHC) promoter. Three-week-old transgenic atria ex-hibited mild hypertrophy. Finally, atrial weight was in-creased 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 trans