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Cardiovascular Research 2003 59(1):86-94; doi:10.1016/S0008-6363(03)00328-6
© 2003 by European Society of Cardiology
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Copyright © 2003, European Society of Cardiology

Titin isoform expression in normal and hypertensive myocardium

Chad M. Warrena, Maria C. Jordanb, Kenneth P. Roosb, Paul R. Krzesinskia and Marion L. Greasera,*

aMuscle Biology Laboratory, University of Wisconsin-Madison, 1805 Linden Dr. West, Madison, WI 53706, USA
bCardiovascular Research Laboratory and Department of Physiology, The David Geffen School of Medicine at UCLA, Los Angeles, CA, USA

mgreaser{at}facstaff.wisc.edu

* Corresponding author. Tel.: +1-608-262-1456; fax: +1-608-265-3110.

Objective: Titin isoform expression patterns were examined to explain previously observed genetic differences in rat cardiac passive tension. Methods: Rat ventricles from male spontaneously hypertensive (SHR) and Wistar–Kyoto (WKY) rats (normotensive) were used to analyze the titin isoform patterns. The hypertensive status was verified by blood pressure measurements and heart weight to body weight ratios. Gel electrophoresis and scanning densitometry were performed to determine ratios of myosin heavy chain and titin isoforms expressed. In situ hybridization using a cRNA probe specific for N2BA titin and a positive control in the N2B unique region was used to demonstrate tissue location of the titin message. Results: Regression analysis of titin isoform ratios, myosin heavy chain isoform ratios, and heart weight to body weight ratios all suggest a smaller proportion of N2BA titin (longer isoform) was expressed in rat left ventricles with increased hypertrophy. In situ hybridization showed that the N2BA and N2B isoforms were co-expressed within most of the cardiomyocytes. Agarose gel electrophoresis demonstrated two different N2BA titin isoforms in all rat ventricles. Conclusions: Expression of less N2BA and more N2B titin in response to pressure overload will result in higher passive tension upon stretch at a given sarcomere length and thus affect cardiac performance.

KEYWORDS Hypertrophy; Hypertension; Ventricular function; Remodeling; Myocytes


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