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DOI: 10.1369/jhc.4A6608.2005
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Journal of Histochemistry and Cytochemistry
Volume 53 (7): 839-844, 2005
Copyright ©The Histochemical Society, Inc.

Cardiomyocyte Remodeling and Sarcomere Addition after Uniaxial Static Strain In Vitro

Ji-Guo Yu and Brenda Russell

Department of Physiology and Biophysics, University of Illinois at Chicago, Chicago, Illinois

Correspondence to: Brenda Russell, PhD, Department of Physiology and Biophysics (M/C 901), University of Illinois at Chicago, 835 S. Wolcott Avenue, Chicago, IL 60612-7342. E-mail: Russell{at}uic.edu

Individual cardiomyocytes are lengthened in dilated cardiomyopathy. However, it is not known how the new sarcomeres are added to preexisting myofibrils. Using a three-dimensional microtextured culturing system, a 10% mechanical static strain was applied to aligned, well-attached cardiomyocytes from neonatal rat. The morphology of the myofibrils and the ends of the myocytes were examined. Disruptions of the sarcomeric pattern for actin showed a progression from weak to intense staining over 4 hr. The lightly stained sarcomeres were common at 1 hr after being strained, peaked at 2 hr, and then subsided. In contrast, the numbers of intensely stained sarcomeres were initially low, peaked at 3 hr, and then began to decline when compared with control values. The myocyte ends showed elongations and convolutions after 3 hr and 4 hr of mechanical strain when observed with {alpha}-actinin and N-cadherin staining. We suggest that myocytes from neonatal rat hearts remodel by insertion of new sarcomeres throughout the cell length and also by enhancement at the intercalated discs. (J Histochem Cytochem 53:839–844, 2005)

Key Words: heart failure • cell shape regulation • length remodeling • muscle adaptation • eccentric hypertrophy • myofibrillogenesis


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