Key result
A 10% mechanical static strain applied to neonatal rat cardiomyocytes induced sarcomere remodeling throughout the cell length and enhancement at the intercalated discs over 4 hours.
In vitro mechanical strain induces cardiomyocyte remodeling via insertion of new sarcomeres throughout the cell and enhancement at intercalated discs.
May explain sarcomere addition in dilated cardiomyopathy; leaves open in vivo translation to adult human myocardium.
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.
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Yu et al. (2005) studied Dilated cardiomyopathy. Mechanical static strain vs. Control was evaluated on Morphology of the myofibrils and the ends of the myocytes. A 10% mechanical static strain applied to neonatal rat cardiomyocytes induced sarcomere remodeling throughout the cell length and enhancement at the intercalated discs over 4 hours.
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