Key result
New single myofibril force assay measures contractility and simulates cardiac cycles in cardiomyopathy tissue.
This novel instrumentation allows for detailed physiological measurement of single myofibril mechanics and simulation of cardiac cycles using frozen tissue samples.
Should not change cardiomyopathy management; extends single-myofibril assays for mutation studies in animal models.
Many causes of heart muscle diseases and skeletal muscle diseases are inherited and caused by mutations in genes of sarcomere proteins which play either a structural or contractile role in the muscle cell. Tissue samples from human hearts with mutations can be obtained but often samples are only a few milligrams and it is necessary to freeze them for storage and transportation. Myofibrils are the fundamental contractile components of the muscle cell and retain all structural elements and contractile proteins performing in contractile event; moreover viable myofibrils can be obtained from frozen tissue.•We are describing a versatile technique for measuring the contractility and its Ca(2+) regulation in single myofibrils. The control of myofibril length, incubation medium and data acquisition is carried out using a digital acquisition board via computer software. Using computer control it is possible not only to measure contractile and mechanical parameters but also simulate complex protocols such as a cardiac cycle to vary length and medium independently.•This single myofibril force assay is well suited for physiological measurements. The system can be adapted to measure tension amplitude, rates of contraction and relaxation, Ca(2+) dependence of these parameters in dose-response measurements, length-dependent activation, stretch response, myofibril elasticity and response to simulated cardiac cycle length changes. Our approach provides an all-round quantitative way to measure myofibrils performance and to observe the effect of mutations or posttranslational modifications. The technique has been demonstrated by the study of contraction in heart with hypertrophic or dilated cardiomyopathy mutations in sarcomere proteins.
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Vikhorev et al. (2016) studied Hypertrophic or dilated cardiomyopathy. Single myofibril force assay was evaluated on Contractile and mechanical parameters. A versatile single myofibril force assay was developed to measure contractility, Ca(2+) regulation, and simulate cardiac cycles in tissue samples with cardiomyopathy mutations.
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