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Modulation of muscle contraction by a cell-permeable peptide.

ABSTRACT: In contrast to immortal cell lines, primary cells are hardly susceptible to intracellular delivery methods such as transfection. In this study, we evaluated the direct delivery of several cell-permeable peptides under noninvasive conditions into living primary adult rat cardiomyocytes. We specifically monitored the functional effects of a cell-permeable peptide containing the 15 amino acid N-terminal peptide from human ventricular light chain-1 (VLC-1) on contraction and intracellular Ca2+ signals after electrical stimulation in primary adult cardiomyocytes. The transducible VLC-1 variant was taken up by cardiomyocytes within 5 min with more than 95% efficiency and localized to sarcomeric structures. Analysis of the functional effects of the cell-permeable VLC-1 revealed an enhancement of the intrinsic contractility of cardiomyocytes without affecting the intracellular Ca2+. Therefore, peptide transduction mediated by cell-penetrating peptides represents not only a unique strategy to enhance heart muscle function with no secondary effect on intracellular Ca2+ but also an invaluable tool for the modulation and manipulation of protein interactions in general and in primary cells.

SUBMITTER: Tunnemann G

PROVIDER: S-EPMC2121654 | biostudies-other | 2007 Dec

REPOSITORIES: biostudies-other

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Project description:Manipulative actions involving unstable interactions with the environment require controlling mechanical impedance through muscle co-contraction. While much research has focused on how the central nervous system (CNS) selects the muscle patterns underlying a desired movement or end-point force, the coordination strategies used to achieve a desired end-point impedance have received considerably less attention. We recorded isometric forces at the hand and electromyographic (EMG) signals in subjects performing a reaching task with an external disturbance. In a virtual environment, subjects displaced a cursor by applying isometric forces and were instructed to reach targets in 20 spatial locations. The motion of the cursor was then perturbed by disturbances whose effects could be attenuated by increasing co-contraction. All subjects could voluntarily modulate co-contraction when disturbances of different magnitudes were applied. For most muscles, activation was modulated by target direction according to a cosine tuning function with an offset and an amplitude increasing with disturbance magnitude. Co-contraction was characterized by projecting the muscle activation vector onto the null space of the EMG-to-force mapping. Even in the baseline the magnitude of the null space projection was larger than the minimum magnitude required for non-negative muscle activations. Moreover, the increase in co-contraction was not obtained by scaling the baseline null space projection, scaling the difference between the null space projections in any block and the projection of the non-negative minimum-norm muscle vector, or scaling the difference between the null space projections in the perturbed blocks and the baseline null space projection. However, the null space projections in the perturbed blocks were obtained by linear combination of the baseline null space projection and the muscle activation used to increase co-contraction without generating any force. The failure of scaling rules in explaining voluntary modulation of arm co-contraction suggests that muscle pattern generation may be constrained by muscle synergies.

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Modulation of muscle contraction by a cell-permeable peptide.

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