Spatiotemporal magnetic fields enhance cytosolic Ca2+ levels and induce actin polymerization via activation of voltage-gated sodium channels in skeletal muscle cells
Language English Country Netherlands Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
29471128
DOI
10.1016/j.biomaterials.2018.02.031
PII: S0142-9612(18)30117-0
Knihovny.cz E-resources
- Keywords
- Alternating magnetic field, Cytosolic calcium, Eddy current, Modeling, Skeletal muscle, Voltage-gated sodium channels,
- MeSH
- Actins metabolism MeSH
- Models, Biological MeSH
- Cell Membrane physiology MeSH
- Cell Line MeSH
- Ion Channel Gating MeSH
- Muscle Fibers, Skeletal metabolism MeSH
- Magnetic Fields MeSH
- Membrane Potentials MeSH
- Myoblasts cytology MeSH
- Mice MeSH
- Polymerization MeSH
- Voltage-Gated Sodium Channels physiology MeSH
- Calcium metabolism MeSH
- Calcium Signaling MeSH
- Cell Survival MeSH
- Animals MeSH
- Check Tag
- Mice MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Actins MeSH
- Voltage-Gated Sodium Channels MeSH
- Calcium MeSH
Cellular function is modulated by the electric membrane potential controlling intracellular physiology and signal propagation from a motor neuron to a muscle fiber resulting in muscle contraction. Unlike electric fields, magnetic fields are not attenuated by biological materials and penetrate deep into the tissue. We used complex spatiotemporal magnetic fields (17-70 mT) to control intracellular signaling in skeletal muscle cells. By changing different parameters of the alternating magnetic field (amplitude, inversion time, rotation frequency), we induced transient depolarization of cellular membranes leading to i) Na+ influx through voltage-gated sodium channels (VGSC), ii) cytosolic calcium increase, and iii) VGSC- and ryanodine receptor-dependent increase of actin polymerization. The ion fluxes occurred only, when the field was applied and returned to baseline after the field was turned off. The 30-s-activation-cycle could be repeated without any loss of signal intensity. By contrast, static magnetic fields of the same strength exhibited no effect on myotube Ca2+ levels. Mathematical modeling suggested a role for the alternating magnetic field-induced eddy current, which mediates a local change in the membrane potential triggering the activation of VGSC. These findings might pave the way for the use of complex magnetic fields to improve function of skeletal muscles in myopathies.
References provided by Crossref.org
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