ArticleMolecular biology of the cell1994
Myotubes from transgenic mdx mice expressing full-length dystrophin show normal calcium regulation.
Article in Molecular biology of the cell, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 27 citations in OpenAlex.
- Wasting mechanisms in muscular dystrophy.The international journal of biochemistry & cell biology · 2013Review
- New insights in the regulation of calcium transfers by muscle dystrophin-based cytoskeleton: implications in DMD.Journal of muscle research and cell motility · 2006Review
- Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice.The Journal of physiology · 2004Article
- Enhanced expression of the alpha 7 beta 1 integrin reduces muscular dystrophy and restores viability in dystrophic mice.The Journal of cell biology · 2001Article
- Mdx myotubes have normal excitability but show reduced contraction-relaxation dynamics.Journal of muscle research and cell motility · 2001Article
- Intracellular calcium signals measured with indo-1 in isolated skeletal muscle fibres from control and mdx mice.The Journal of physiology · 1999Article
- Understanding dystrophinopathies: an inventory of the structural and functional consequences of the absence of dystrophin in muscles of the mdx mouse.Journal of muscle research and cell motility · 1999Review
- Regulation of cytosolic calcium in skeletal muscle cells of the mdx mouse under conditions of stress.British journal of pharmacology · 1996Article
- The dystrophin superfamily: variability and complexity.Journal of muscle research and cell motility · 1994Review
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A lack of dystrophin results in muscle degeneration in Duchenne muscular dystrophy. Dystrophin-deficient human and mouse muscle cells have higher resting levels of intracellular free calcium ([Ca2+]i) and show a related increase in single-channel open probabilities of calcium leak channels. Elevated [Ca2+]i results in high levels of calcium-dependent proteolysis, which in turn increases calcium leak channel activity. This process could initiate muscle degeneration by further increasing [Ca2+]i and proteolysis in a positive feedback loop. Here, we tested the direct effect of restoration of dystrophin on [Ca2+]i and channel activity in primary myotubes from mdx mice made transgenic for full-length dystrophin. Transgenic mdx mice have been previously shown to have normal dystrophin localization and no muscle degeneration. Fura-2 calcium measurements and single-channel patch recordings showed that resting [Ca2+]i levels and open probabilities of calcium leak channels of transgenic mdx myotubes were similar to normal levels and significantly lower than mdx littermate controls (mdx) that lack dystrophin. Thus, restoration of normal calcium regulation in transgenic mdx mice may underlie the resulting absence of degeneration.
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