ArticleThe Journal of biological chemistry2011
Mitochondrial calcium uptake regulates rapid calcium transients in skeletal muscle during excitation-contraction (E-C) coupling.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 59 papers.
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Who cites it
59 citing papers in PubMed, 84 citations in OpenAlex.
- MCU genetically altered mice suggest how mitochondrial CaTrends in endocrinology and metabolism: TEM · 2024Review
- Targeting mitochondrial CaThe Journal of physiology · 2024Review
- Reorganization of mitochondria-organelle interactions during postnatal development in skeletal muscle.The Journal of physiology · 2024Article
- Aberrant evoked calcium signaling and nAChR cluster morphology in aFrontiers in cell and developmental biology · 2024Article
- Isolation of Mitochondria from Murine Skeletal Muscle.Methods in molecular biology (Clifton, N.J.) · 2024Article
- Exercise metabolism and adaptation in skeletal muscle.Nature reviews. Molecular cell biology · 2023Review
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- Mitochondrial Dysfunction in Intensive Care Unit-Acquired Weakness and Critical Illness Myopathy: A Narrative Review.International journal of molecular sciences · 2023Review
- Potential Applications for Growth Hormone Secretagogues Treatment of Amyotrophic Lateral Sclerosis.Current neuropharmacology · 2023Article
- Review
- A controversial issue: Can mitochondria modulate cytosolic calcium and contraction of skeletal muscle fibers?The Journal of general physiology · 2022Review
- Butyrate Ameliorates Mitochondrial Respiratory Capacity of The Motor-Neuron-like Cell Line NSC34-G93A, a Cellular Model for ALS.Biomolecules · 2022Article
- Review
- Excitation-contraction coupling in mammalian skeletal muscle: Blending old and last-decade research.Frontiers in physiology · 2022Review
- Comprehensive Simulation of CaInternational journal of molecular sciences · 2021Article
- Ryanodine receptor leak triggers fiber CaScience advances · 2021Article
- MG53 Preserves Neuromuscular Junction Integrity and Alleviates ALS Disease Progression.Antioxidants (Basel, Switzerland) · 2021Article
- Old and new biomarkers for volumetric muscle loss.Current opinion in pharmacology · 2021Review
- Butyrate Feeding Reverses CypD-Related Mitoflash Phenotypes in Mouse Myofibers.International journal of molecular sciences · 2021Article
- CaNeuroscience letters · 2021Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Defective coupling between sarcoplasmic reticulum and mitochondria during control of intracellular Ca(2+) signaling has been implicated in the progression of neuromuscular diseases. Our previous study showed that skeletal muscles derived from an amyotrophic lateral sclerosis (ALS) mouse model displayed segmental loss of mitochondrial function that was coupled with elevated and uncontrolled sarcoplasmic reticulum Ca(2+) release activity. The localized mitochondrial defect in the ALS muscle allows for examination of the mitochondrial contribution to Ca(2+) removal during excitation-contraction coupling by comparing Ca(2+) transients in regions with normal and defective mitochondria in the same muscle fiber. Here we show that Ca(2+) transients elicited by membrane depolarization in fiber segments with defective mitochondria display an ~10% increased amplitude. These regional differences in Ca(2+) transients were abolished by the application of 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid, a fast Ca(2+) chelator that reduces mitochondrial Ca(2+) uptake. Using a mitochondria-targeted Ca(2+) biosensor (mt11-YC3.6) expressed in ALS muscle fibers, we monitored the dynamic change of mitochondrial Ca(2+) levels during voltage-induced Ca(2+) release and detected a reduced Ca(2+) uptake by mitochondria in the fiber segment with defective mitochondria, which mirrored the elevated Ca(2+) transients in the cytosol. Our study constitutes a direct demonstration of the importance of mitochondria in shaping the cytosolic Ca(2+) signaling in skeletal muscle during excitation-contraction coupling and establishes that malfunction of this mechanism may contribute to neuromuscular degeneration in ALS.
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