ArticleThe Journal of physiology2008
Reactive oxygen species contribute to Ca2+ signals produced by osmotic stress in mouse skeletal muscle fibres.
Article in The Journal of physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 71 citations in OpenAlex.
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- Enzymatically dissociated muscle fibers display rapid dedifferentiation and impaired mitochondrial calcium control.iScience · 2022Article
- Exogenous Melatonin Ameliorates the Negative Effect of Osmotic Stress in Human and Bovine Ovarian Stromal Cells.Antioxidants (Basel, Switzerland) · 2022Article
- PTRH2: an adhesion regulated molecular switch at the nexus of life, death, and differentiation.Cell death discovery · 2020Review
- The roles of reactive oxygen species and antioxidants in cryopreservation.Bioscience reports · 2019Review
- Stretching magnitude-dependent inactivation of AKT by ROS led to enhanced p53 mitochondrial translocation and myoblast apoptosis.Molecular biology of the cell · 2019Article
- Calcium-induced release of calcium in muscle: 50 years of work and the emerging consensus.The Journal of general physiology · 2018Review
- Osmolality Selectively Offsets the Impact of Hyperthermia on Mouse Skeletal MuscleFrontiers in physiology · 2018Article
- Hyponatraemia-induced rhabdomyolysis complicated by anuric acute kidney injury: a renal replacement conundrum.BMJ case reports · 2016Article
- Regulation of NADPH oxidases in skeletal muscle.Free radical biology & medicine · 2016Review
- Proof of concept: hypovolemic hyponatremia may precede and augment creatine kinase elevations during an ultramarathon.European journal of applied physiology · 2016Article
- Absence of Dystrophin Disrupts Skeletal Muscle Signaling: Roles of Ca2+, Reactive Oxygen Species, and Nitric Oxide in the Development of Muscular Dystrophy.Physiological reviews · 2016Review
- Age-dependent uncoupling of mitochondria from Ca2⁺ release units in skeletal muscle.Oncotarget · 2015Article
- Osmosensation in TRPV2 dominant negative expressing skeletal muscle fibres.The Journal of physiology · 2015Article
- Effects of N-acetylcysteine on isolated mouse skeletal muscle: contractile properties, temperature dependence, and metabolism.Pflugers Archiv : European journal of physiology · 2014Article
- Assessment of calcium sparks in intact skeletal muscle fibers.Journal of visualized experiments : JoVE · 2014Article
- Mechanical stretch-induced activation of ROS/RNS signaling in striated muscle.Antioxidants & redox signaling · 2014Review
- Dysferlin stabilizes stress-induced Ca2+ signaling in the transverse tubule membrane.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca(2+) sparks, localized elevations in cytosolic [Ca(2+)], are rarely detected in intact adult mammalian skeletal muscle under physiological conditions. However, they have been observed in permeabilized cells and in intact fibres subjected to stresses, such as osmotic shock and strenuous exercise. Our previous studies indicated that an excess in cellular reactive oxygen species (ROS) generation over the ROS scavenging capabilities could be one of the up-stream causes of Ca(2+) spark appearance in permeabilized muscle fibres. Here we tested whether the cytosolic ROS balance is compromised in intact skeletal muscle fibres that underwent osmotic shock and whether this misbalance contributes to unmasking Ca(2+) sparks. Spontaneous Ca(2+) sparks and the rate of ROS generation were assessed with single photon confocal microscopy and fluorescent indicators fluo-4, CM-H(2)DCFDA and MitoSOX Red. Osmotic shock produced spontaneous Ca(2+) sparks and a concomitant significant increase in ROS production. Preincubation of muscle cells with ROS scavengers (e.g. MnTBAP, Mn-cpx 3, TIRON) nearly eliminated Ca(2+) sparks. In addition, inhibitors of NAD(P)H oxidase (DPI and apocynin) significantly reduced ROS production and suppressed the appearance of Ca(2+) sparks. Taken together, the data suggest that ROS contribute to the abnormal Ca(2+) spark activity in mammalian skeletal muscle subjected to osmotic stress and also indicate that NAD(P)H oxidase is a possible source of ROS. We propose that ROS-dependent Ca(2+) sparks are an important component of adaptive/maladaptive muscle responses under various pathological conditions such as eccentric stretch, osmotic changes during ischaemia and reperfusion, and some muscle diseases.
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