ArticleThe Journal of physiology2006
Functional role of store-operated and stretch-activated channels in murine adult skeletal muscle fibres.
Article in The Journal of physiology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 75 citations in OpenAlex.
- Piezo1 Regulates the Skeletal Muscle Length-Tension Relationship Through Channel-Independent Mechanotransduction.Biomolecules · 2026Article
- Reduced voltage-activated Ca2+ release flux in muscle fibers from a rat model of Duchenne dystrophy.The Journal of general physiology · 2025Article
- TRPCs: Influential Mediators in Skeletal Muscle.Cells · 2020Review
- The Emerging Roles of Nicotinamide Adenine Dinucleotide Phosphate Oxidase 2 in Skeletal Muscle Redox Signaling and Metabolism.Antioxidants & redox signaling · 2019Review
- Effects of adrenaline on contractility and endurance of isolated mammalian soleus with different calcium concentrations.Journal of muscle research and cell motility · 2019Article
- An Anabolic Signaling Response of Rat Soleus Muscle to Eccentric Contractions Following Hindlimb Unloading: A Potential Role of Stretch-Activated Ion Channels.International journal of molecular sciences · 2019Article
- GsMTx4-D provides protection to the D2.mdx mouse.Neuromuscular disorders : NMD · 2018Article
- The Complex Role of Store Operated Calcium Entry Pathways and Related Proteins in the Function of Cardiac, Skeletal and Vascular Smooth Muscle Cells.Frontiers in physiology · 2018Review
- 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
- Extracellular Ca2+-induced force restoration in K+-depressed skeletal muscle of the mouse involves an elevation of [K+]i: implications for fatigue.Journal of applied physiology (Bethesda, Md. : 1985) · 2015Article
- Protonation of the human PIEZO1 ion channel stabilizes inactivation.The Journal of biological chemistry · 2015Article
- Ca2+-dependent regulations and signaling in skeletal muscle: from electro-mechanical coupling to adaptation.International journal of molecular sciences · 2015Review
- Age-dependent changes in diastolic Ca(2+) and Na(+) concentrations in dystrophic cardiomyopathy: Role of Ca(2+) entry and IP3.Biochemical and biophysical research communications · 2014Article
- The excitation-contraction coupling mechanism in skeletal muscle.Biophysical reviews · 2014Review
- Article
- Quantifying SOCE fluorescence measurements in mammalian muscle fibres. The effects of ryanodine and osmotic shocks.Journal of muscle research and cell motility · 2013Article
- Skeletal muscle hypertrophy and regeneration: interplay between the myogenic regulatory factors (MRFs) and insulin-like growth factors (IGFs) pathways.Cellular and molecular life sciences : CMLS · 2013Review
- Gravitational force modulates G2/M phase exit in mechanically unloaded myoblasts.Cell cycle (Georgetown, Tex.) · 2013Article
- Inhibition of iPLA2 β and of stretch-activated channels by doxorubicin alters dystrophic muscle function.British journal of pharmacology · 2013Article
- Partial opening and subconductance gating of mechanosensitive ion channels in dystrophic skeletal muscle.The Journal of physiology · 2012Article
Corrections and comments
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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
In skeletal muscle, Ca(2+) is implicated in contraction, and in regulation of gene expression. An alteration of [Ca(2+)](i) homeostasis is responsible, at least partially, for the muscle degeneration that occurs after eccentric contractions in Duchenne muscular dystrophy, a disease characterized by the loss of the cytoskeletal protein dystrophin. Using patch clamp in the cell-attached configuration, we characterized the store-operated channels (SOCs) and the stretch-activated channels (SACs) present in isolated mouse skeletal muscle. SOCs were voltage independent, had a unitary conductance between 7 and 8 pS (110 mm Ca(2+) in the pipette), and their open probability increased when the sarcoplasmic reticulum was depleted by thapsigargin. These SOCs were identical to those previously described in the pathophysiology of Duchenne muscular dystrophy. Under the same experimental conditions, we detected a channel activity that was increased by applying a negative pressure to the patch electrode. The SACs responsible for this current had the same unitary conductance and current-voltage relationship as those observed for SOCs. SOCs and SACs had a similar sensitivity to pharmacological agents such as Gd(3+), SKF-96365, 2-aminoethoxydiphenyl borate and GsMTx4 toxin. Moreover, stimulation with IGF-1 increased the occurrence of the activity of both channel types. Together, these observations suggest that SOCs and SACs might belong to the same population or share common constituents. From a functional point of view, treatment of soleus muscle with SKF-96365 or GsMTx4 toxin increased its sensitivity to a fatigue protocol, suggesting that the influx of Ca(2+) that occurs through these channels during contraction is also involved in force maintaining during repeated stimulations.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.