ArticleJournal of muscle research and cell motility2014
Three calpain isoforms are autolyzed in rat fast-twitch muscle after eccentric contractions.
Article in Journal of muscle research and cell motility, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- Calpain-3 Is Not a Sodium Dependent Protease and Simply Requires Calcium for Activation.International journal of molecular sciences · 2023Article
- Mechanisms of eccentric contraction-induced muscle damage and nutritional supplementations for mitigating it.Journal of muscle research and cell motility · 2022Review
- Efficacy of leupeptin in treating ischemia in a rat hind limb model.Physiological reports · 2022Article
- Myofibrillar function differs markedly between denervated and dexamethasone-treated rat skeletal muscles: Role of mechanical load.PloS one · 2019Article
- Article
- Insertion sequence 1 from calpain-3 is functional in calpain-2 as an internal propeptide.The Journal of biological chemistry · 2018Article
- Preconditioning contractions prevent the delayed onset of myofibrillar dysfunction after damaging eccentric contractions.The Journal of physiology · 2018Article
- Past injurious exercise attenuates activation of primary calcium-dependent injury pathways in skeletal muscle during subsequent exercise.Physiological reports · 2018Article
- Electrical Stimulation Prevents Preferential Skeletal Muscle Myosin Loss in Steroid-Denervation Rats.Frontiers in physiology · 2018Article
- l-arginine ingestion inhibits eccentric contraction-induced proteolysis and force deficit via S-nitrosylation of calpain.Physiological reports · 2018Article
- Elucidating a molecular mechanism that the deterioration of porcine meat quality responds to increased cortisol based on transcriptome sequencing.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The present study investigated changes in autolysis of three calpain isoforms in skeletal muscles undergoing eccentric contractions (ECC), leading to prolonged force deficits. Rat extensor digitorum longus and tibialis anterior muscles were exposed to 200-repeated ECC in situ, excised immediately after or 3 or 6 days after cessation of ECC, and used for measures of force output and for biochemical analyses. Full restoration of tetanic force in ECC-treated muscles was not attained until 6 days of recovery. Maximal calpain activity determined by a fluorogenic substrate was unaltered immediately after ECC, but increased to 313 and 450 % after 3 and 6 days, respectively. Increases in the amount of autolyzed calpain-3 were apparent immediately and developed progressively with recovery time, whereas elevations of autolyzed μ- and m-calpain occurred after 3 and 6 days, respectively. The protein content was augmented only in m-calpain. It is suggested that the three calpain isoforms may be involved in the dismantling, repair, remodeling and/or regeneration processes in ECC-treated muscles.
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Registered trials
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.