ArticleExperimental eye research2010
Superior calcium homeostasis of extraocular muscles.
Article in Experimental eye research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Cellular pathogenesis of Duchenne muscular dystrophy: progressive myofibre degeneration, chronic inflammation, reactive myofibrosis and satellite cell dysfunction.European journal of translational myology · 2023Article
- Complexity of skeletal muscle degeneration: multi-systems pathophysiology and organ crosstalk in dystrophinopathy.Pflugers Archiv : European journal of physiology · 2021Review
- Mass Spectrometric Profiling of Extraocular Muscle and Proteomic Adaptations in theLife (Basel, Switzerland) · 2021Article
- Article
- The panniculus carnosus muscle: A novel model of striated muscle regeneration that exhibits sex differences in the mdx mouse.Scientific reports · 2019Article
- Extraocular muscle function is impaired inThe Journal of general physiology · 2019Article
- Stimulation of TLR3 triggers release of lysosomal ATP in astrocytes and epithelial cells that requires TRPML1 channels.Scientific reports · 2018Article
- Robust lysosomal calcium signaling through channel TRPML1 is impaired by lysosomal lipid accumulation.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018Article
- Changes in calsequestrin, TNF-α, TGF-β and MyoD levels during the progression of skeletal muscle dystrophy in mdx mice: a comparative analysis of the quadriceps, diaphragm and intrinsic laryngeal muscles.International journal of experimental pathology · 2015Article
- Expression of calcium-buffering proteins in rat intrinsic laryngeal muscles.Physiological reports · 2015Article
- What has the mdx mouse model of Duchenne muscular dystrophy contributed to our understanding of this disease?Journal of muscle research and cell motility · 2015Review
- Extraocular muscle satellite cells are high performance myo-engines retaining efficient regenerative capacity in dystrophin deficiency.Developmental biology · 2015Article
- Comparative proteomic profiling of soleus, extensor digitorum longus, flexor digitorum brevis and interosseus muscles from the mdx mouse model of Duchenne muscular dystrophy.International journal of molecular medicine · 2013Article
- Analysis of spontaneous and nerve-evoked calcium transients in intact extraocular muscles in vitro.Experimental eye research · 2012Article
- How to make rapid eye movements "rapid": the role of growth factors for muscle contractile properties.Pflugers Archiv : European journal of physiology · 2011Article
- Genome-Wide Association Study and Rare Variant Association Studies of Strabismus in theOphthalmology scienceArticle
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Extraocular muscles (EOMs) are a unique group of skeletal muscles with unusual physiological properties such as being able to undergo rapid twitch contractions over extended periods and escape damage in the presence of excess intracellular calcium (Ca(2+)) in Duchenne's muscular dystrophy (DMD). Enhanced Ca(2+) buffering has been proposed as a contributory mechanism to explain these properties; however, the mechanisms are not well understood. We investigated mechanisms modulating Ca(2+) levels in EOM and tibialis anterior (TA) limb muscles. Using Fura-2 based ratiometric Ca(2+) imaging of primary myotubes we found that EOM myotubes reduced elevated Ca(2+) ˜2-fold faster than TA myotubes, demonstrating more efficient Ca(2+) buffering. Quantitative PCR (qPCR) and western blotting revealed higher expression of key components of the Ca(2+) regulation system in EOM, such as the cardiac/slow isoforms sarcoplasmic Ca(2+)-ATPase 2 (Serca2) and calsequestrin 2 (Casq2). Interestingly EOM expressed monomeric rather than multimeric forms of phospholamban (Pln), which was phosphorylated at threonine 17 (Thr17) but not at the serine 16 (Ser16) residue. EOM Pln remained monomeric and unphosphorylated at Ser16 despite protein kinase A (PKA) treatment, suggesting differential signalling and modulation cascades involving Pln-mediated Ca(2+) regulation in EOM. Increased expression of Ca(2+)/SR mRNA, proteins, differential post-translational modification of Pln and superior Ca(2+) buffering is consistent with the improved ability of EOM to handle elevated intracellular Ca(2+) levels. These characteristics provide mechanistic insight for the potential role of superior Ca(2+) buffering in the unusual physiology of EOM and their sparing in DMD.
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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.