ArticleJournal of the neurological sciences2011
Reduced resting potentials in dystrophic (mdx) muscle fibers are secondary to NF-κB-dependent negative modulation of ouabain sensitive Na+-K+ pump activity.
Article in Journal of the neurological sciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- The effect of muscle oxygenation on neuromuscular efficiency and force complexity.European journal of applied physiology · 2026Article
- Longitudinal Follow-Up of Patients With Duchenne Muscular Dystrophy Using QuantitativeJournal of cachexia, sarcopenia and muscle · 2025Article
- Longitudinal assessment of skeletal muscle functional mechanics in the DE50-MD dog model of Duchenne muscular dystrophy.Disease models & mechanisms · 2023Article
- Short-Term Mild Hypoxia Modulates Na,K-ATPase to Maintain Membrane Electrogenesis in Rat Skeletal Muscle.International journal of molecular sciences · 2022Article
- The Donnan-dominated resting state of skeletal muscle fibers contributes to resilience and longevity in dystrophic fibers.The Journal of general physiology · 2022Article
- Chronic Ouabain Prevents Na,K-ATPase Dysfunction and Targets AMPK and IL-6 in Disused Rat Soleus Muscle.International journal of molecular sciences · 2021Article
- Skeletal Muscle Na,K-ATPase as a Target for Circulating Ouabain.International journal of molecular sciences · 2020Article
- Cholesterol and the Safety Factor for Neuromuscular Transmission.International journal of molecular sciences · 2019Review
- Cardiac glycoside bufalin blocks cancer cell growth by inhibition of Aurora A and Aurora B activation via PI3K-Akt pathway.Oncotarget · 2018Article
- Specialized Functional Diversity and Interactions of the Na,K-ATPase.Frontiers in physiology · 2016Review
- Dystrophin restoration therapy improves both the reduced excitability and the force drop induced by lengthening contractions in dystrophic mdx skeletal muscle.Skeletal muscle · 2016Article
- Genetic evidence in the mouse solidifies the calcium hypothesis of myofiber death in muscular dystrophy.Cell death and differentiation · 2015Review
- The effect of specific IKKβ inhibitors on the cytosolic expression of IκB-α and the nuclear expression of p65 in dystrophic (MDX) muscle.American journal of translational research · 2015Article
- Na+ dysregulation coupled with Ca2+ entry through NCX1 promotes muscular dystrophy in mice.Molecular and cellular biology · 2014Article
- Dual effects of ouabain on the regulation of proliferation and apoptosis in human umbilical vein endothelial cells: involvement of Na(+)-K(+)-ATPase α-subunits and NF-κB.International journal of clinical and experimental medicine · 2014Article
- Acute failure of action potential conduction in mdx muscle reveals new mechanism of contraction-induced force loss.The Journal of physiology · 2013Article
- Increased resting intracellular calcium modulates NF-κB-dependent inducible nitric-oxide synthase gene expression in dystrophic mdx skeletal myotubes.The Journal of biological chemistry · 2012Article
- Recovery of electrogenesis in skeletal muscles after cell therapy of myodystrophy in MDX mice.Doklady biological sciences : proceedings of the Academy of Sciences of the USSR, Biological sciences sectionsArticle
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5 authors at 1 institution in 1 country.
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Abstract
To examine potential mechanisms for the reduced resting membrane potentials (RPs) of mature dystrophic (mdx) muscle fibers, the Na(+)-K(+) pump inhibitor ouabain was added to freshly isolated nondystrophic and mdx fibers. Ouabain produced a 71% smaller depolarization in mdx fibers than in nondystrophic fibers, increased the [Na(+)](i) in nondystrophic fibers by 40%, but had no significant effect on the [Na(+)](i) of mdx fibers, which was approximately double that observed in untreated nondystrophic fibers. Western blots indicated no difference in total and phosphorylated Na(+)-K(+) ATPase catalytic α1 subunit between nondystrophic and mdx muscle. Examination of the effects of the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) indicated that direct application of the drug slowly hyperpolarized mdx fibers (7 mV in 90 min) but had no effect on nondystrophic fibers. Pretreatment with ouabain abolished this hyperpolarization, and pretreatment with PDTC restored ouabain-induced depolarization and reduced [Na(+)](i). Administration of an NF-κB inhibitor that utilizes a different mechanism for reducing nuclear NF-κB activation, ursodeoxycholic acid (UDCA), also hyperpolarized mdx fibers. These results suggest that in situ Na(+)-K(+) pump activity is depressed in mature dystrophic fibers by NF-κB dependent modulators, and that this reduced pump activity contributes to the weakness characteristic of dystrophic muscle.
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