ArticlePloS one2012
Fatigue and muscle atrophy in a mouse model of myasthenia gravis is paralleled by loss of sarcolemmal nNOS.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 33 citations in OpenAlex.
- Relationship between fatigue and quantitative electromyography findings in patients with myasthenia gravis.Heliyon · 2024Article
- Blocking interleukin-23 ameliorates neuromuscular and thymic defects in myasthenia gravis.Journal of neuroinflammation · 2023Article
- Sympathetic neuropathology is revealed in muscles affected by amyotrophic lateral sclerosis.Frontiers in physiology · 2023Article
- Alteration of the Neuromuscular Junction and Modifications of Muscle Metabolism in Response to Neuron-Restricted Expression of the CHMP2BBiomolecules · 2022Article
- Assessment of Sarcopenia and Obesity in Patients with Myasthenia Gravis Using Dual-Energy X-ray Absorptiometry: A Cross-Sectional Study.Journal of personalized medicine · 2021Article
- Over-Dose Lithium Toxicity as an Occlusive-like Syndrome in Rats and Gastric Pentadecapeptide BPC 157.Biomedicines · 2021Article
- Aberrant NLRP3 Inflammasome Activation Ignites the Fire of Inflammation in Neuromuscular Diseases.International journal of molecular sciences · 2021Review
- Dystrophin R16/17 protein therapy restores sarcolemmal nNOS in trans and improves muscle perfusion and function.Molecular medicine (Cambridge, Mass.) · 2019Article
- Dystrophin R16/17-syntrophin PDZ fusion protein restores sarcolemmal nNOSμ.Skeletal muscle · 2018Article
- Hypermagnesemia disturbances in rats, NO-related: pentadecapeptide BPC 157 abrogates, L-NAME and L-arginine worsen.Inflammopharmacology · 2017Article
- Amyotrophic Lateral Sclerosis and Myasthenia Gravis Overlap Syndrome: A Review of Two Cases and the Associated Literature.Frontiers in neurology · 2017Article
- Response: "Commentary: A Hypothesis for Examining Skeletal Muscle Biopsy-Derived Sarcolemmal nNOSµ as Surrogate for Enteric nNOSα Function". nNOS(skeletal muscle) may be Evidentiary for Enteric NO-Transmission Despite nNOSµ/α Differences.Frontiers in medicine · 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
- Sarcolemmal targeting of nNOSμ improves contractile function of mdx muscle.Human molecular genetics · 2016Article
- Nonmechanical Roles of Dystrophin and Associated Proteins in Exercise, Neuromuscular Junctions, and Brains.Brain sciences · 2015Article
- A Hypothesis for Examining Skeletal Muscle Biopsy-Derived Sarcolemmal nNOSμ as Surrogate for Enteric nNOSα Function.Frontiers in medicine · 2015Article
- Nuclear recruitment of neuronal nitric-oxide synthase by α-syntrophin is crucial for the induction of mitochondrial biogenesis.The Journal of biological chemistry · 2014Article
- Molecular handoffs in nitrergic neurotransmission.Frontiers in medicine · 2014Review
- Skeletal muscle function during exercise-fine-tuning of diverse subsystems by nitric oxide.International journal of molecular sciences · 2013Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myasthenia Gravis (MG) patients suffer from chronic fatigue of skeletal muscles, even after initiation of proper immunosuppressive medication. Since the localization of neuronal nitric oxide synthase (nNOS) at the muscle membrane is important for sustained muscle contraction, we here study the localization of nNOS in muscles from mice with acetylcholine receptor antibody seropositive (AChR+) experimental autoimmune MG (EAMG). EAMG was induced in 8 week-old male mice by immunization with AChRs purified from torpedo californica. Sham-injected wild type mice and mdx mice, a model for Duchenne muscular dystrophy, were used for comparison. At EAMG disease grade 3 (severe myasthenic weakness), the triceps, sternomastoid and masseter muscles were collected for analysis. Unlike in mdx muscles, total nNOS expression as well as the presence of its binding partner syntrophin α-1, were not altered in EAMG. Immunohistological and biochemical analysis showed that nNOS was lost from the muscle membrane and accumulated in the cytosol, which is likely the consequence of blocked neuromuscular transmission. Atrophy of all examined EAMG muscles were supported by up-regulated transcript levels of the atrogenes atrogin-1 and MuRF1, as well as MuRF1 protein, in combination with reduced muscle fiber diameters. We propose that loss of sarcolemmal nNOS provides an additional mechanism for the chronic muscle fatigue and secondary muscle atrophy in EAMG and MG.
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