ArticlePloS one2014
The role of muscle microRNAs in repairing the neuromuscular junction.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 64 citations in OpenAlex.
- Cerebellar microRNA-206 tunes Purkinje neuron firing dynamics to control sensorimotor gating.bioRxiv : the preprint server for biology · 2026Article
- Novel Translational Concept: Axon-to-Muscle Exosomal Signaling as an Emerging Therapeutic Target in Spinal Muscular Atrophy.Biomedicines · 2025Review
- Hochuekkito accelerates recovery from cisplatin induced-muscle atrophy accompanied by slow-twitch fiber-specific microRNA upregulation in mice.Frontiers in pharmacology · 2025Article
- Regulation of miR-206 in denervated and dystrophic muscles, and its effect on acetylcholine receptor clustering.Journal of cell science · 2024Article
- AAV1.tMCK.NT-3 gene therapy improves phenotype inBrain communications · 2024Article
- The roles of miRNAs in adult skeletal muscle satellite cells.Free radical biology & medicine · 2023Review
- Article
- The Cellular and Molecular Signature of ALS in Muscle.Journal of personalized medicine · 2022Review
- Postnatal Protein Intake as a Determinant of Skeletal Muscle Structure and Function in Mice-A Pilot Study.International journal of molecular sciences · 2022Article
- Response of plasma microRNAs to nusinersen treatment in patients with SMA.Annals of clinical and translational neurology · 2022Article
- Argonaute 2 is lost from neuromuscular junctions affected with amyotrophic lateral sclerosis in SOD1Scientific reports · 2022Article
- Neuromuscular Junction Dysfunction in Amyotrophic Lateral Sclerosis.Molecular neurobiology · 2022Review
- An Emerging Role for Epigenetics in Cerebral Palsy.Journal of personalized medicine · 2021Review
- RNA Deregulation in Amyotrophic Lateral Sclerosis: The Noncoding Perspective.International journal of molecular sciences · 2021Review
- Age-Related Alterations at Neuromuscular Junction: Role of Oxidative Stress and Epigenetic Modifications.Cells · 2021Review
- The microRNA miR-133b functions to slow Duchenne muscular dystrophy pathogenesis.The Journal of physiology · 2021Article
- AAV1.NT-3 gene therapy in a CMT2D model: phenotypic improvements inBrain communications · 2021Article
- Article
- Study on variation trend of repetitive nerve stimulation waveform in amyotrophic lateral sclerosis.Chinese medical journal · 2019Article
- Conditional Overexpression of rtn4al in Muscle of Adult Zebrafish Displays Defects Similar to Human Amyotrophic Lateral Sclerosis.Marine biotechnology (New York, N.Y.) · 2019Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
microRNAs have been implicated in mediating key aspects of skeletal muscle development and responses to diseases and injury. Recently, we demonstrated that a synaptically enriched microRNA, miR-206, functions to promote maintenance and repair of the neuromuscular junction (NMJ); in mutant mice lacking miR-206, reinnervation is impaired following nerve injury and loss of NMJs is accelerated in a mouse model of amyotrophic lateral sclerosis (ALS). Here, we asked whether other microRNAs play similar roles. One attractive candidate is miR-133b because it is in the same transcript that encodes miR-206. Like miR-206, miR-133b is concentrated near NMJs and induced after denervation. In miR-133b null mice, however, NMJ development is unaltered, reinnervation proceeds normally following nerve injury, and disease progression is unaffected in the SOD1(G93A) mouse model of ALS. To determine if miR-206 compensates for the loss of miR-133b, we generated mice lacking both microRNAs. The phenotype of these double mutants resembled that of miR-206 single mutants. Finally, we used conditional mutants of Dicer, an enzyme required for the maturation of most microRNAs, to generate mice in which microRNAs were depleted from skeletal muscle fibers postnatally, thus circumventing a requirement for microRNAs in embryonic muscle development. Reinnervation of muscle fibers following injury was impaired in these mice, but the defect was similar in magnitude to that observed in miR-206 mutants. Together, these results suggest that miR-206 is the major microRNA that regulates repair of the NMJ following nerve injury.
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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.