ArticleIn vitro cellular & developmental biology. Animal2021
RGMa can induce skeletal muscle cell hyperplasia via association with neogenin signalling pathway.
Article in In vitro cellular & developmental biology. Animal, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- Evaluation of a serum protein signature as monitoring biomarker for Duchenne muscular dystrophy in a long-term clinical trial with corticosteroids.Skeletal muscle · 2026Trial
- The uncoordinated-5 homologue A is a key receptor in netrin-ligand-mediated fast-twitch myotube formation in male mice.Physiological reports · 2026Article
- RGMa Nuclear Localization in Skeletal Muscle Cells Reveals a Novel Role in Cell Viability and Proliferation.Cells · 2026Article
- Evaluation of a serum protein signature as monitoring biomarker for Duchenne Muscular Dystrophy in a long-term clinical trial with corticosteroids.medRxiv : the preprint server for health sciences · 2026Article
- Large-scale serum protein biomarkers discovery associated with function and clinical milestones in Duchenne muscular dystrophy.Nature communications · 2025Observational
- Article
- Loss of Neogenin alters branchial arch development and leads to craniofacial skeletal defects.Frontiers in cell and developmental biology · 2024Article
- Transcriptomic characterization of the molecular mechanisms induced by RGMa during skeletal muscle nuclei accretion and hypertrophy.BMC genomics · 2022Article
- Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Although originally discovered inducing important biological functions in the nervous system, repulsive guidance molecule a (RGMa) has now been identified as a player in many other processes and diseases, including in myogenesis. RGMa is known to be expressed in skeletal muscle cells, from somites to the adult. Functional in vitro studies have revealed that RGMa overexpression could promote skeletal muscle cell hypertrophy and hyperplasia, as higher efficiency in cell fusion was observed. Here, we extend the potential role of RGMa during C2C12 cell differentiation in vitro. Our results showed that RGMa administrated as a recombinant protein during late stages of C2C12 myogenic differentiation could induce myoblast cell fusion and the downregulation of different myogenic markers, while its administration at early stages induced the expression of myogenic markers with no detectable morphological effects. We also found that RGMa effects on skeletal muscle hyperplasia are performed via neogenin receptor, possibly as part of a complex with other proteins. Additionally, we observed that RGMa-neogenin is not playing a role as an inhibitor of the BMP signalling in skeletal muscle cells. This work contributes to placing RGMa as a component of the mechanisms that determine skeletal cell fusion via neogenin receptor.
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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 Socratic graph.