ArticleGlia2020
Gpr126/Adgrg6 contributes to the terminal Schwann cell response at the neuromuscular junction following peripheral nerve injury.
Article in Glia, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 39 citations in OpenAlex.
- Adhesion G-Protein Coupled Receptors in Neurological and Psychiatric Disorders.Journal of psychiatry and brain science · 2025Article
- Macrophage induces angiogenesis via HIF signaling in denervated muscle following nerve injury.Scientific reports · 2025Article
- Basic Pathological Mechanisms in Peripheral Nerve Diseases.International journal of molecular sciences · 2025Review
- FK506 Enhancement of Neuromuscular Junction Recovery After Nerve Injury Is Macrophage-Dependent.Muscle & nerve · 2025Article
- RUNX1 promotes denervation-induced muscle atrophy by activating the JUNB/NF-κB pathway and driving M1 macrophage polarization.Open life sciences · 2025Article
- Absence of T-box transcription factor 21 limits neuromuscular junction recovery after nerve injury inFrontiers in cell and developmental biology · 2025Article
- Schwann Cells as Orchestrators of Nerve Repair: Implications for Tissue Regeneration and Pathologies.Cold Spring Harbor perspectives in biology · 2024Review
- Origin, identity, and function of terminal Schwann cells.Trends in neurosciences · 2024Review
- Heterologous fibrin biopolymer as an emerging approach to peripheral nerve repair: a scoping review.The journal of venomous animals and toxins including tropical diseases · 2024Article
- Structure, ligands, and roles of GPR126/ADGRG6 in the development and diseases.Genes & diseases · 2024Review
- A screen of pharmacologically active compounds to identify modulators of the Adgrg6/Gpr126 signalling pathway in zebrafish embryos.Basic & clinical pharmacology & toxicology · 2023Article
- Models and methods to study Schwann cells.Journal of anatomy · 2022Review
- Adhesion G protein-coupled receptors: structure, signaling, physiology, and pathophysiology.Physiological reviews · 2022Review
- Progress in perisynaptic Schwann cell and neuromuscular junction research.Neural regeneration research · 2022Article
- Neuroimmune interactions and immunoengineering strategies in peripheral nerve repair.Progress in neurobiology · 2022Review
- Lessons from Injury: How Nerve Injury Studies Reveal Basic Biological Mechanisms and Therapeutic Opportunities for Peripheral Nerve Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- T-box transcription factor 21 is expressed in terminal Schwann cells at the neuromuscular junction.Muscle & nerve · 2021Article
- Terminal Schwann Cell Aging: Implications for Age-Associated Neuromuscular Dysfunction.Aging and disease · 2021Review
- The adhesion GPCR Adgrg6 (Gpr126): Insights from the zebrafish model.Genesis (New York, N.Y. : 2000) · 2021Review
- Macrophage roles in peripheral nervous system injury and pathology: Allies in neuromuscular junction recovery.Molecular and cellular neurosciences · 2021Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Gpr126/Adgrg6 is an adhesion G protein-coupled receptor essential for Schwann cell (SC) myelination with important contributions to repair after nerve crush injury. Despite critical functions in myelinating SCs, the role of Gpr126 within nonmyelinating terminal Schwann cells (tSCs) at the neuromuscular junction (NMJ), is not known. tSCs have important functions in synaptic maintenance and reinnervation, and after injury tSCs extend cytoplasmic processes to guide regenerating axons to the denervated NMJ. In this study, we show that Gpr126 is expressed in tSCs, and that absence of Gpr126 in SCs (SC-specific Gpr126 knockout, cGpr126) results in a NMJ maintenance defect in the hindlimbs of aged mice, but not in young adult mice. After nerve transection and repair, cGpr126 mice display delayed NMJ reinnervation, altered tSC morphology with decreased S100β expression, and reduced tSC cytoplasmic process extensions. The immune response promoting reinnervation at the NMJ following nerve injury is also altered with decreased macrophage infiltration, Tnfα, and anomalous cytokine expression compared to NMJs of control mice. In addition, Vegfa expression is decreased in muscle, suggesting that cGpr126 non-cell autonomously modulates angiogenesis after nerve injury. In sum, cGpr126 mice demonstrated delayed NMJ reinnervation and decreased muscle mass following nerve transection and repair compared to control littermates. The integral function of Gpr126 in tSCs at the NMJ provides the framework for new therapeutic targets for neuromuscular disease.
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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.