ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018
mTORC1 Is Transiently Reactivated in Injured Nerves to Promote c-Jun Elevation and Schwann Cell Dedifferentiation.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.
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49 citing papers in PubMed, 83 citations in OpenAlex.
- Myelination and Remyelination in Peripheral Nerve Injury: Mechanisms, Regulation, and Therapeutic Perspectives.MedComm · 2026Review
- Macrophage Dab1 Links Early Hypoxia to Adaptive Angiogenesis to Drive Peripheral Nerve Repair.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Genetically targeted mTORC1 inhibitor reveals transcriptional control by nuclear mTORC1.Nature chemical biology · 2026Article
- Sympathetic nerve-fibroblast crosstalk drives nerve injury, fibroblast activation, and matrix remodeling in pancreatic cancer.JCI insight · 2026Article
- Lactate: elucidating its indispensable role in human health.Molecular cancer · 2026Review
- Multi-omic identification of perineurial hyperplasia and lipid-associated nerve macrophages in human polyneuropathies.Nature communications · 2025Article
- Hypoxia-induced conversion of sensory Schwann cells into repair cells is regulated by HDAC8.Nature communications · 2025Article
- Schwann cells in the inner ear: development, disease, and regeneration.Frontiers in cellular neuroscience · 2025Review
- Pharmacologically targeting Schwann cells to improve regeneration following nerve damage.Frontiers in cell and developmental biology · 2025Review
- Unraveling the immune system's role in peripheral nerve regeneration: a pathway to enhanced healing.Frontiers in immunology · 2025Review
- Role of theBiomedicines · 2024Article
- TFEB/3 Govern Repair Schwann Cell Generation and Function Following Peripheral Nerve Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- OPALIN is an LGI1 receptor promoting oligodendrocyte differentiation.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- p53 modulates kinase inhibitor resistance and lineage plasticity in NF1-related MPNSTs.Oncogene · 2024Article
- Mechanisms driving fasting-induced protection from genotoxic injury in the small intestine.American journal of physiology. Gastrointestinal and liver physiology · 2024Article
- The role of TSC1 and TSC2 proteins in neuronal axons.Molecular psychiatry · 2024Review
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- Mechanosensitive channel of large conductance enhances the mechanical stretching-induced upregulation of glycolysis and oxidative metabolism in Schwann cells.Cell communication and signaling : CCS · 2024Article
- Sustainable Release Selenium Laden with SiOInternational journal of nanomedicine · 2024Article
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Corrections and comments
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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
Schwann cells (SCs) are endowed with a remarkable plasticity. When peripheral nerves are injured, SCs dedifferentiate and acquire new functions to coordinate nerve repair as so-called repair SCs. Subsequently, SCs redifferentiate to remyelinate regenerated axons. Given the similarities between SC dedifferentiation/redifferentiation in injured nerves and in demyelinating neuropathies, elucidating the signals involved in SC plasticity after nerve injury has potentially wider implications. c-Jun has emerged as a key transcription factor regulating SC dedifferentiation and the acquisition of repair SC features. However, the upstream pathways that control c-Jun activity after nerve injury are largely unknown. We report that the mTORC1 pathway is transiently but robustly reactivated in dedifferentiating SCs. By inducible genetic deletion of the functionally crucial mTORC1-subunit Raptor in mouse SCs (including male and female animals), we found that mTORC1 reactivation is necessary for proper myelin clearance, SC dedifferentiation, and consequently remyelination, without major alterations in the inflammatory response. In the absence of mTORC1 signaling, c-Jun failed to be upregulated correctly. Accordingly, a c-Jun binding motif was found to be enriched in promoters of genes with reduced expression in injured mutants. Furthermore, using cultured SCs, we found that mTORC1 is involved in c-Jun regulation by promoting its translation, possibly via the eIF4F-subunit eIF4A. These results provide evidence that proper c-Jun elevation after nerve injury involves also mTORC1-dependent post-transcriptional regulation to ensure timely dedifferentiation of SCs.
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