ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012
p38 MAPK activation promotes denervated Schwann cell phenotype and functions as a negative regulator of Schwann cell differentiation and myelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 81 papers, 1 of them a synthesis that pooled it.
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Who cites it
81 citing papers in PubMed, 1 synthesis or guideline pooled it, 137 citations in OpenAlex.
- Pooled it
- miRNome Expression Analysis Reveals New Players on Leprosy Immune Physiopathology.Frontiers in immunology · 2018Trial
- Molecular Mediators Associated With Myelination, Demyelination, and Remyelination in the Peripheral Nervous System.Journal of the peripheral nervous system : JPNS · 2026Review
- Source-Dependent Mitochondrial Transplantation Drives Schwann Cell Bioenergetic Reprogramming and Peripheral Nerve Regeneration.Advanced healthcare materials · 2026Article
- Review
- Influence of ApoE genotype on doxorubicin-induced cognitive impairment in juvenile rats.Scientific reports · 2025Article
- Pharmacologically targeting Schwann cells to improve regeneration following nerve damage.Frontiers in cell and developmental biology · 2025Review
- The Multi-targeted Effect of Fascaplysin on the Proliferation and Dedifferentiation of Schwann Cells Inhibits Peripheral Nerve Degeneration by Blocking CDK4/6 and Androgen Receptor.Experimental neurobiology · 2024Article
- Genes in Axonal Regeneration.Molecular neurobiology · 2024Review
- Targeting the Hippo pathway in Schwann cells ameliorates peripheral nerve degeneration via a polypharmacological mechanism.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 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
- Neurotrophin-3 promotes peripheral nerve regeneration by maintaining a repair state of Schwann cells after chronic denervation via the TrkC/ERK/c-Jun pathway.Journal of translational medicine · 2023Article
- The Effect of Distraction Osteogenesis on Peripheral Nerve Regeneration in Rats: A Preliminary StudyJournal of tissue engineering and regenerative medicine · 2023Article
- Traumatic and Diabetic Schwann Cell Demyelination Is Triggered by a Transient Mitochondrial Calcium Release through Voltage Dependent Anion Channel 1.Biomedicines · 2022Article
- Photodynamic Activity of Protoporphyrin IX-Immobilized Cellulose Monolith for Nerve Tissue Regeneration.International journal of molecular sciences · 2022Article
- Review: Myelin clearance is critical for regeneration after peripheral nerve injury.Frontiers in neurology · 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
- The Effects of Insulin on Immortalized Rat Schwann Cells, IFRS1.International journal of molecular sciences · 2021Article
- A glycolytic shift in Schwann cells supports injured axons.Nature neuroscience · 2020Article
- Article
21 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
11 authors at 6 institutions in 5 countries.
Funding
Abstract
Physical damage to the peripheral nerves triggers Schwann cell injury response in the distal nerves in an event termed Wallerian degeneration: the Schwann cells degrade their myelin sheaths and dedifferentiate, reverting to a phenotype that supports axon regeneration and nerve repair. The molecular mechanisms regulating Schwann cell plasticity in the PNS remain to be elucidated. Using both in vivo and in vitro models for peripheral nerve injury, here we show that inhibition of p38 mitogen-activated protein kinase (MAPK) activity in mice blocks Schwann cell demyelination and dedifferentiation following nerve injury, suggesting that the kinase mediates the injury signal that triggers distal Schwann cell injury response. In myelinating cocultures, p38 MAPK also mediates myelin breakdown induced by Schwann cell growth factors, such as neuregulin and FGF-2. Furthermore, ectopic activation of p38 MAPK is sufficient to induce myelin breakdown and drives differentiated Schwann cells to acquire phenotypic features of immature Schwann cells. We also show that p38 MAPK concomitantly functions as a negative regulator of Schwann cell differentiation: enforced p38 MAPK activation blocks cAMP-induced expression of Krox 20 and myelin proteins, but induces expression of c-Jun. As expected of its role as a negative signal for myelination, inhibition of p38 MAPK in cocultures promotes myelin formation by increasing the number as well as the length of individual myelin segments. Altogether, our data identify p38 MAPK as an important regulator of Schwann cell plasticity and differentiation.
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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.