ArticleBioMed research international2014
Nerve injury-induced c-Jun activation in Schwann cells is JNK independent.
Article in BioMed research international, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 39 citations in OpenAlex.
- Myelination and Remyelination in Peripheral Nerve Injury: Mechanisms, Regulation, and Therapeutic Perspectives.MedComm · 2026Review
- Endogenous Network Modeling Reveals Mechanisms of Repair Schwann Cell Decline and Potential Recovery Targets.Biology · 2026Article
- New insights into the influence of temperature on axonal transport and function in myelinated regions of Schwann cells.iScience · 2025Review
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- Article
- Roles of ERK signaling pathway in regulating myelination of the peripheral nervous system.Frontiers in molecular neuroscience · 2025Review
- DA.Frontiers in cell and developmental biology · 2025Article
- Influencing factors and repair advancements in rodent models of peripheral nerve regeneration.Regenerative medicine · 2024Review
- 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 Dynamics of Nerve Degeneration and Regeneration in a Healthy Milieu and in Diabetes.International journal of molecular sciences · 2023Review
- Perioperative Suppression of Schwann Cell Dedifferentiation Reduces the Risk of Adenomyosis Resulting from Endometrial-Myometrial Interface Disruption in Mice.Biomedicines · 2022Article
- Melatonin signalling in Schwann cells during neuroregeneration.Frontiers in cell and developmental biology · 2022Review
- Injury-Induced HSP27 Expression in Peripheral Nervous Tissue Is Not Associated with Any Alteration in Axonal Outgrowth after Immediate or Delayed Nerve Repair.International journal of molecular sciences · 2021Article
- Cell Shape and Matrix Stiffness Impact Schwann Cell Plasticity via YAP/TAZ and Rho GTPases.International journal of molecular sciences · 2021Article
- Single-Cell Regulatory Network Inference and Clustering Identifies Cell-Type Specific Expression Pattern of Transcription Factors in Mouse Sciatic Nerve.Frontiers in cellular neuroscience · 2021Article
- Meta-Analysis Reveals Transcription Factor Upregulation in Cells of Injured Mouse Sciatic Nerve.Frontiers in cellular neuroscience · 2021Article
- Interaction between Schwann cells and other cells during repair of peripheral nerve injury.Neural regeneration research · 2021Article
- Satellite glial cells promote regenerative growth in sensory neurons.Nature communications · 2020Article
- Lipid metabolism adaptations are reduced in human compared to murine Schwann cells following injury.Nature communications · 2020Article
- Redefining the heterogeneity of peripheral nerve cells in health and autoimmunity.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We investigated (a) if activation of the mitogen activated protein kinase (MAPK) pathway was linked to the stress activated protein kinase (SAPK) pathway and (b) if JNK was required for activation of c-Jun in Schwann cells of rat sciatic nerve following injury. To this aim, ERK1/2 and the transcription factors c-Jun and ATF-3 were studied by immunohistochemistry in segments of transected nerves. We utilized pharmacological inhibitors of both signal transduction pathways in vitro to determine the effects on downstream signalling events, such as c-Jun activation, and on Schwann cell survival and proliferation. A transection induces c-Jun and ATF-3 transcription in Schwann cells. These events are followed by Schwann cell activation of c-Jun in the injured nerve. The MAPK inhibitor U0126 blocked ERK1/2 activation and reduced Schwann cell proliferation as well as induction of c-Jun transcription. The JNK inhibitor SP600125 reduced Schwann cell proliferation, but did not affect the expression of ERK1/2 or injury-induced increases in c-Jun or ATF-3 levels. Importantly, nerve injury induces Schwann cell activation of c-Jun by phosphorylation, which, in contrast to in sensory neurons, is JNK independent. MAP kinases, other than JNK, can potentially activate c-Jun in Schwann cells following injury; information that is crucial to create new nerve reconstruction strategies.
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Registered trials
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