ArticleMolecular neurobiology2014
Oncostatin M reduces lesion size and promotes functional recovery and neurite outgrowth after spinal cord injury.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- When Bone Forms Where It Shouldn't: Heterotopic Ossification in Muscle Injury and Disease.International journal of molecular sciences · 2025Review
- Traumatic brain injury and post-injury sleep fragmentation differentially alter the microglial transcriptome.Frontiers in immunology · 2025Article
- Oncostatin M enhances the lengthening of sensory nerves and skin hypersensitivity.Frontiers in immunology · 2025Article
- Diversity of Microglia-Derived Molecules with Neurotrophic Properties That Support Neurons in the Central Nervous System and Other Tissues.Molecules (Basel, Switzerland) · 2024Review
- Interleukins in Epilepsy: Friend or Foe.Neuroscience bulletin · 2024Review
- Elamipretide reduces pyroptosis and improves functional recovery after spinal cord injury.CNS neuroscience & therapeutics · 2023Article
- N6-methyladenosine RNA is modified in the rat hippocampus following traumatic brain injury with hypothermia treatment.Frontiers in neuroscience · 2023Article
- The clinical relevance of OSM in inflammatory diseases: a comprehensive review.Frontiers in immunology · 2023Review
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- Topotecan Reduces Neuron Death after Spinal Cord Injury by Suppressing Caspase-1-Dependent Pyroptosis.Molecular neurobiology · 2022Article
- Oncostatin M triggers brain inflammation by compromising blood-brain barrier integrity.Acta neuropathologica · 2022Article
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- Dermatologic comorbidities of the patients with severe COVID-19: A case-control study.Dermatologic therapy · 2021Article
- HDAC8 Inhibition Reduces Lesional Iba-1+ Cell Infiltration after Spinal Cord Injury without Effects on Functional Recovery.International journal of molecular sciences · 2020Article
- Oncostatin M-induced astrocytic tissue inhibitor of metalloproteinases-1 drives remyelination.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Oncostatin M, an Underestimated Player in the Central Nervous System.Frontiers in immunology · 2019Review
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- Macrophage-derived oncostatin M contributes to human and mouse neurogenic heterotopic ossifications.JCI insight · 2017Article
- Neuron and microglia/macrophage-derived FGF10 activate neuronal FGFR2/PI3K/Akt signaling and inhibit microglia/macrophages TLR4/NF-κB-dependent neuroinflammation to improve functional recovery after spinal cord injury.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The family of interleukin (IL)-6 like cytokines plays an important role in the neuroinflammatory response to injury by regulating both neural as well as immune responses. Here, we show that expression of the IL-6 family member oncostatin M (OSM) and its receptor is upregulated after spinal cord injury (SCI). To reveal the relevance of increased OSM signaling in the pathophysiology of SCI, OSM was applied locally after spinal cord hemisection in mice. OSM treatment significantly improved locomotor recovery after mild and severe SCI. Improved recovery in OSM-treated mice was associated with a reduced lesion size. OSM significantly diminished astrogliosis and immune cell infiltration. Thus, OSM limits secondary damage after CNS trauma. In vitro viability assays demonstrated that OSM protects primary neurons in culture from cell death, suggesting that the underlying mechanism involves direct neuroprotective effects of OSM. Furthermore, OSM dose-dependently promoted neurite outgrowth in cultured neurons, indicating that the cytokine plays an additional role in CNS repair. Indeed, our in vivo experiments demonstrate that OSM treatment increases plasticity of serotonergic fibers after SCI. Together, our data show that OSM is produced at the lesion site, where it protects the CNS from further damage and promotes recovery.
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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.