ArticleMolecular and cellular biochemistry2013
Signaling pathways regulating dose-dependent dual effects of TNF-α on primary cultured Schwann cells.
Article in Molecular and cellular biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 28 citations in OpenAlex.
- Cross-species TNF-α signaling in mosquitoes promotes malaria transmission.EMBO reports · 2026Article
- Development ofBeilstein journal of nanotechnology · 2026Article
- Muscle-derived TRAIL negatively regulates myogenic differentiation.Experimental cell research · 2020Article
- Effects of NP-1 on proliferation, migration, and apoptosis of Schwann cell line RSC96 through the NF-κB signaling pathway.American journal of translational research · 2020Article
- Nuclear Factor-κB Dysregulation and α-Synuclein Pathology: Critical Interplay in the Pathogenesis of Parkinson's Disease.Frontiers in aging neuroscience · 2020Review
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- Valproate reduces neuroinflammation and neuronal death in a rat chronic constriction injury model.Scientific reports · 2018Article
- Comparative transcriptomic profiling of peripheral efferent and afferent nerve fibres at different developmental stages in mice.Scientific reports · 2018Article
- Chronic TNFα Exposure Induces Robust Proliferation of Olfactory Ensheathing Cells, but not Schwann Cells.Neurochemical research · 2017Article
- IL-22 Impedes the Proliferation of Schwann cells: Transcriptome Sequencing and Bioinformatics Analysis.Molecular neurobiology · 2017Article
- Article
- SCY1-Like 1-Binding Protein 1 (SCYL1BP1) Suppressed Sciatic Nerve Regeneration by Enhancing the RhoA Pathway.Molecular neurobiology · 2016Article
- Hypoxia-Induced Upregulation of miR-132 Promotes Schwann Cell Migration After Sciatic Nerve Injury by Targeting PRKAG3.Molecular neurobiology · 2016Article
- Spatiotemporal Expression of Poly(rC)-Binding Protein PCBP2 Modulates Schwann Cell Proliferation After Sciatic Nerve Injury.Cellular and molecular neurobiology · 2016Article
- Effects of tumor necrosis factor alpha blocker adalimumab in experimental spinal cord injury.Journal of Korean Neurosurgical Society · 2015Article
- Dysregulated expression of death, stress and mitochondrion related genes in the sciatic nerve of presymptomatic SOD1(G93A) mouse model of Amyotrophic Lateral Sclerosis.Frontiers in cellular neuroscience · 2015Article
- Up-regulation of HDAC4 is associated with Schwann cell proliferation after sciatic nerve crush.Neurochemical research · 2014Article
- Differential gene expression in proximal and distal nerve segments of rats with sciatic nerve injury during Wallerian degeneration.Neural regeneration research · 2014Article
- Article
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
After peripheral nerve injury, Schwann cells are rapidly activated to participate in the regenerative process and modulate local immune reactions. Tumor necrosis factor-α (TNF-α), one of the major initiators of the inflammatory cascade, has been known to exert pleiotropic functions during peripheral nerve injury and regeneration. In this study, we aimed to investigate the in vitro effects of TNF-α on peripheral neural cells. First, gene-microarray analysis was applied to the RNA samples extracted from injured peripheral nerves, providing the information of gene interactions post nerve injury. Then, after primary cultured Schwann cells were treated with increasing dosages (0-40 ng/ml) of TNF-α, cell proliferation and migration were examined by EdU incorporation and a transwell-based assay, and cell apoptosis was observed and quantified by electron microscopy and Annexin V-FITC assay, respectively. The results showed that lower dosages of TNF-α increased cell proliferation and migration, whereas higher dosages of TNF-α decreased cell proliferation and migration and enhanced cell apoptosis. The tests using a chemical inhibitor of TNF-α further confirmed the above effects of TNF-α. To understand how TNF-α produced the dose-dependent dual effects on primary cultured Schwann cells, we performed co-immunoprecipitation, Western blot analysis, and immunocytochemistry to decipher the complex network of biochemical pathways involving many signaling molecules, i.e., TNF receptor-associated death domain, Fas-associated death domain, receptor interacting protein, JNK, NF-κB p65, and caspases, thus assuming the mechanisms by which TNF-α activated the death and survival pathways and achieved a balance between the two opposite actions in primary cultured Schwann cells.
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