ArticleMediators of inflammation2014
The role of IL-17 promotes spinal cord neuroinflammation via activation of the transcription factor STAT3 after spinal cord injury in the rat.
Article in Mediators of inflammation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 67 citations in OpenAlex.
- Regulatory effect of inflammatory mediators in spinal cord injury.Frontiers in immunology · 2025Review
- RETRACTION: ET-1 Promotes Differentiation of Periodontal Ligament Stem Cells Into Osteoblasts Through ETR, MAPK, and Wnt/β-Catenin Signaling Pathways Under Inflammatory Microenvironment.Mediators of inflammation · 2025Article
- Identification of Ifitm1 as a Pivotal Gene in Mouse Spinal Cord Injury Using Comprehensive Machine Learning Algorithms.Mediators of inflammation · 2025Article
- Unveiling vital biomarkers and immune infiltration profiles in endoplasmic reticulum stress following spinal cord injury.Scientific reports · 2024Article
- Acute spinal cord injury serum biomarkers in human and rat: a scoping systematic review.Spinal cord series and cases · 2024Article
- Interleukin-17: A Putative Novel Pharmacological Target for Pathological Pain.Current neuropharmacology · 2024Review
- Long-term changes of Th17 and regulatory T cells in peripheral blood of dogs with spinal cord injury after intervertebral disc herniation.BMC veterinary research · 2023Article
- Neutrophil-derived interleukin-17A participates in neuroinflammation induced by traumatic brain injury.Neural regeneration research · 2023Article
- Patients with Chronic Spinal Cord Injury and a Long Period of Evolution Exhibit an Altered Cytokine Production by CD4 and CD8 T Cell Populations.International journal of molecular sciences · 2023Article
- Biomarkers for predicting the severity of spinal cord injury by proteomic analysis.Frontiers in molecular neuroscience · 2023Article
- Interleukin-17 as a potential therapeutic target for chronic pain.Frontiers in immunology · 2022Review
- Revealing Potential Spinal Cord Injury Biomarkers and Immune Cell Infiltration Characteristics in Mice.Frontiers in genetics · 2022Article
- Inhibition of miR-145-5p Reduces Spinal Cord Injury-Induced Inflammatory and Oxidative Stress Responses via Affecting Nurr1-TNF-α Signaling Axis.Cell biochemistry and biophysics · 2021Article
- Interleukin-17A regulates ependymal cell proliferation and functional recovery after spinal cord injury in mice.Cell death & disease · 2021Article
- MiR-495 regulates cell proliferation and apoptosis in HAnnals of translational medicine · 2021Article
- Mesenchymal stem cell-derived exosomes: therapeutic opportunities and challenges for spinal cord injury.Stem cell research & therapy · 2021Review
- Inhibition of RNF6 alleviates traumatic brain injury by suppressing STAT3 signaling in rats.Brain and behavior · 2020Article
- Promoting functions of microRNA-29a/199B in neurological recovery in rats with spinal cord injury through inhibition of the RGMA/STAT3 axis.Journal of orthopaedic surgery and research · 2020Article
- MicroRNA-15a inhibits inflammatory response and apoptosis after spinal cord injury via targeting STAT3.European review for medical and pharmacological sciences · 2019Article
- Synthesis and Characterization of a Silica-Based Drug Delivery System for Spinal Cord Injury Therapy.Nano-micro letters · 2019Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
designIn this study, we investigated the role of IL-17 via activation of STAT3 in the pathophysiology of SCI.
objectiveThe purpose of the experiments is to study the expression of IL-17 and related cytokines via STAT3 signaling pathways, which is caused by the acute inflammatory response following SCI in different periods via establishing an acute SCI model in rat.
methodsBasso, Beattie, and Bresnahan hind limb locomotor rating scale was used to assess the rat hind limb motor function. Immunohistochemistry was used to determine the expression levels of IL-17 and p-STAT3 in spinal cord tissues. Western blotting analysis was used to determine the protein expression of p-STAT3 in spinal cord tissue. RT-PCR was used to analyze the mRNA expression of IL-17 and IL-23p19 in the spleen tissue. ELISA was used to determine the peripheral blood serum levels of IL-6, IL-21, and IL-23.
resultsCompared to the sham-operated group, the expression levels of IL-17, p-STAT3, IL-6, IL-21, and IL-23 were significantly increased and peaked at 24 h after SCI. The increased levels of cytokines were correlated with the SCI disease stages.
conclusionIL-17 may play an important role in promoting spinal cord neuroinflammation after SCI via activation of STAT3.
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