ArticleCNS neuroscience & therapeutics2023
Protein arginine methyltransferase 8 regulates ferroptosis and macrophage polarization in spinal cord injury via glial cell-derived neurotrophic factor.
Article in CNS neuroscience & therapeutics, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Deferoxamine mitigates neuronal loss following spinal cord injury via ferroptosis inhibition and Nrf2/HO‑1 pathway activation.International journal of molecular medicine · 2026Article
- The expression of glial cell-derived neurotrophic factor in the hippocampal tissue of rats with vascular dementia and its correlation with molecular pathways involved in learning and memory impairment.Journal of bioenergetics and biomembranes · 2026Article
- Ferroptosis in Spine-Related Diseases: Mechanistic Insights and Potential Therapeutic Targets.Cellular and molecular neurobiology · 2026Review
- CARD9 Conveys Pancreatic Islet Sympathetic Nervous β2 Signals to Reshape Macrophage Creatine Metabolism in Type 1 Diabetes.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Engineered CCR2 positive macrophages coordinate immunoregulation with neural regeneration and matrix remodeling after spinal cord injury.Theranostics · 2026Article
- Exosomal miR-494 from Bone Marrow Mesenchymal Stem Cells Attenuates Ferroptosis and Enhances Spinal Cord Injury Repair by Modulating the SIRT1/HO-1 Pathway.Molecular neurobiology · 2025Article
- Arginine methylation in cancer: mechanisms and therapeutic implications.Biomarker research · 2025Review
- Current and Emerging Therapies for Targeting Protein Arginine Methyltransferases (PRMTs) in Cancer.International journal of molecular sciences · 2025Review
- Microglia and programmed cell death in spinal cord injury: beyond apoptosis.Frontiers in cell and developmental biology · 2025Review
- Protein arginine methyltransferase 8 regulates ferroptosis and macrophage polarization in spinal cord injury via glial cell-derived neurotrophic factor.CNS neuroscience & therapeutics · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveTo explore the influence of protein arginine methyltransferase 8 (PRMT8) regulating glial cell-derived neurotrophic factor (GDNF) on neuron ferroptosis and macrophage polarization in spinal cord injury (SCI).
methodsA rat model of SCI was established through an injury induced by an external force. Basso, Beattie, and Bresnahan score, hematoxylin and eosin staining, and immunofluorescence were used, respectively, to detect changes in rat locomotion, spinal cord histopathology, and NeuN expression in the spinal cord. Iron content in the spinal cord and levels of malondialdehyde and glutathione were measured using detection kits. Transmission electron microscopy was used to reveal the morphological characteristics of mitochondria. Western blotting was performed to detect PRMT8, GDNF, cystine/glutamate transporter XCT, glutathione peroxidase 4, 4-hydroxynonenal, heme oxygenase-1, inducible nitric oxide synthase (iNOS), CD16, and arginase 1 (Arg1). The expression levels of iNOS and Arg1 in the spinal cord were visualized by immunofluorescence. ELISA was performed to measure the expression levels of IL-6, IL-1β, and TNF-α. Rat dorsal root ganglion (DRG) neurons and RMa-bm rat macrophages were treated with lipopolysaccharide under hypoxic conditions. The viability and iron content of the neurons were detected using Cell Counting Kit-8 and a specific probe, respectively. Flow cytometry and immunofluorescence were used to assess macrophage polarization. Chromatin immunoprecipitation was used to identify the binding of PRMT8 to the GDFN promoter.
resultsNeuronal ferroptosis and M1 macrophage polarization were promoted, and PRMT8 expression was downregulated in SCI. PRMT8 overexpression exerted therapeutic effects on injured DRG neurons and RMa-bm cells. Moreover, PRMT8 overexpression inhibited ferroptosis and M1 macrophage polarization in rats with SCI. PRMT8 promoted GDNF expression by catalyzing H3K4 methylation. Knockdown of GDNF counteracted the therapeutic effects of PRMT8 overexpression.
conclusionOverexpression of PRMT8 may inhibit ferroptosis and M1 macrophage polarization by increasing GDNF expression, thereby alleviating SCI.
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