ArticleFrontiers in neuroscience2024
Targeting transcription factor pu.1 for improving neurologic outcomes after spinal cord injury.
Article in Frontiers in neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- A Unified Framework for Spinal Cord Injury Repair: Metabolic-Nutritional Microenvironment Remodeling, Immune Modulation, and Neural Regeneration.Molecular neurobiology · 2026Review
- Arachidonic acid metabolism in spinal cord injury.Journal of advanced research · 2026Review
- Neuronal SPI1 suppression enhances axonal regeneration after spinal cord injury through Rassf10 downregulation.Burns & trauma · 2026Article
- The Utility of Metabolomics in Spinal Cord Injury: Opportunities for Biomarker Discovery and Neuroprotection.International journal of molecular sciences · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: After spinal cord injury (SCI), lipid metabolism dysregulation at the lesion site exacerbates secondary damage. The transcription factor pu.1 has been implicated as a negative regulator of multiple lipid metabolism-related genes and pathways. However, its role in post-SCI lipid metabolism remains unclear. Methods: We employed a mouse model of complete T10 crush SCI. Non-targeted metabolomics and bioinformatics analysis were utilized to investigate lipid metabolism at the lesion site after SCI. Polarized light imaging was used to evaluate the presence of cholesterol crystals. DB1976, a specific inhibitor of pu.1, was administered to examine its impact on local lipid metabolism after SCI. Immunofluorescence staining was performed to assess pu.1 expression and distribution, and to evaluate lipid droplet formation, astrocytic/fibrotic scar development, inflammatory cell infiltration, and tight junctions within the vasculature. Results: Non-targeted metabolomics and bioinformatics analyses revealed significant alterations in lipid metabolism components after SCI. Moreover, immunofluorescence staining and polarized light imaging demonstrated substantial BODIPY Conclusion: Our study reveals a significant correlation between lipid metabolism disturbance post-SCI and transcription factor pu.1 upregulation, specifically in macrophages/microglia at the lesion site. Thus, targeted pu.1 modulation has the potential to yield promising results by substantially diminishing the deposition of lipid metabolism byproducts at the lesion site and fostering a milieu conducive to SCI repair.
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Registered trials
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