ArticleCell death discovery2025
ELAVL1-mediated USP29 mRNA degradation activates TAK1 driving M1 microglial polarization and neural stem cell differentiation dysregulation in spinal cord injury.
Article in Cell death discovery, 2025. 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.
- Neuroprotective Role of E3 Ubiquitin Ligase TRIM2 in Parkinson's Disease: Attenuation of Oxidative Stress and Apoptosis via Promoting ELAVL1 Ubiquitination.CNS neuroscience & therapeutics · 2026Article
- RNA-binding proteins: a comprehensive review of multifaceted regulatory mechanisms in neuroinflammation and implications in the pathogenesis of neurological disorders.Journal of neuroinflammation · 2026Review
- HMC3 revealed: how much do these "Microglia" really tell us?Frontiers in immunology · 2026Review
- CD63Frontiers in cellular and infection microbiology · 2026Article
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Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Spinal cord injury (SCI) represents a profound neurological condition characterized by motor dysfunction and sensory impairment. Microglial polarization significantly influences neurorepair and regeneration post SCI. This study aims to investigate the regulatory role of the ELAV-like RNA binding protein 1 (ELAVL1)-ubiquitin-specific peptidase 29 (USP29)-transforming growth factor beta-activated kinase 1 (TAK1) axis in microglial polarization and its effects on differentiation of neural stem cells (NSCs). A rat model of SCI was established via spinal cord transection at the tenth thoracic vertebra segment, followed by short hairpin RNA (shRNA) lentivirus infection. Motor function and coordination were evaluated while histopathological analysis of spinal cord tissues was conducted. Microglial polarization and NSC differentiation were assessed via immunofluorescence and Western blot analysis. In cellular experiments, lipopolysaccharide (LPS) was utilized to induce M1 polarization in HMC3 cells, with polarization status determined by flow cytometry, immunofluorescence, and WB. Co-immunoprecipitation, GST pull-down, and ubiquitination assays elucidated USP29 effects on TAK1 ubiquitination and activation. In SCI rat spinal cord tissues and LPS-treated HMC3 cells, we observed upregulation of ELAVL1 and phosphorylated level of TAK1, while USP29 expression was downregulated. ELAVL1 was found to bind USP29 mRNA, promoting its degradation and suppressing USP29 expression. USP29 directly interacted with TAK1, inhibiting its ubiquitination and phosphorylation. Knockdown of ELAVL1 significantly enhanced USP29 mRNA stability, inhibited TAK1 activation, promoted M2 microglial polarization, and suppressed M1 polarization. In vivo downregulation of ELAVL1 promoted the differentiation of NSCs into neurons by inhibiting M1 polarization and promoting M2 polarization, thereby improving motor function, alleviating nerve injury, and facilitating spinal cord repair. ELAVL1 exacerbates SCI pathology by degrading USP29 mRNA, thereby activating TAK1 and driving M1 microglial polarization. Targeting the ELAVL1-USP29-TAK1 axis may offer therapeutic potential for enhancing neurorepair in SCI. Schematic diagram of the ELAVL1-USP29-TAK1 axis mediating M1 microglial polarization and NSC differentiation dysregulation exacerbating SCI.
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Registered trials
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