ArticleCellular & molecular biology letters2024
Acid-sensing ion channel-1 contributes to the failure of myelin sheath regeneration following spinal cord injury by transcellular delivery of PGE2.
Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Photobiomodulation‑Engineered Extracellular Vesicles Enhance Neural Differentiation via UFL1‑Mediated UFMylation in Spinal Cord Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Arachidonic acid metabolism in spinal cord injury.Journal of advanced research · 2026Review
- PTGS2 as a potential target for apigenin to promote spinal cord injury repair.Journal of bioenergetics and biomembranes · 2026Article
- RPS3-Enriched Extracellular Vesicles Mediate Liver-Spinal Cord Inter-Organ Communication.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Navigating the Lipid Landscape: The Role of Fatty Acid Synthase in Neural Stem Cell Fate and Central Nervous System Function.Molecular neurobiology · 2025Review
- Neural Stem Cell-Derived Extracellular Vesicles for Advanced Neural Repair.Journal of neurochemistry · 2025Review
- Extracellular Vesicles as Emerging Therapeutic Strategies in Spinal Cord Injury: Ready to Go.Biomedicines · 2025Review
- Apigenin Suppresses NLRP3 Inflammasome Activation and Pyroptosis and Promotes Functional Recovery by Promoting Mitophagy in Experimental Spinal Cord Injured Rats.Journal of inflammation research · 2025Article
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Abstract
backgroundTraumatic injuries to spinal cord lead to severe motor, sensory, and autonomic dysfunction. The accumulation of inhibitory compounds plays a pivotal role in the secondary damage to sparing neural tissue and the failure of axonal regeneration and remyelination. Acid-sensing ion channel-1(ASIC1A) is widely activated following neurotrauma, including spinal cord injury (SCI). However, its role in SCI remains elusive.
methodsThe effects of acidic environment on the differentiation and genes changes of neural stem cells (NSCs) were assessed by immunofluorescence staining and RNA-sequencing analysis, respectively. The expression of ASIC1A and prostaglandin endoperoxide synthase 2 (PTGS2) were detected by western blot and immunofluorescence staining. The concentration of prostaglandin E2 (PGE2) within NSC-derived extracellular vesicles were evaluated by ELISA. Small-interfering RNAs (siRNAs) were used to knock down Asic1a and Ptgs2 expression in NSCs. The myelin sheath regeneration and axonal remyelination in rats and Asic1a-KO mice were assessed by immunofluorescence staining.
resultsFollowing injury to the spinal cord, ASIC1A was found to be colocalized and upregulated in NSCs. ASIC1A activation prevents the differentiation of NSCs into oligodendrocytes by upregulating PTGS2, which leads to increased production and release of PGE2 within extracellular vesicles (EVs). ASIC1A or PTGS2 deficiency in NSCs counters the ASIC1A-related effects on mediating NSC differentiation by reducing PGE2 expression within NSC-derived EVs. Furthermore, intervention in ASIC1A signaling by administration of ASIC1A inhibitors or genetic deletion of ASIC1A demonstrated a pronounced advantage in enhancing myelin sheath regeneration and axonal remyelination.
conclusionsThe activation of ASIC1A prevents NSC differentiation into oligodendrocytes via the transcellular NSC-to-NSC delivery of PGE2, resulting in the failure of myelin sheath regeneration and axonal remyelination following SCI. The inhibition of ASIC1A presents a promising therapeutic strategy for the treatment of SCI.
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