ArticleCNS neuroscience & therapeutics2024
Vof16-miR-185-5p-GAP43 network improves the outcomes following spinal cord injury via enhancing self-repair and promoting axonal growth.
Article in CNS neuroscience & therapeutics, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 13 citations in OpenAlex.
- Smart-responsive electrospun scaffolds (SRES) for neural repair: Recent advances and future prospects.Bioactive materials · 2026Review
- Research Progress on Spinal Cord Repair Based on Regulation of the Neuroregenerative Microenvironment.Cellular and molecular neurobiology · 2026Review
- The Specialized Proresolving Mediator Maresin 1 Alleviated Neuropathic Pain Exacerbated by High-Fat Diet via Regulating Neuroinflammation.Pain research & management · 2026Article
- Cryptic Splicing of GAP43 mRNA is a Novel Hallmark of TDP-43-Associated ALS and AD.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The promise of mitochondria in the treatment of glioblastoma: a brief review.Discover oncology · 2025Review
- Targeting LncRNA-Vof16: A Novel Therapeutic Strategy for Neuropathic Pain Relief.CNS neuroscience & therapeutics · 2025Article
- NcRNAs: a potential treatment for spinal cord injury.Frontiers in cellular neuroscience · 2025Review
- An unstable variant of GAP43 leads to neurodevelopmental deficiency.Scientific reports · 2024Article
- Research progress on long non‑coding RNAs in non‑infectious spinal diseases (Review).Molecular medicine reports · 2024Review
- NeuroAiDBiomedicines · 2024Article
- Vof16-miR-185-5p-GAP43 network improves the outcomes following spinal cord injury via enhancing self-repair and promoting axonal growth.CNS neuroscience & therapeutics · 2024Article
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Authors and funding
13 authors at 4 institutions in 2 countries.
Funding
Abstract
introductionSelf-repair of spinal cord injury (SCI) has been found in humans and experimental animals with partial recovery of neurological functions. However, the regulatory mechanisms underlying the spontaneous locomotion recovery after SCI are elusive.
aimsThis study was aimed at evaluating the pathological changes in injured spinal cord and exploring the possible mechanism related to the spontaneous recovery.
resultsImmunofluorescence staining was performed to detect GAP43 expression in lesion site after spinal cord transection (SCT) in rats. Then RNA sequencing and gene ontology (GO) analysis were employed to predict lncRNA that correlates with GAP43. LncRNA smart-silencing was applied to verify the function of lncRNA vof16 in vitro, and knockout rats were used to evaluate its role in neurobehavioral functions after SCT. MicroRNA sequencing, target scan, and RNA22 prediction were performed to further explore the underlying regulatory mechanisms, and miR-185-5p stands out. A miR-185-5p site-regulated relationship with GAP43 and vof16 was determined by luciferase activity analysis. GAP43-silencing, miR-185-5p-mimic/inhibitor, and miR-185-5p knockout rats were also applied to elucidate their effects on spinal cord neurite growth and neurobehavioral function after SCT. We found that a time-dependent increase of GAP43 corresponded with the limited neurological recovery in rats with SCT. CRNA chip and GO analysis revealed lncRNA vof16 was the most functional in targeting GAP43 in SCT rats. Additionally, silencing vof16 suppressed neurite growth and attenuated the motor dysfunction in SCT rats. Luciferase reporter assay showed that miR-185-5p competitively bound the same regulatory region of vof16 and GAP43.
conclusionsOur data indicated miR-185-5p could be a detrimental factor in SCT, and vof16 may function as a ceRNA by competitively binding miR-185-5p to modulate GAP43 in the process of self-recovery after SCT. Our study revealed a novel vof16-miR-185-5p-GAP43 regulatory network in neurological self-repair after SCT and may underlie the potential treatment target for SCI.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.