ArticleCNS neuroscience & therapeutics2023
Depletion of SASH1, an astrocyte differentiation-related gene, contributes to functional recovery in spinal cord injury.
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 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- SASH1 as a Context-Dependent Multi-Docking Scaffold Linking Receptor Signaling to Cytoskeletal Dynamics.International journal of molecular sciences · 2026Review
- Neuronal SPI1 suppression enhances axonal regeneration after spinal cord injury through Rassf10 downregulation.Burns & trauma · 2026Article
- RNA Interference and Its Key Targets for Spinal Cord Injury Therapy: What Is Known So Far?International journal of molecular sciences · 2025Review
- Gliogenesis but not neurogenesis occurs during the acute phase of vestibular compensation after unilateral vestibular neurectomy.IBRO neuroscience reports · 2025Article
- Neural stem cells fate under neuroinflammatory conditions and oxidative stress response.Frontiers in cellular neuroscience · 2025Review
- Research on stem cell therapy for spinal cord injury: a bibliometric and visual analysis from 2018-2023.Frontiers in genetics · 2024Review
- Depletion of SASH1, an astrocyte differentiation-related gene, contributes to functional recovery in spinal cord injury.CNS neuroscience & therapeutics · 2023Article
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Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsThis study aimed to evaluate the effects of the depletion of SAM and SH3 domain-containing protein 1 (SASH1) on functional recovery after spinal cord injury (SCI) and to investigate the possible mechanism of SASH1 knockdown in astrocytes facilitating axonal growth.
methodsSCI model was established in adult rats. SASH1 small interfering RNA (siSASH1) was used to investigate its function. Hindlimb motor function was evaluated by the Basso-Bresnahan-Beattie (BBB) assay. The gene expressions were evaluated by the methods of qRT-PCR, Western-blotting, ELISA, and immunohistochemistry.
resultsSASH1 knockdown improved the BBB scores after SCI and significantly reduced GFAP expression. In cultured spinal astrocytes, siSASH1 treatment decreased interferon-γ release and increased brain-derived neurotrophic factor (BDNF) release. When cocultured with SASH1-knockdown astrocytes, axonal growth increased. The neuronal tropomyosin receptor kinase B (BDNF receptor) expression increased, especially in the axonal tips. SASH1 expression increased while NSCs differentiated into glial cells, instead of neurons. After SASH1 depletion, differentiated NSCs maintained a higher level of Nestin protein and an increase in BDNF release.
conclusionsThese results indicate that SASH1 acts as an astrocytic differentiation-maintaining protein, and SASH1 downregulation limits glial activation and contributes toward functional recovery after SCI.
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