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  4. Lentivirus-mediated overexpression of netrin-1/ DCC co-expression promotes axonal regeneration and functional recovery in spinal cord injury via the inhibition of the NgR1-RhoA-ROCK signaling pathway

Lentivirus-mediated overexpression of netrin-1/ DCC co-expression promotes axonal regeneration and functional recovery in spinal cord injury via the inhibition of the NgR1-RhoA-ROCK signaling pathway

Translational Neuroscience, 2025 · DOI: https://doi.org/10.1515/tnsci-2025-0365 · Published: January 27, 2025

Spinal Cord InjuryRegenerative MedicineNeurology

Simple Explanation

Spinal cord injury (SCI) causes disabilities due to lack of neurotrophic factors and presence of inhibitory factors for axonal regeneration. This study investigates Netrin-1's role in promoting axonal regeneration by binding to the DCC receptor after SCI. A Netrin-1/DCC co-expression lentiviral vector was constructed to assess the effect of Netrin-1 on the NgR1-RhoA-ROCK signaling pathway in an SCI model. Results suggest that Netrin-1 has neuroprotective effects by inhibiting this pathway after binding to DCC. The study aims to understand the mechanisms by which Netrin-1 promotes axon regeneration and regulates the NgR1-RhoA-ROCK signaling pathway after nerve injury, potentially opening new avenues for clinical treatment of SCI.

Study Duration
Not specified
Participants
Adult Sprague–Dawley (SD) rats (200–250 g)
Evidence Level
Not specified

Key Findings

  • 1
    SCI injury decreases the expression of Netrin-1 in spinal cord tissue, suggesting Netrin-1 plays a role after SCI.
  • 2
    Increasing the expression of Netrin-1 contributes to the long-term motor function recovery in rats after SCI.
  • 3
    Netrin-1 promotes axon regeneration by binding to DCC and inhibiting the NgR1-RhoA-ROCK signaling pathway.

Research Summary

This study investigates the role of Netrin-1 and its receptor DCC in promoting axonal regeneration and functional recovery after spinal cord injury (SCI) in rats. The findings suggest that Netrin-1, by binding to DCC, inhibits the NgR1-RhoA-ROCK signaling pathway, leading to enhanced axon regeneration and improved motor function recovery. The research provides a mechanism-based bio-repair strategy for SCI, potentially leading to new clinical treatments that stimulate axon growth and facilitate functional recovery.

Practical Implications

Therapeutic Target Identification

Netrin-1/DCC and NgR1-RhoA-ROCK signaling pathway may be potential therapeutic targets for SCI.

Bio-repair Strategies

The study supports the development of bio-repair strategies based on promoting Netrin-1/DCC interaction to stimulate axon growth.

Clinical Application Potential

The findings open new avenues for clinical treatment of SCI by targeting the NgR1-RhoA-ROCK pathway.

Study Limitations

  • 1
    The study is limited to a rat model and may not directly translate to human outcomes.
  • 2
    The exact duration of the study or long-term effects of Netrin-1/DCC overexpression are not clearly specified.
  • 3
    The study does not fully address the potential side effects or off-target effects of lentivirus-mediated gene delivery.

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