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  4. Olig2-Induced Semaphorin Expression Drives Corticospinal Axon Retraction After Spinal Cord Injury

Olig2-Induced Semaphorin Expression Drives Corticospinal Axon Retraction After Spinal Cord Injury

Cerebral Cortex, 2020 · DOI: 10.1093/cercor/bhaa142 · Published: November 1, 2020

Spinal Cord InjuryRegenerative MedicineGenetics

Simple Explanation

After a spinal cord injury, the body's ability to repair damaged nerve connections is limited. This study investigates how certain molecules, called semaphorins, might prevent nerve fibers from regrowing after such an injury. Researchers found that after a spinal cord injury, the levels of specific semaphorins increase. These molecules then cause nerve fibers to retract, further hindering the healing process. The study also discovered that a protein called Olig2 is responsible for increasing the production of these inhibitory semaphorins after a spinal cord injury. By controlling Olig2, it may be possible to reduce the levels of semaphorins and promote nerve regeneration.

Study Duration
Not specified
Participants
Adult C57BL/6 J mice, Two rhesus monkeys
Evidence Level
Not specified

Key Findings

  • 1
    Expression of multiple semaphorin family members (Sema3a, Sema3b, Sema3c, Sema3d, Sema3g, Sema4c, Sema4d, Sema5a, Sema6a, and Sema6d) was elevated one week post-injury in mice.
  • 2
    Genetic deletion of Sema6d, PlexinA1, or Nrp1 suppresses dieback of CST fibers after SCI in mice.
  • 3
    Olig2 regulates semaphorin expression after SCI, as evidenced by decreased Sema5a and Sema6d expression in Olig2-deleted mice.

Research Summary

This study investigates the role of semaphorins in axon repulsion after spinal cord injury (SCI), identifying that the expression of multiple semaphorin family members is induced by Olig2. Genetic evidence demonstrates that this molecular system creates an inhibitory environment for injured corticospinal axons following SCI. The research reveals that transcriptional regulation of semaphorins by Olig2 is essential for semaphorin induction after SCI, contributing to a suppressive environment for axonal growth.

Practical Implications

Therapeutic Target

Targeting the Olig2 transcriptional machinery could be a novel therapeutic strategy to enhance regeneration after SCI by preventing expression of multiple inhibitory molecules simultaneously.

Understanding Inhibitory Barriers

The study highlights the importance of understanding transcriptional control machinery as a far-reaching extrinsic mechanism that can impede axonal growth, providing insights for future research.

Combination Therapies

Additional methods that modulate scar tissue formation may be needed to overcome the strict inhibitory barrier to axon regrowth, suggesting the potential of combination therapies.

Study Limitations

  • 1
    The study did not observe any marked increase in axon regeneration into and beyond the lesion core despite semaphorin deletion.
  • 2
    Olig2 deletion may have additional effects on the repair process, such as glial scar formation, which requires further investigation.
  • 3
    It is technically difficult to pharmaceutically inhibit transcription factors, posing a challenge for direct therapeutic translation.

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