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  4. Transient activation of Wnt/β-catenin signaling reporter in fibrotic scar formation after compression spinal cord injury in adult mice

Transient activation of Wnt/β-catenin signaling reporter in fibrotic scar formation after compression spinal cord injury in adult mice

Biochem Biophys Res Commun, 2018 · DOI: 10.1016/j.bbrc.2018.02.004 · Published: February 19, 2018

Spinal Cord InjuryGeneticsResearch Methodology & Design

Simple Explanation

After a spinal cord injury, scar tissue forms, which can hinder the regeneration of nerve fibers. This study looked at the role of Wnt/β-catenin signaling, a communication pathway between cells, in the formation of this scar tissue. The researchers used a spinal cord injury model in mice and found that Wnt/β-catenin signaling was temporarily activated in fibroblast-like cells, which are cells that contribute to the formation of the scar. This suggests that Wnt signaling may play a role in the development of fibrotic scars after spinal cord injury. Understanding this process could lead to new therapies to control scar formation and promote nerve regeneration.

Study Duration
21 days
Participants
Adult TOPgal transgenic mice (2-4 months old)
Evidence Level
Not specified

Key Findings

  • 1
    Wnt/β-catenin signaling reporter TOPgal positive cells appeared at the lesion site by 5 days, peaked on 7 days, and diminished by 14 days post injury.
  • 2
    These transiently TOPgal positive cells are a group of Fibronectin(+);GFAP(−) fibroblast-like cells in the core scar region.
  • 3
    Some of these TOPgal positive cells are proliferative, suggesting a role of Wnt/β-catenin signaling in the expansion of fibroblasts and the formation of the fibrotic scar.

Research Summary

This study investigates the role of Wnt/β-catenin signaling in fibrotic scar formation following spinal cord injury (SCI) in adult mice using a compression-SCI model and TOPgal reporter mice. The results demonstrate a transient activation of Wnt/β-catenin signaling in Fibronectin(+);GFAP(−) fibroblast-like cells within the core scar region after SCI. The findings suggest that Wnt signaling may play a key role in fibrotic scar formation after traumatic SCI, providing a potential therapeutic target for controlling scar formation and enhancing regeneration.

Practical Implications

Therapeutic Target Identification

Wnt signaling could be a novel therapeutic target for controlling scar formation and enhanced regeneration after SCI.

Understanding Fibrosis

The results provide new insights into the function of Wnt/β-catenin signaling in fibrotic scar formation after adult neural injury.

Clinical Translation Potential

Targeting Wnt signaling to modulate fibrotic scar formation could improve recovery outcomes for SCI patients.

Study Limitations

  • 1
    The cellular origins of the TOPgal(+) cells and the role of Wnt signaling in the initiation of the potential transformation from pericytes to fibroblasts after SCI remain to be addressed in future studies.
  • 2
    The TOPgal reporter may visualize only the most intensively activated Wnt signaling in the cells.
  • 3
    The effects of upregulated Wnt signaling with respect to myelin loss, modulation of axonal regeneration, and neural precursor differentiation are controversial, and may vary with the injury model.

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