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  4. AP-1cFos/JunB/miR-200a regulate the pro-regenerative glial cell response during axolotl spinal cord regeneration

AP-1cFos/JunB/miR-200a regulate the pro-regenerative glial cell response during axolotl spinal cord regeneration

Communications Biology, 2019 · DOI: https://doi.org/10.1038/s42003-019-0335-4 · Published: March 4, 2019

Regenerative MedicineNeurologyGenetics

Simple Explanation

Salamanders can regenerate their spinal cords after injury. Glial cells help with this process by creating a supportive environment for new axons to grow. This study looks at how certain molecules, specifically AP-1cFos/JunB and miR-200a, control this helpful glial cell response in axolotls. Axolotl glial cells up-regulate AP-1cFos/JunB after injury, which promotes a pro-regenerative glial cell response. Injury induced upregulation of miR-200a in glial cells supresses c-Jun expression in these cells. The research showed that miR-200a inhibits reactive gliosis in axolotl glial cells during spinal cord regeneration, which is different from what happens in mammals where reactive gliosis leads to scar formation that hinders regeneration.

Study Duration
Not specified
Participants
Axolotls (3-5 cm in length)
Evidence Level
Not specified

Key Findings

  • 1
    Axolotl glial cells upregulate a non-canonical AP-1 complex, AP-1cFos/JunB, after spinal cord injury, unlike mammals where AP-1cFos/cJun is upregulated and promotes glial scar formation.
  • 2
    miR-200a is upregulated in axolotl glial cells after spinal cord injury and directly represses c-Jun expression, preventing the formation of the AP-1cFos/cJun complex.
  • 3
    Inhibition of miR-200a leads to defects in axon regeneration and altered expression of genes involved in reactive gliosis, glial scar formation, and extracellular matrix remodeling.

Research Summary

This study investigates the molecular mechanisms underlying the pro-regenerative glial cell response in axolotls after spinal cord injury, focusing on the roles of AP-1 transcription factors and miR-200a. The research identifies that axolotl glial cells upregulate a non-canonical AP-1 complex, AP-1cFos/JunB, and that miR-200a represses c-Jun expression, preventing the formation of the canonical AP-1cFos/cJun complex, which is associated with glial scar formation in mammals. The study demonstrates that miR-200a plays a crucial role in inhibiting reactive gliosis and promoting a pro-regenerative environment in the axolotl spinal cord, highlighting key differences between regenerative and non-regenerative responses to spinal cord injury.

Practical Implications

Regenerative Therapies

Understanding the role of AP-1cFos/JunB and miR-200a in axolotl spinal cord regeneration could lead to new therapeutic strategies for promoting regeneration in mammals after spinal cord injury.

Targeting Reactive Gliosis

Identifying miR-200a as an inhibitor of reactive gliosis suggests that modulating miR-200a levels could be a potential approach to prevent glial scar formation and promote axon regeneration.

Comparative Biology

Comparing the molecular mechanisms of spinal cord regeneration in axolotls and mammals can provide valuable insights into the regenerative potential of different species and identify key factors that are necessary for successful regeneration.

Study Limitations

  • 1
    The study is limited by the availability of axolotl-specific antibodies, which makes it difficult to confirm protein expression levels.
  • 2
    The study uses a chemically synthesized miR-200a inhibitor rather than a knockout strategy, which may not completely eliminate miR-200a function.
  • 3
    The RNA sequencing data includes mRNA from various cell types in the spinal cord, not just glial cells, which may complicate the interpretation of gene expression changes.

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