Xenopus laevis neural stem progenitor cells exhibit a transient metabolic shift toward glycolysis during spinal cord regeneration

Front. Cell Dev. Biol., 2025 · DOI: 10.3389/fcell.2025.1529093 · Published: January 29, 2025

Simple Explanation

Spinal cord injury in mammals often leads to permanent damage due to limited regeneration. However, some animals like Xenopus laevis tadpoles can regenerate their spinal cords. This study explores how mitochondria, the cell's energy producers, and cellular metabolism change during this regeneration process. The research found that after spinal cord injury in Xenopus laevis tadpoles, neural stem cells undergo a quick shift in how they produce energy. Instead of relying on mitochondria, they temporarily switch to glycolysis, a process that breaks down glucose for energy. This metabolic shift is accompanied by changes in the structure and location of mitochondria within these stem cells. These changes are believed to be necessary for the regeneration process to occur successfully.

Study Duration

Not specified

Participants

Xenopus laevis embryos and tadpoles

Evidence Level

Original Research

Key Findings

1
Mitochondria are primarily located in neural stem progenitor cells (NSPCs) near the spinal cord's central canal, exhibiting an apical distribution. After SCI, this arrangement is disrupted.
2
Following spinal cord injury (SCI), there is a temporary decrease in the number of mitochondria per cell section, coupled with an increase in mitochondrial area and circularity within NSPCs.
3
SCI induces a shift toward glycolytic metabolism in NSPCs, indicated by increased transcript levels and enzyme activity of glycolytic genes, alongside a transient decrease in mitochondrial membrane potential.

Research Summary

This study investigates the mitochondrial and metabolic response of neural stem progenitor cells (NSPCs) during spinal cord regeneration in Xenopus laevis. The research reveals that mitochondria undergo a rapid response after spinal cord injury (SCI). Mitochondria, typically located in the apical region of NSPCs, redistribute following SCI. There is also a decrease in mitochondrial number per cell section and an increase in mitochondrial size and circularity. The study demonstrates a transient metabolic shift toward glycolysis in NSPCs post-SCI. This shift, along with mitochondrial morphology changes, suggests a tightly regulated metabolic adaptation essential for spinal cord regeneration.

Practical Implications

Therapeutic Targets

The findings provide potential therapeutic targets for promoting CNS regeneration by manipulating mitochondrial dynamics and metabolic pathways.

Understanding Regeneration

The research enhances our understanding of the molecular basis of spinal cord regeneration, particularly the role of mitochondrial dynamics and metabolic shifts in NSPCs.

Conserved Mechanisms

The study supports the idea that conserved metabolic responses, such as aerobic glycolysis, are crucial across different regenerative models.

Study Limitations

1
Transcript levels do not always predict protein levels or function.
2
Changes in mitochondrial mass could not be ruled out.
3
The exact mechanisms regulating mitochondrial dynamics and metabolic shifts on NSPC survival, proliferation, and differentiation require further investigation.

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