Evaluation of transcriptomic changes after photobiomodulation in spinal cord injury

Scientific Reports, 2025 · DOI: https://doi.org/10.1038/s41598-025-87300-4 · Published: January 29, 2025

Spinal Cord Injury Bioinformatics Rehabilitation

Simple Explanation

Spinal cord injury (SCI) often leads to permanent disabilities because the body struggles to repair damaged nerve cells. There are currently no effective treatments to promote nerve regeneration after SCI. Photobiomodulation (PBM) is a therapy that uses red or near-infrared light to stimulate cells, particularly mitochondria, which are the powerhouses of cells. PBM has shown promise in helping to restore function after SCI in animal models. This study examines how PBM affects gene activity in rats with SCI. Researchers analyzed the genes that were turned on or off after PBM treatment to understand how it promotes nerve regeneration and reduces cell death.

Study Duration

3 days

Participants

Adult 6-8-week-old male Sprague-Dawley rats (n=4 per group)

Evidence Level

In-vivo model

Key Findings

1
PBM treatment resulted in 1275 differentially expressed genes (DEGs), with 397 upregulated and 878 downregulated, indicating a significant change in gene expression patterns after PBM.
2
Pathway analysis revealed a significant enrichment of “neuron projection morphogenesis,” suggesting PBM promotes neuroregeneration. Key pathways like Notch3, Slit1/Robo2, and Sema3g were upregulated.
3
Downregulation of metabolism-associated pathways suggests that PBM may help avert acute post-injury mitochondrial dysfunction, supporting the idea that PBM helps protect nerve cells after injury.

Research Summary

This study uses a transcriptomic approach to investigate the mechanisms by which photobiomodulation (PBM) exerts its effects on spinal cord injury (SCI) in rats. The findings indicate that PBM promotes neuroregeneration and suppresses apoptosis after SCI by influencing various gene expression pathways. The results suggest that PBM's supportive action on mitochondrial function may allow energy conservation in the acute post-injury phase, reducing ribosomal stress responses and minimizing apoptotic processes.

Practical Implications

Clinical Translation

Provides a well-defined rationale for using PBM medical devices in clinical contexts for spinal cord injury.

Therapeutic Target Identification

Highlights specific transcriptional changes associated with neuroprotection and axonal regeneration, offering new therapeutic targets for improving outcomes after SCI.

Optimization of PBM Parameters

Insights gained may lead to improvements in the design of PBM parameters to achieve optimal effects in treating CNS injuries.

Study Limitations

1
Use of a single set of PBM parameters with a single timepoint post-injury limits the insights derived.
2
Lack of a Sham control group for comparison of metabolic activity-related transcription.
3
Tissue used was a homogenate of the entire injury site, precluding resolution of mechanisms to specific cell types.

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