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  4. Vitamin D Promotes Remyelination by Suppressing c-Myc and Inducing Oligodendrocyte Precursor Cell Differentiation after Traumatic Spinal Cord Injury

Vitamin D Promotes Remyelination by Suppressing c-Myc and Inducing Oligodendrocyte Precursor Cell Differentiation after Traumatic Spinal Cord Injury

International Journal of Biological Sciences, 2022 · DOI: 10.7150/ijbs.73673 · Published: August 29, 2022

Spinal Cord InjuryRegenerative MedicineNutrition & Dietetics

Simple Explanation

This study investigates how vitamin D (VitD) impacts the recovery process after a traumatic spinal cord injury (TSCI), specifically focusing on remyelination, the repair of the protective coating around nerve fibers. The research used rat models of TSCI, with some rats having normal VitD levels and others being VitD-deficient, to mimic real-world scenarios where people might have different VitD levels before an injury. The findings suggest that VitD supplementation after TSCI can improve motor function, especially in individuals with sufficient VitD levels prior to the injury, by promoting the differentiation of cells that help rebuild the myelin sheath.

Study Duration
8 weeks
Participants
60 male Sprague Dawley rats and 18 male C57/6N mice
Evidence Level
Not specified

Key Findings

  • 1
    VitD treatment post-TSCI effectively improved hindlimb movement in rats with normal VitD level irrespective of injury severity.
  • 2
    VitD rescued oligodendrocytes from apoptotic cell death in vitro and enhanced their myelinating ability towards dorsal root axons.
  • 3
    Enhanced myelination was mediated by increased oligodendrocyte precursor cells (OPCs) differentiation into oligodendrocytes in concert with c-Myc downregulation and suppressed OPCs proliferation.

Research Summary

This study demonstrates the therapeutic potential of VitD after TSCI by improving the integrity of myelin sheath through c-Myc suppression. Although the mechanisms of injury and pathophysiological alterations differ between contusion and transection injury, VitD treatment effectively improved hindlimb movement in animals without prior VitD-deficiency irrespective of injury severity. The study also demonstrates a novel function of VitD as a potent regulator of OLs survival and OPCs differentiation, and provided translational implications for combination therapy with OPCs transplantation and VitD supplementation to enhance the chances of OPCs survival while promoting in situ differentiation.

Practical Implications

Clinical Assessments

Highlights the importance of routine assessments of serum 25(OH)D levels in TSCI patients.

Treatment Strategies

Provides a strong reason to test the effect of VitD treatment in the clinical setting as it is a safe, well-tolerated and readily accessible agent.

Combination Therapy

Suggests translational implications for combination therapy with OPCs transplantation and VitD supplementation to enhance the chances of OPCs survival while promoting in situ differentiation.

Study Limitations

  • 1
    Whether animals with prior VitD-deficiency and severe injury would benefit from a higher dosage of VitD supplementation requires further investigations.
  • 2
    Given that the serum VitD levels were only assessed at 8w post-TSCI, it is not clear whether the observed reduction of serum VitD occurs at an earlier stage or at the late stage during recovery.
  • 3
    While serum VitD level post-TSCI seem to be a critical determinant in motor recovery, it is not clear whether serum calcium was in fact involved in functional improvements.

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