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Determining Immune System Suppression versus CNS Protection for Pharmacological Interventions in Autoimmune Demyelination
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Versican promotes T helper 17 cytotoxic inflammation and impedes oligodendrocyte precursor cell remyelination

Samira Ghorbani1, Emily Jelinek1, Rajiv Jain1

  • 1Hotchkiss Brain Institute and Department of Clinical Neurosciences, University of Calgary, Calgary, Canada.

Nature Communications
|May 4, 2022
PubMed

Insights

Versican-V1 in multiple sclerosis (MS) lesions inhibits oligodendrocyte precursor cells and promotes neuroinflammation, hindering myelin repair. Lowering CSPGs may offer dual repair and immunomodulatory therapy for MS.

Area of Science:

  • Neuroscience
  • Immunology
  • Regenerative Medicine

Background:

  • Remyelination failure in multiple sclerosis (MS) exacerbates disability.
  • Neuroinflammation and chondroitin sulfate proteoglycans (CSPGs) inhibit repair.
  • The specific CSPG involved in MS lesion pathology is unknown.

Purpose of the Study:

  • Identify the CSPG member inhibiting remyelination in MS.
  • Investigate versican-V1's role in oligodendrocyte precursor cell (OPC) function and neuroinflammation.
  • Evaluate therapeutic strategies targeting versican-V1.

Main Methods:

  • Correlating versican-V1 expression with OPC presence in MS and experimental autoimmune encephalomyelitis (EAE) lesions.
  • Assessing versican-V1's effects on OPCs and T helper 17 (Th17) cell polarization in vitro.
  • Administering difluorosamine to EAE mice to modulate versican-V1 and Th17 levels, and assess remyelination.

Main Results:

  • High versican-V1 expression correlates with reduced premyelinating oligodendrocytes in MS lesions.
  • Versican-V1 selectively upregulates in EAE lesions and inhibits OPCs in vitro.
  • Versican-V1 promotes Th17 polarization, and Th17 cells become more toxic to OPCs.
  • Difluorosamine treatment reduced versican-V1 and Th17 frequency while enhancing remyelination in EAE mice.

Conclusions:

  • Lesion-elevated versican-V1 directly impairs OPCs and indirectly inhibits remyelination via Th17-mediated neuroinflammation.
  • Targeting CSPGs presents a potential dual therapeutic strategy for MS repair and immunomodulation.

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