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  11. Neurotropic Murine Β-coronavirus Infection Causes Differential Expression Of Connexin 47 In Oligodendrocyte Subpopulations Associated With Demyelination.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Neurotropic Murine Β-coronavirus Infection Causes Differential Expression Of Connexin 47 In Oligodendrocyte Subpopulations Associated With Demyelination.

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Neurotropic Murine β-Coronavirus Infection Causes Differential Expression of Connexin 47 in Oligodendrocyte Subpopulations Associated with Demyelination.

Soubhik Das1, Archana Kumari Shaw2, Subhajit Das Sarma2

  • 1Biotechnology Research and Innovation Council - National Institute of Biomedical Genomics (BRIC-NIBMG), Kalyani, 741251, West Bengal, India.

Molecular Neurobiology
|September 18, 2024

View abstract on PubMed

Summary
This summary is machine-generated.
Keywords:
Connexin 43Connexin 47Gap junctionMouse β-coronavirus

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Oligodendroglial gap junctions (GJs) involving connexin 47 (Cx47) are lost in mature cells during demyelination, hindering repair. Oligodendrocyte precursor cells may offer a pathway for restoring GJ function in the central nervous system (CNS).

Area of Science:

  • Neuroscience
  • Cell Biology
  • Immunology

Background:

  • Gap junctions (GJs) are vital for oligodendrocyte survival and central nervous system (CNS) myelination.
  • Mouse hepatitis virus (MHV) infection causes demyelination, mimicking human multiple sclerosis (MS).

Purpose of the Study:

  • To investigate spatiotemporal changes in connexin 47 (Cx47) and connexin 43 (Cx43) expression during MHV-induced demyelination.
  • To understand the association between GJ changes and demyelination in the CNS.

Main Methods:

  • Intracerebral infection of mice with neurotropic MHV.
  • Analysis of Cx47 and Cx43 expression in oligodendrocytes and astrocytes at different time points post-infection.
  • Assessment of demyelination severity in distinct spinal cord regions.
Oligodendrocytes
Spinal cord demyelination

Main Results:

  • Persistent loss of Cx47 GJs in mature oligodendrocytes, even in non-lesioned areas, after initial Cx43 GJ loss in astrocytes during acute infection.
  • Re-emergence of astroglial Cx43 GJs post-viral clearance, but failed re-establishment of Cx47 GJs in mature oligodendrocytes.
  • Oligodendrocyte precursor cells showed Cx47 GJ expression at later demyelinating stages.
  • Thoracic spinal cord exhibited the most severe demyelination, correlating with differential Cx47 GJ expression in oligodendrocyte lineage cells.

Conclusions:

  • Loss of Cx47 GJs in mature oligodendrocytes contributes to persistent demyelination after MHV clearance.
  • Oligodendrocyte precursor cells expressing Cx47 GJs may be crucial for CNS repair and remyelination.
  • Regional differences in demyelination are linked to dynamic changes in oligodendrocyte GJ expression, suggesting a mechanism for progressive demyelination.