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Sublytic terminal complement complexes decrease P0 Gene expression in Schwann cells.

S M Dashiell1, C L Koski

  • 1Department of Pathology, University of Maryland School of Medicine, Baltimore, USA.

Journal of Neurochemistry
|December 3, 1999
PubMed
Summary
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Sublytic complement activation on Schwann cells (SchCs) reduces myelin gene expression, potentially contributing to peripheral nerve demyelination. This study investigated the impact of terminal complement complexes (TCCs) on myelin gene regulation in SchCs.

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Complement cascade activation can lead to myelin destruction in peripheral nerves.
  • Schwann cells (SchCs) express terminal complement complexes (TCCs) during inflammatory neuropathy but resist lysis.
  • The functional impact of sublytic TCC deposition on SchCs remains largely unknown.

Purpose of the Study:

  • To investigate the effects of sublytic complement activation on myelin gene expression in SchCs.
  • To determine whether TCCs modulate myelin gene expression at posttranscriptional and transcriptional levels.

Main Methods:

  • Cultured SchCs expressing protein zero (P0) were treated with antibody and normal human serum (NHS) complement.
  • P0 mRNA degradation was assessed using actinomycin D.

Related Experiment Videos

  • P0 gene transcription was analyzed using a P0 promoter/luciferase reporter construct.
  • c-jun mRNA expression was monitored.

    • Main Results:

    • Sublytic TCCs decreased P0 mRNA content by 71% within 12 hours.
    • Enhanced P0 mRNA degradation was observed, with levels declining 50% in the presence of actinomycin D.
    • TCC formation significantly reduced P0 mRNA levels.
    • Sublytic TCCs inhibited P0 gene transcription by 70%.
    • c-jun mRNA was upregulated by sublytic TCCs prior to P0 mRNA reduction.

    Conclusions:

    • Sublytic complement activation on SchCs leads to decreased expression of myelin genes like P0 at both transcriptional and posttranscriptional levels.
    • This downregulation of essential myelin genes may contribute to peripheral nerve demyelination.
    • Upregulation of c-jun suggests a potential signaling pathway involved in complement-mediated modulation of myelin gene expression.