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Sublytic complement attack induces cell cycle in oligodendrocytes

H G Rus1, F Niculescu, M L Shin

  • 1Department of Pathology, University of Maryland School of Medicine, Baltimore, MD 21201, USA.

Journal of Immunology (Baltimore, Md. : 1950)
|June 15, 1996
PubMed
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Terminal complement complexes (TCC) activate oncogenes like c-jun in oligodendrocytes (OLG), stimulating cell cycle entry and reducing apoptosis. This response may aid OLG in inflammation.

Area of Science:

  • Neuroimmunology
  • Cellular Biology
  • Molecular Neuroscience

Background:

  • Oligodendrocytes (OLG) are crucial for myelin maintenance in the central nervous system.
  • The complement system, particularly terminal complement complexes (TCC), plays a role in neuroinflammation.
  • Sublytic complement attack on OLG affects myelin protein mRNA decay.

Purpose of the Study:

  • To investigate if TCC stimulate cell cycle entry in differentiated OLG.
  • To determine the relationship between TCC-induced cell cycle entry and oncogene expression.
  • To elucidate the molecular pathways involved in OLG response to complement activation.

Main Methods:

  • Measurement of oncogene mRNA expression (c-jun, JunD, c-fos) and AP-1 DNA-binding activity.
  • Assessment of [3H]thymidine uptake to quantify cell proliferation.

Related Experiment Videos

  • Analysis of c-jun NH2-terminal kinase (JNK) activity.
  • Inhibition studies using antisense c-jun oligonucleotides.
  • Evaluation of cyclin-dependent kinase (cdk) activation (cdk2, cdk4, cyclin D2).
  • Quantification of OLG undergoing apoptotic cell death.

    • Main Results:

    • TCC assembly rapidly induced c-jun, JunD, and c-fos mRNA expression and AP-1 DNA-binding activity.
    • TCC increased [3H]thymidine uptake, indicating cell cycle entry, which was inhibited by c-jun antisense oligonucleotides.
    • JNK activity significantly increased within 20 minutes of TCC assembly.
    • Complement activation modulated cdk2 and cdk4/cyclin D2 activity, promoting G1/S transition.
    • Sublytic TCC significantly reduced spontaneous OLG apoptotic cell death.

    Conclusions:

    • Sublytic TCC activate the JNK pathway, leading to c-jun induction and subsequent OLG cell cycle entry.
    • Complement-mediated stimulation of OLG proliferation and reduced apoptosis may be a protective mechanism during inflammation.
    • These findings reveal a novel role for complement in regulating OLG fate and function in the context of CNS inflammation.