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Terminal complement complexes induce cell cycle entry in oligodendrocytes through mitogen activated protein kinase

H Rus1, F Niculescu, T Badea

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

Immunopharmacology
|February 26, 1998
PubMed
Summary

Complement attack (C5b-9) activates mitogen-activated protein kinase (MAPK) pathways, driving oligodendrocytes (OLG) into cell cycle S phase. This study reveals MAPK

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Role of the C5b-9 complement complex in cell cycle and apoptosis.

Immunological reviews·2001

Area of Science:

  • Neuroscience
  • Immunology
  • Cell Biology

Background:

  • Oligodendrocytes (OLG) express proto-oncogenes and enter the cell cycle upon sublytic complement attack via C5b-9 assembly.
  • The role of the mitogen-activated protein kinase (MAPK) pathway in C5b-9-induced oligodendrocyte cell cycle entry requires elucidation.

Purpose of the Study:

  • To investigate whether the mitogen-activated protein kinase (MAPK) pathway mediates cell cycle induction by C5b-9 in oligodendrocytes (OLG).

Main Methods:

  • Oligodendrocytes (OLG) were treated with C5b-9 and C5b6 complement components.
  • Activation of ERK1, c-jun NH2-terminal kinases 1 (JNK1), Raf-1, and MEK1 was assessed.
  • The effect of PD098,059, a MEK1 inhibitor, on DNA synthesis and proto-oncogene mRNA expression was evaluated.
  • p70 S6 kinase activation was also measured.

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Main Results:

  • C5b-9, but not C5b6, transiently activated ERK1 and JNK1 in OLG within 20 minutes.
  • Upstream kinases Raf-1 and MEK1 were activated by C5b-9.
  • PD098,059 completely abolished C5b-9-induced DNA synthesis and partially inhibited c-fos mRNA expression.
  • p70 S6 kinase was also activated by C5b-9.

Conclusions:

  • Mitogen-activated protein kinase (MAPK) pathways play a significant role in inducing oligodendrocytes (OLG) to enter S phase from G0/G1.
  • The ERK1 pathway is crucial for C5b-9-mediated DNA synthesis in OLG.