IL-17A activates ERK1/2 and enhances differentiation of oligodendrocyte progenitor cells

Jane M. Rodgers, Andrew P. Robinson, Elen S. Rosler, Karen Lariosa-Willingham, Rachael E. Persons, Jason C. Dugas, Stephen D. Miller*

*Corresponding author for this work

Research output: Contribution to journalArticlepeer-review

20 Scopus citations

Abstract

Inflammatory signals present in demyelinated multiple sclerosis lesions affect the reparative remyelination process conducted by oligodendrocyte progenitor cells (OPCs). Interferon-γ (IFN-γ), tumor necrosis factor-α (TNF-α), and interleukin (IL)-6 have differing effects on the viability and growth of OPCs, however the effects of IL-17A are largely unknown. Primary murine OPCs were stimulated with IL-17A and their viability, proliferation, and maturation were assessed in culture. IL-17A-stimulated OPCs exited the cell cycle and differentiated with no loss in viability. Expression of the myelin-specific protein, proteolipid protein, increased in a cerebellar slice culture assay in the presence of IL-17A. Downstream, IL-17A activated ERK1/2 within 15 min and induced chemokine expression in 2 days. These results demonstrate that IL-17A exposure stimulates OPCs to mature and participate in the inflammatory response.

Original languageEnglish (US)
Pages (from-to)768-779
Number of pages12
JournalGlia
Volume63
Issue number5
DOIs
StatePublished - May 1 2015

Keywords

  • Chemokine
  • ERK
  • Inflammation
  • Interleukin-17
  • Myelin
  • Oligodendrocyte

ASJC Scopus subject areas

  • Neurology
  • Cellular and Molecular Neuroscience

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