Format

Send to

Choose Destination
See comment in PubMed Commons below
PLoS One. 2012;7(8):e43338. doi: 10.1371/journal.pone.0043338. Epub 2012 Aug 29.

Interferon gamma and sonic hedgehog signaling are required to dysregulate murine neural stem/precursor cells.

Author information

  • 1Department of Neurology, Heinrich-Heine-University, Düsseldorf, North Rhine-Westphalia, Germany. Janine.Walter@googlemail.com

Abstract

BACKGROUND:

The pro-inflammatory cytokine interferon gamma (IFNγ), a key player in various neurological diseases, was recently shown to induce a dysregulated phenotype in neural stem/precursor cells (NSPCs) that is characterized by the simultaneous expression of glial and neuronal markers and irregular electrophysiological properties. Thus far, the mechanisms of this phenomenon have remained unclear.

METHODOLOGY/PRINCIPAL FINDINGS:

To determine if binding of the signal transducers and activators of transcription (Stat 1) to the sonic hedgehog (SHH) promoter is important for this phenomenon to occur, chromatin immunoprecipitation and pharmacological inhibition studies were performed. We report here that the activation of both the Stat 1 and SHH pathways is necessary to elicit the dysregulated phenotype.

CONCLUSIONS/SIGNIFICANCE:

Thus, blocking these pathways might preserve functional differentiation of NSPCs under inflammatory conditions leading to more effective regeneration.

[PubMed - indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Public Library of Science Icon for PubMed Central
    Loading ...
    Write to the Help Desk