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Expression pattern of the transcription factor Olig2 in response to brain injuries: implications for neuronal repair.

Abstract
Despite the presence of neural stem cells and ongoing neurogenesis in some regions of the adult mammalian brain, neurons are not replaced in most brain regions after injury. With the aim to unravel factors contributing to the failure of neurogenesis in the injured cerebral cortex, we examined the expression of cell fate determinants after acute brain injuries, such as stab wound or focal ischemia, and in a model of chronic amyloid deposition. Although none of the neurogenic factors, such as Pax6, Mash1, Ngn2, was detected in the injured parenchyma, we observed a strong up-regulation of the bHLH transcription factor Olig2, but not Olig1, upon acute and chronic injury. To examine the function of Olig2 in brain lesion, we injected retroviral vectors containing a dominant negative form of Olig2 into the lesioned cortex 2 days after a stab wound. Antagonizing Olig2 function resulted in a significant number of infected cells generating immature neurons that were not observed after injection of the control virus. These data, therefore, imply Olig2 as a repressor of neurogenesis in cells reacting to brain injury and open innovative perspectives toward evoking endogenous neuronal repair.
AuthorsAnnalisa Buffo, Milan R Vosko, Dilek Ertürk, Gerhard F Hamann, Mathias Jucker, David Rowitch, Magdalena Götz
JournalProceedings of the National Academy of Sciences of the United States of America (Proc Natl Acad Sci U S A) Vol. 102 Issue 50 Pg. 18183-8 (Dec 13 2005) ISSN: 0027-8424 [Print] United States
PMID16330768 (Publication Type: Comparative Study, Journal Article, Research Support, Non-U.S. Gov't)
Chemical References
  • Basic Helix-Loop-Helix Transcription Factors
  • Nerve Tissue Proteins
  • Olig2 protein, mouse
  • Bromodeoxyuridine
Topics
  • Animals
  • Basic Helix-Loop-Helix Transcription Factors (metabolism)
  • Bromodeoxyuridine
  • Cell Proliferation
  • Cerebral Cortex (injuries, metabolism, pathology)
  • Genetic Vectors
  • Mice
  • Mice, Transgenic
  • Nerve Regeneration (physiology)
  • Nerve Tissue Proteins (metabolism)
  • Neurons (physiology)
  • Plaque, Amyloid (pathology)
  • Retroviridae
  • Up-Regulation

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