Email updates

Keep up to date with the latest news and content from BMC Neuroscience and BioMed Central.

This article is part of the supplement: Annual Meeting of the Study Group Neurochemistry. International Conference of the Gesellschaft für Biochemie und Molekularbiologie 2006 (GBM 2006): Molecular pathways in health and disease of the nervous system

Open Access Poster presentation

Tumor necrosis factor alpha induced proliferation of adult neural stem cells is mediated via NF-κB

Darius Widera*, Ilja Mikenberg, Margitta Elvers, Christian Kaltschmidt and Barbara Kaltschmidt

  • * Corresponding author: Darius Widera

Author Affiliations

University of Witten/Herdecke, Institute for Neurobiochemistry, Witten, Germany

For all author emails, please log on.

BMC Neuroscience 2007, 8(Suppl 1):P1  doi:10.1186/1471-2202-8-S1-P1

The electronic version of this article is the complete one and can be found online at:


Published:23 March 2007

© 2007 Widera et al; licensee BioMed Central Ltd.

Poster presentation

Brain inflammation is a very complex phenomenon with several related aspects. Besides the neurodegenerative effect of inflammation, inflammatory signals exert a positive influence on neural stem cell proliferation, migration and differentiation. Large parts of the inflammatory signal transduction can be considered as an innate immune response triggered by TNF. The purpose of the present study was to investigate the signal transduction mechanisms induced by TNF.

Here we show that TNF-mediated signal transduction cascade results in increased proliferation of neural stem cells (NSCs).

TNF strongly activated the transcription factor NF-κB as showed by immunocytochemical analysis and reporter gene assays. Furthermore, TNF treatment significantly up-regulated the Cyclin D1 level, which correlated with increased proliferation of NSCs.

Since the proliferation of most tumour cells described up to date has been shown to be largely NF-κB and Cyclin D1 dependant, this study might provide a common denominator between neural stem cell and tumour cell proliferation control. Understanding of these mechanisms might be important to avoid side effects of tumor therapy (unintended killing of stem cells by NF-κB inhibition). On the other hand, understanding proliferation control of stem cells might be crucial for future therapeutic strategies.