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Open Access Highly Accessed Research article

Both systemic and local application of Granulocyte-colony stimulating factor (G-CSF) is neuroprotective after retinal ganglion cell axotomy

Tobias Frank1, Johannes CM Schlachetzki1, Bettina Göricke12, Katrin Meuer1, Gundula Rohde12, Gunnar PH Dietz123, Mathias Bähr12, Armin Schneider4 and Jochen H Weishaupt12*

  • * Corresponding author: Jochen H Weishaupt jweisha@gwdg.de

  • † Equal contributors

Author Affiliations

1 Department of Neurology, University Medical Center Göttingen, Robert-Koch-Strasse 40, 37075 Göttingen, Germany

2 DFG-Research Center for Molecular Physiology of the Brain (CMPB), Humboldtallee 23, Göttingen, Germany

3 H Lundbeck A/S, 2500 Valby, Denmark

4 Sygnis Bioscience, Im Neuenheimer Feld 515, 69120 Heidelberg, Germany

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BMC Neuroscience 2009, 10:49  doi:10.1186/1471-2202-10-49

Published: 14 May 2009

Abstract

Background

The hematopoietic Granulocyte-Colony Stimulating Factor (G-CSF) plays a crucial role in controlling the number of neutrophil progenitor cells. Its function is mediated via the G-CSF receptor, which was recently found to be expressed also in the central nervous system. In addition, G-CSF provided neuroprotection in models of neuronal cell death. Here we used the retinal ganglion cell (RGC) axotomy model to compare effects of local and systemic application of neuroprotective molecules.

Results

We found that the G-CSF receptor is robustly expressed by RGCs in vivo and in vitro. We thus evaluated G-CSF as a neuroprotectant for RGCs and found a dose-dependent neuroprotective effect of G-CSF on axotomized RGCs when given subcutaneously. As stem stell mobilization had previously been discussed as a possible contributor to the neuroprotective effects of G-CSF, we compared the local treatment of RGCs by injection of G-CSF into the vitreous body with systemic delivery by subcutaneous application. Both routes of application reduced retinal ganglion cell death to a comparable extent. Moreover, G-CSF enhanced the survival of immunopurified RGCs in vitro.

Conclusion

We thus show that G-CSF neuroprotection is at least partially independent of potential systemic effects and provide further evidence that the clinically applicable G-CSF could become a treatment option for both neurodegenerative diseases and glaucoma.