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Editors Selection IGR 11-3
Basic Research: Granulocyte-colony stimulating factor and neuroprotection
Comment by Neville Osborne on:
24387 Both systemic and local application of Granulocyte-colony stimulating factor (G-CSF) is neuroprotective after retinal ganglion cell axotomy, Frank T; Schlachetzki JCM; Goricke B et al., BMC Neuroscience, 2009; 10: 49
Granulocyte colony-stimulating factor (G-CSF), also known as colonystimulating factor 3 (CSF-3), is a colony-stimulating factor hormone that functions as a glycoprotein, growth factor or cytokine. It is produced by a number of different tissues to stimulate the production of bone marrow granulocytes and stem cells. It also stimulates the survival, proliferation, differentiation, and function of neutrophil precursors and mature neutrophils by actions that involve various signal transduction pathways. It is used in the clinic to treat patients with chemotherapyinduced neutropenia and therefore has a tested safety profile. The study by Frank et al. (1229) impressively provides evidence for the first time that G-CSF might be considered as a future treatment option for neurodegenerative diseases like glaucoma. They show that G-CSF receptor immunoreactivity is specifically located to rat ganglion cell perikarya and by implication their activation by G-CSF enhances the survival of the neurones. They show that subcutaneous or intravitreal injection of G-CSF by different regimes enhanced the survival of retinal ganglion cells in the rat retina where ganglion cell death was elicited by optic nerve axotomy.
G-CSF receptor immunoreactivity is specifically located to rat ganglion cell perikarya and by implication their activation by G-CSF enhances the survival of the neurones
Importantly, this occurred even if G-CSF was injected subcutaneously two hours after optic nerve transaction. Moreover, evidence is provided to suggest that G-CSF might elicit some of its neuroprotective action by a direct action on retinal ganglion cell G-CSF receptors. To do this, the authors used purified rat ganglion cells maintained in culture and triggered apoptosis by neurotrophic factor withdrawal. Here like in the animal studies, G-CSF significantly attenuated ganglion cell death. The overall conclusion from this manuscript is that G-CSF is a potent neuroprotective agent for ganglion cells of the retina. Its potential use in diseases like glaucoma where ganglion cells are primarily affected is therefore one that requires consideration. However, since G-CSF has multiple additional functions not directly related to neuroprotection its continuous use to treat glaucoma where the disease is often manageable might be a matter of concern.
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