G-CSF administration is neuroprotective following transient cerebral ischemia even in the absence of a functional NOS-2 gene |
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Authors: | Claire L Gibson Philip MW Bath and Sean P Murphy |
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Institution: | 1Institute of Neuroscience, University of Nottingham, Nottingham, UK;2School of Psychology, University of Leicester, Leicester, UK |
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Abstract: | Granulocyte colony-stimulating factor (G-CSF) is a candidate neuroprotective factor following cerebral ischemia. To determine whether G-CSF acts partly through the inhibition of nitric oxide synthase (NOS)-2 expression, we administered G-CSF to male NOS-2−/− mice after cerebral ischemia. Although male NOS-2−/− mice exhibit resistance to the gross effects of cerebral ischemia, they display neuronal loss and skilled motor deficits following cerebral ischemia. Administration of G-CSF during reperfusion reduced motor deficit and neuronal loss. Thus, G-CSF is still effective in NOS-2 gene-deficient mice, suggesting that part of the mechanism of action is independent of NOS-2. |
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Keywords: | focal ischemia G-CSF neuroprotection nitric oxide NOS-2 |
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