Abstract
In the present study, we evaluated the potential neuroprotective effect of granulocyte colony-stimulating factor (G-CSF), a hematopoietic growth factor in two different culture models in which dopaminergic (DA) neurons die selectively: first, in a culture model in which death of DA neurons occurs spontaneously and second, in a toxin-based paradigm, the in vitro 1-methyl-4-phenylpyridinium model of PD. In neither of the two models, a treatment with G-CSF, could prevent or halt the progressive neurodegeneration. However, we cannot rule out that G-CSF might exert neuroprotective or even deleterious effects in in vivo models of PD, based on the significant increase in the number of microglial cells observed after G-CSF treatment.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
MeSH terms
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1-Methyl-4-phenylpyridinium / toxicity
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Analysis of Variance
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Animals
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CD11b Antigen / metabolism
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Cell Count / methods
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Cell Death / drug effects*
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Cell Proliferation / drug effects
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Cells, Cultured
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Cytarabine / toxicity
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Dopamine / metabolism*
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Dose-Response Relationship, Drug
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Drug Interactions
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Embryo, Mammalian
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Glial Fibrillary Acidic Protein / metabolism
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Granulocyte Colony-Stimulating Factor / pharmacology*
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Herbicides / toxicity
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Immunohistochemistry / methods
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Microglia / drug effects
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Microglia / metabolism
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Microtubule-Associated Proteins / metabolism
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Neurons / cytology
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Neurons / drug effects*
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Neurons / metabolism
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Rats
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Thymidine / pharmacokinetics
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Tritium / pharmacokinetics
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Tyrosine 3-Monooxygenase / metabolism
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Vimentin / metabolism
Substances
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CD11b Antigen
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Glial Fibrillary Acidic Protein
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Herbicides
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MAP2 protein, rat
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Microtubule-Associated Proteins
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Vimentin
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Cytarabine
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Tritium
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Granulocyte Colony-Stimulating Factor
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Tyrosine 3-Monooxygenase
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1-Methyl-4-phenylpyridinium
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Thymidine
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Dopamine