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Granulocyte-colony stimulating factor attenuates striatal degeneration with activating survival pathways in 3-nitropropionic acid model of Huntington's disease

Cited 23 time in Web of Science Cited 26 time in Scopus
Authors
Lee, S. T.; Park, J. E.; Kim, D. H.; Kim, S.; Im, W. S.; Kang, L.; Jung, S. H.; Kim, M. W.; Chu, K.; Kim, M.
Issue Date
2008-01-02
Publisher
Elsevier
Citation
Brain Res. 2008 Feb 15;1194:130-7. Epub 2007 Dec 7.
Keywords
AnimalsCorpus Striatum/drug effects/*pathologyDisease Models, AnimalDrug InteractionsGene Expression Regulation/drug effects/physiologyGranulocyte Colony-Stimulating Factor/*therapeutic useHuntington Disease/*chemically induced/*complicationsIn Situ Nick-End LabelingMale*Neurodegenerative Diseases/drug therapy/etiology/pathology*Nitro CompoundsOrganic Chemicals/diagnostic use*Propionic AcidsRatsRats, Inbred LewSignal Transduction/*drug effects/physiologyStatistics, Nonparametric
Abstract
Huntington's disease (HD) has a mitochondrial dysfunction causing the vulnerability to the excitotoxicity and activations of multiple cell death pathways. Recent evidences suggest that the hematopoietic cytokine, granulocyte-colony stimulating factor (G-CSF), exerts pleiotropic neuroprotection in acute neural injury with activating various survival pathways. Thus, we investigated whether G-CSF can modulate neurodegeneration in an HD animal model induced by 3-nitropropionic acid (3NP), which inhibits mitochondrial succinate dehydrogenase complex II. Either G-CSF (50 microg/kg/day) or saline (as vehicle) was administered intraperitoneally for 5 days with 3NP (63 mg/kg/day) continuous osmotic pump infusion into male Lewis rats. We measured motor scales (0-8) daily and sacrificed rats at 5 days. We observed that G-CSF receptors were expressed in 3NP-induced degenerating striatum. Rats treated with G-CSF showed less degree of neurologic deficits. In the G-CSF-treated rats, the striatal lesion volume measured by Nissl staining, TUNEL+ apoptotic cells, Fluorojade C+ degenerating neurons, and c-Jun+ cells were all decreased. In western blotting, G-CSF activated survival pathways including p-ERK, p-eNOS, p-STAT3, and p-Akt. In summary, G-CSF was found to have neuroprotective effects and save striatal cells through activations of survival pathways in the 3NP-induced striatal degeneration model for HD.
ISSN
0006-8993 (Print)
Language
English
URI
http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6SYR-4R98K8V-1&_user=10&_rdoc=1&_fmt=&_orig=search&_sort=d&_docanchor=&view=c&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=a4237208943899212b2792b39b036aa5

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=18166168

http://hdl.handle.net/10371/22332
DOI
https://doi.org/10.1016/j.brainres.2007.11.058
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College of Medicine/School of Medicine (의과대학/대학원)Neuroscience (뇌신경과학전공)Journal Papers (저널논문_뇌신경과학전공)
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