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Granulocyte-colony stimulating factor attenuates striatal degeneration with activating survival pathways in 3-nitropropionic acid model of Huntington's disease.
Brain Res. 2008 Feb 15; 1194:130-7.BR

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.

Authors+Show Affiliations

Department of Neurology, Clinical Research Institute, Seoul National University Hospital, Seoul, South Korea.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18166168

Citation

Lee, Soon-Tae, et al. "Granulocyte-colony Stimulating Factor Attenuates Striatal Degeneration With Activating Survival Pathways in 3-nitropropionic Acid Model of Huntington's Disease." Brain Research, vol. 1194, 2008, pp. 130-7.
Lee ST, Park JE, Kim DH, et al. Granulocyte-colony stimulating factor attenuates striatal degeneration with activating survival pathways in 3-nitropropionic acid model of Huntington's disease. Brain Res. 2008;1194:130-7.
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. (2008). Granulocyte-colony stimulating factor attenuates striatal degeneration with activating survival pathways in 3-nitropropionic acid model of Huntington's disease. Brain Research, 1194, 130-7. https://doi.org/10.1016/j.brainres.2007.11.058
Lee ST, et al. Granulocyte-colony Stimulating Factor Attenuates Striatal Degeneration With Activating Survival Pathways in 3-nitropropionic Acid Model of Huntington's Disease. Brain Res. 2008 Feb 15;1194:130-7. PubMed PMID: 18166168.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Granulocyte-colony stimulating factor attenuates striatal degeneration with activating survival pathways in 3-nitropropionic acid model of Huntington's disease. AU - Lee,Soon-Tae, AU - Park,Jung-Eun, AU - Kim,Dong-Hyun, AU - Kim,Seungchan, AU - Im,Woo-Seok, AU - Kang,Lami, AU - Jung,Se Hee, AU - Kim,Min-Wook, AU - Chu,Kon, AU - Kim,Manho, Y1 - 2007/12/07/ PY - 2007/07/13/received PY - 2007/11/24/revised PY - 2007/11/27/accepted PY - 2008/1/2/pubmed PY - 2008/5/31/medline PY - 2008/1/2/entrez SP - 130 EP - 7 JF - Brain research JO - Brain Res VL - 1194 N2 - 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. SN - 0006-8993 UR - https://www.unboundmedicine.com/medline/citation/18166168/Granulocyte_colony_stimulating_factor_attenuates_striatal_degeneration_with_activating_survival_pathways_in_3_nitropropionic_acid_model_of_Huntington's_disease_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0006-8993(07)02843-0 DB - PRIME DP - Unbound Medicine ER -