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Reduction in programmed cell death and improvement in functional outcome of transient focal cerebral ischemia after administration of granulocyte-macrophage colony-stimulating factor in rats. Laboratory investigation

Authors
 TaeHo Kong  ;  Jung-Kyoung Choi  ;  Hyeonseon Park  ;  Byung Hyune Choi  ;  Brian Jeffrey Snyder  ;  Shefqat Bukhari  ;  Na-Kyeong Kim  ;  Xian Huang  ;  So Ra Park  ;  Hyung Chun Park  ;  Yoon Ha 
Citation
 JOURNAL OF NEUROSURGERY, Vol.111(1) : 155-163, 2009 
Journal Title
JOURNAL OF NEUROSURGERY
ISSN
 0022-3085 
Issue Date
2009
MeSH
Animals ; Apoptosis/drug effects* ; Cell Line, Tumor ; Cerebral Infarction/drug therapy ; Cerebral Infarction/metabolism ; Cerebral Infarction/pathology ; Disease Models, Animal ; Gene Expression/drug effects ; Glutamic Acid/metabolism ; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology* ; Humans ; Ischemic Attack, Transient/drug therapy* ; Ischemic Attack, Transient/metabolism ; Ischemic Attack, Transient/pathology* ; Leukocytes, Mononuclear/drug effects ; Male ; Mesenchymal Stromal Cells/drug effects ; Motor Activity/drug effects ; Neuroblastoma ; Neuroprotective Agents/pharmacology* ; Neurotoxins/metabolism ; RNA, Messenger/metabolism ; Rats ; Rats, Sprague-Dawley ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/genetics ; Receptors, Granulocyte-Macrophage Colony-Stimulating Factor/metabolism ; Recovery of Function/drug effects '
Keywords
cerebral ischemia ; neuroprotection ; granulocyte-macrophage colony-stimulating factor
Abstract
OBJECT: Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a potent hematopoietic growth factor that both enhances the survival and drives the differentiation and proliferation of myeloid lineage cells. Recent studies have suggested that GM-CSF has a neuroprotective effect against CNS injury. In this paper, the authors investigated the neuroprotective effect of GM-CSF on neuron survival and locomotor behavior in a rat model of focal cerebral ischemic injury.

MATERIALS: To understand its neuroprotective effect in vitro, GM-CSF was administered to a glutamate-induced excitotoxicity neuronal injury cell culture model that mimics the pathophysiology of focal hypoxic cerebral injury. In the animal study, the authors prepared a rat focal cerebral ischemia model by occluding the unilateral middle cerebral artery. They then examined the effects of GM-CSF administration on changes in infarct volume, apoptosis-related gene expression, and improvement in locomotor behavior.

RESULTS: Treatment with GM-CSF significantly increased cell viability in a cell culture model of glutamate-induced neuronal injury. Furthermore, in vivo administration of GM-CSF at 60 microg/kg body weight daily for 5 consecutive days beginning immediately after injury decreased infarction volume, altered the expression of several apoptosis-related genes (Bcl-2, Bax, caspase 3, and p53), and improved locomotor behavior in the focal cerebral ischemia model.

CONCLUSIONS: The GM-CSF had neuroprotective effects in in vitro and in vivo experiments and resulted in decreased infarction volume and improved locomotor behavior. Although the specific mechanism involved in stroke recovery was not fully elucidated as it was not the primary focus of this study, administration of GM-CSF appeared to decrease the extent of neuronal apoptosis by modulating the expression of several apoptosis-related genes such as Bcl-2, Bax, caspase 3, and p53. Further investigations are necessary to better understand the role of GM-CSF on neural regeneration during the recovery phase of a stroke, as well as the intracellular signal transduction pathways that mediate neuroprotection.
Full Text
http://thejns.org/doi/abs/10.3171/2008.12.JNS08172
DOI
10.3171/2008.12.JNS08172
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Neurosurgery (신경외과학교실) > 1. Journal Papers
Yonsei Authors
Ha, Yoon(하윤)
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/103901
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