<B>Object</B><P>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 studi...
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https://www.riss.kr/link?id=A107595953
2009
-
SCI,SCIE,SCOPUS
학술저널
155-163(9쪽)
0
상세조회0
다운로드다국어 초록 (Multilingual Abstract)
<B>Object</B><P>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 studi...
<B>Object</B><P>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.</P><B>Materials</B><P>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.</P><B>Results</B><P>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 μg/kg body weight daily for 5 consecutive days beginning immediately after injury decreased infarction volume, altered the expression of several apoptosis-related genes (<I>Bcl-2, Bax, caspase 3,</I> and <I>p53</I>), and improved locomotor behavior in the focal cerebral ischemia model.</P><B>Conclusions</B><P>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 <I>Bcl-2, Bax, caspase 3, and p53</I>. 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.</P>
심혈관 및 신경계 생체조직장기 개발 센터 (1355060303) / 2009 / 보건의료기술연구개발 / 김수현 / 한국과학기술연구원 / 보건복지가족부 / 1,834,000,000
인하대학교 의학전문대학원 사업단 (1345095835) / 2009 / 2단계 연구중심대학 육성(0.5) / 박인선 / 인하대학교 / 교육과학기술부 / 676,000,000
심혈관 및 신경계 생체조직장기 개발 센터 (1355060303) / 2009 / 보건의료기술연구개발 / 김수현 / 한국과학기술연구원 / 보건복지가족부 / 1,834,000,000
인하대학교 의학전문대학원 사업단 (1345095835) / 2009 / 2단계 연구중심대학 육성(0.5) / 박인선 / 인하대학교 / 교육과학기술부 / 676,000,000