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rdf:type |
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lifeskim:mentions |
umls-concept:C0037083,
umls-concept:C0205374,
umls-concept:C0205421,
umls-concept:C0332206,
umls-concept:C0392756,
umls-concept:C0521390,
umls-concept:C0917798,
umls-concept:C1336644,
umls-concept:C1710082,
umls-concept:C1749467,
umls-concept:C1883709,
umls-concept:C2348867
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pubmed:issue |
2
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pubmed:dateCreated |
2010-6-14
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pubmed:abstractText |
Mechanisms underlying delayed selective neuronal death after global cerebral ischemia remain to be clarified. Here, we report a critical role for tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) in the pathogenesis of cerebral ischemia. C57BL/6j mice were subjected to transient global brain ischemia. RT-PCR and immunohistochemistry showed that the expression of TRAIL and DR5 was upregulated following transient ischemia-reperfusion. Dual immunofluorescence analysis indicated that TRAIL expression was significantly more pronounced in astrocytes and activated microglia/macrophages, whereas DR5 expression was more pronounced in neurons, which had a good correlation with the distribution of apoptotic cells. Treatment with soluble DR5 reduced ischemic cell death after transient global ischemia through blocking the interaction of endogenous TRAIL with DR5. These results indicate that TRAIL plays a deleterious role in the pathogenesis of delayed neuronal damage after global cerebral ischemia and inhibition of TRAIL function in the brain may represent a novel neuroprotective strategy to treat ischemic stroke.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Aug
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pubmed:issn |
1095-953X
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pubmed:author |
pubmed-author:ChenYouhai HYH,
pubmed-author:LiangXiaohongX,
pubmed-author:LiuKejingK,
pubmed-author:LiuYugangY,
pubmed-author:MaXuelianX,
pubmed-author:OnoH MHM,
pubmed-author:SunWenshengW,
pubmed-author:WangLimeiL,
pubmed-author:WeiXinbingX,
pubmed-author:YangMingfengM,
pubmed-author:ZhouZhiqiangZ
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pubmed:issnType |
Electronic
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pubmed:volume |
39
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
138-47
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pubmed:meshHeading |
pubmed-meshheading:20359534-Animals,
pubmed-meshheading:20359534-Apoptosis,
pubmed-meshheading:20359534-Brain,
pubmed-meshheading:20359534-DNA Fragmentation,
pubmed-meshheading:20359534-Disease Models, Animal,
pubmed-meshheading:20359534-Gene Expression Regulation,
pubmed-meshheading:20359534-Glial Fibrillary Acidic Protein,
pubmed-meshheading:20359534-In Situ Nick-End Labeling,
pubmed-meshheading:20359534-Ischemic Attack, Transient,
pubmed-meshheading:20359534-Male,
pubmed-meshheading:20359534-Mice,
pubmed-meshheading:20359534-Mice, Inbred C57BL,
pubmed-meshheading:20359534-Neural Cell Adhesion Molecules,
pubmed-meshheading:20359534-Neurons,
pubmed-meshheading:20359534-Receptors, TNF-Related Apoptosis-Inducing Ligand,
pubmed-meshheading:20359534-Signal Transduction,
pubmed-meshheading:20359534-Statistics, Nonparametric,
pubmed-meshheading:20359534-TNF-Related Apoptosis-Inducing Ligand
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pubmed:year |
2010
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pubmed:articleTitle |
Blocking TRAIL-DR5 signaling with soluble DR5 reduces delayed neuronal damage after transient global cerebral ischemia.
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pubmed:affiliation |
Department of Physiology, Shandong University School of Medicine, 44#, Wenhua Xi Road, Jinan, Shandong, 250012, P.R. China. cuimin@sdu.edu.cn <cuimin@sdu.edu.cn>
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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