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Title: Neuroprotection against ischaemic brain injury by a GluR6-9c peptide containing the TAT protein transduction sequence
Author: Pei, DS ; Wang, XT ; Liu, Y ; Sun, YF ; Guan, QH ; Wang, W ; Yan, JZ ; Zong, YY ; Xu, TL(徐天乐) ; Zhang, GY
Source: BRAIN
Issued Date: 2006
Volume: 129, Issue:pt 2, Pages:465-479
Keyword: cerebral ischaemia ; glutamate receptor 6 (GluR6) ; mixed lineage kinase-3 (MLK3) ; c-Jun N-terminal kinase (JNK) ; Tat protein ; RECEPTOR-MEDIATED RESPONSES ; PROGRAMMED CELL-DEATH ; C-JUN ; CEREBRAL-ISCHEMIA ; GLUR6-DEFICIENT MICE ; HIPPOCAMPAL-NEURONS ; KINASE ACTIVATION ; KAINATE RECEPTORS ; RAT HIPPOCAMPUS ; MIXED LINEAGE
Subject: Neurosciences & Neurology
Corresponding Author: Zhang, GY (reprint author), Xuzhou Med Coll, Res Ctr Biochem & Mol Biol, 84 W Huaihai Rd, Xuzhou 221002, Jiangsu, Peoples R China,gyzhang@xzmc.edu.cn
English Abstract: It is well documented that N-methyl-D-aspartate and alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptors play a pivotal role in ischaemic brain injury. Recent studies have shown that kainate (KA) receptors are involved in neuronal cell death induced by seizure, which is mediated by the GluR6 center dot PSD-95 center dot MLK3 signalling module and subsequent c-Jun N-terminal kinase (JNK) activation. Here we investigate whether GluR6 mediated JNK activation is correlated with ischaemic brain injury. Our results show that cerebral ischaemia followed by reperfusion can enhance the assembly of the GluR6 center dot PSD-95 center dot MLK3 signalling module and JNK activation. As a result, activated JNK can not only phosphorylate the transcription factor c-Jun and up-regulate Fas L expression but can also phosphorylate 14-3-3 and promote Bax translocation to mitochondria, increase the release of cytochrome c and increase caspase-3 activation. These results indicate that GluR6 mediated JNK activation induced by ischaemia/reperfusion ultimately results in neuronal cell death via nuclear and non-nuclear pathways. Furthermore, the peptides we constructed, Tat-GluR6-9c, show a protective role against neuronal death induced by cerebral ischaemia/reperfusion through inhibiting the GluR6 mediated signal pathway. In summary, our results indicate that the KA receptor subunit GluR6 mediated JNK activation is involved in ischaemic brain injury and provides a new approach for stroke therapy.
Indexed Type: SCI
Language: 英语
Content Type: 期刊论文
URI: http://ir.sibs.ac.cn/handle/331001/1840
Appears in Collections:神经所(总)_期刊论文

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Recommended Citation:
Pei, DS; Wang, XT; Liu, Y; Sun, YF; Guan, QH; Wang, W; Yan, JZ; Zong, YY; Xu, TL; Zhang, GY.Neuroprotection against ischaemic brain injury by a GluR6-9c peptide containing the TAT protein transduction sequence,BRAIN,2006,129():465-479
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