کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
4341892 | 1295849 | 2006 | 19 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroprotection against ischemic brain injury by a small peptide inhibitor of c-Jun N-terminal kinase (JNK) via nuclear and non-nuclear pathways
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کلمات کلیدی
TBSTJIP-1Poly-ADP-ribose-polymeraseGluR6activator-protein 1MLKMAPKKKGlutamate receptor 6SP600125PARPAP-1JnkTris-buffered saline with 0.1% Tween 20DTTPMSFJBDBSA - BSAc-Jun N-terminal kinase - C-Jun N-terminal kinasec-Jun N-terminal protein kinase - C-Jun N-terminal protein kinaseI/R - I / RMAPK - MAPKMAPK kinase - MAPK کینازMKK - MCCbovine serum albumin - آلبومین سرم گاوischemia/reperfusion - ایسکمی / رپرفیوژنcerebral ischemia/reperfusion - ایسکمی مغزی / reperfusiondithiothreitol - دیتیوتریتولFas Ligand - فاس لیگاندFasL - فاسدphenylmethylsulfonyl fluoride - فنیل متیل سولفونیل فلورایدhuman immunodeficiency virus-type 1 - نقص ایمنی بدن ویروس نوع 1HIV-1 - ویروس اچ آی وی نوع یکmitogen-activated protein kinase - پروتئین کیناز فعال با mitogenmitogen-activated protein kinase kinase kinase - پروتئین کیناز کیناز کیناز پروتئین فعال MitogenMixed-lineage kinase - کیناز مخلوط
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله

چکیده انگلیسی
Our previous studies and the others have strongly suggested that c-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in ischemic brain injury. Here we reported that Tat-JNK binding domain (JBD) of JNK-interacting protein-1 (JIP-1), a smaller 11-mer peptide corresponding to residues 153-163 of murine JIP-1 conjugated to Tat peptide, perturbed the assembly of JIP-1-JNK3 complexes, thus inhibiting the activation of JNK3 induced by ischemia/reperfusion in the vulnerable hippocampal CA1 subregion. As a result, Tat-JBD diminished the increased phosphorylation of c-Jun (a nuclear substrate of JNK) and the increased expression of Fas ligand induced by ischemia/reperfusion in the vulnerable hippocampal CA1 subregion. At the same time, through inhibiting phosphorylation of Bcl-2 (a cytosolic target of JNK) and the release of Bax from Bcl-2/Bax dimers, Tat-JBD attenuated Bax translocation to mitochondria and the release of cytochrome c induced by ischemia/reperfusion. Furthermore, the activation of caspase3 and hydrolyzation of poly-ADP-ribose-polymerase induced by brain ischemia/reperfusion were also significantly suppressed by preinfusion of the peptide Tat-JBD. Importantly, Tat-JBD showed neuroprotective effects on ischemic brain damage in vivo, and administration of the peptide after ischemia also achieved the same effects as preinfusion of the peptide did. Thus, our findings imply that Tat-JBD induced neuroprotection against ischemia/reperfusion in rat hippocampal CA1 region via inhibiting nuclear and non-nuclear pathways of JNK signaling. Taken together, these results indicate that Tat-JBD peptide provides a promising therapeutic approach for ischemic brain injury.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 139, Issue 2, 2006, Pages 609-627
Journal: Neuroscience - Volume 139, Issue 2, 2006, Pages 609-627
نویسندگان
Q.-H. Guan, D.-S. Pei, Y.-Y. Zong, T.-L. Xu, G.-Y. Zhang,