کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6278171 | 1295800 | 2009 | 11 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Neuroprotection of preconditioning against ischemic brain injury in rat hippocampus through inhibition of the assembly of GluR6-PSD95-mixed lineage kinase 3 signaling module via nuclear and non-nuclear pathways
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کلمات کلیدی
JnkTris-buffered saline with 0.1% Tween 20activator-protein 1GluR6pNPPJNK3MLK3PMSFNMDAN-methyl-d-aspartateTBSTPSD-95AP-1c-Jun N-terminal kinase - C-Jun N-terminal kinaseDMSO - DMSOI/R - I / Rp-nitrophenyl phosphate - p-نیترفنیل فسفاتischemia/reperfusion - ایسکمی / رپرفیوژنCerebral ischemia - ایسکمی مغزیc-Jun - جون ژوئنDimethyl sulfoxide - دیمتیل سولفواکسیدmixed lineage kinase 3 - رده بندی کیناز 3 مخلوطFas Ligand - فاس لیگاندFasL - فاسدphenylmethylsulfonyl fluoride - فنیل متیل سولفونیل فلورایدPreconditioning - پیش شرط بندیKainite - کاینیت
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
Our previous studies showed that the assembly of the GluR6-PSD95-mixed lineage kinase 3 (MLK3) signaling module played an important role in rat ischemic brain injury. In this study, we aimed to elucidate whether ischemic preconditioning could downregulate the assembly of the GluR6-PSD95-MLK3 signaling module and suppress the activation of MLK3, MKK4/7, and c-Jun N-terminal kinase (JNK). As a result, ischemic preconditioning could not only inhibit the assembly of the GluR6-PSD95-MLK3 signaling module, diminish the phosphorylation of the transcription factor c-Jun, downregulate Fas ligand expression, attenuate the phosphorylation of 14-3-3 and Bcl-2 and the translocation of Bax to mitochondria, but also increase the release of cytochrome c and the activation of caspase-3. In contrast, both GluR6 antisense ODNs (oligodeoxynucleotides) and 6,7,8,9-tetrahydro-5-nitro-1 H-benz[g]indole-2,3-dione-3-oxime (NS102), an antagonist of GluR6 receptor, prevented the above effects of preconditioning, which shows that suppressing the expression of GluR6 or inhibiting GluR6 activity contributes negatively to preconditioning-induced ischemia tolerance. Taken together, our results indicate that preconditioning can inhibit the over-assembly of the GluR6-PSD95-MLK3 signaling module and the JNK3 activation. GluR6 subunit-containing kainite receptors play an important role in the preconditioning-induced neuronal survival and provide new insight into stroke therapy.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 161, Issue 2, 30 June 2009, Pages 370-380
Journal: Neuroscience - Volume 161, Issue 2, 30 June 2009, Pages 370-380
نویسندگان
Y. Du, C. Li, W.-W. Hu, Y.-J. Song, G.-Y. Zhang,