کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6270691 | 1614737 | 2016 | 31 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
TRESK contributes to pain threshold changes by mediating apoptosis via MAPK pathway in the spinal cord
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کلمات کلیدی
TRESKTWLK2PJnkMIP-2DRGERKMWTMCP-1SNIc-Jun N-terminal kinase - C-Jun N-terminal kinaseMAPK - MAPKSpared nerve injury - آسیب عصب آسیب دیدهinterleukin - اینترلوکینanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancestandard error of mean - خطای استاندارد میانگینNeuropathic pain - درد نوروپاتیکthermal withdrawal latency - زمان تأخیر حرارتیnormal saline - سالین نرمالSpinal cord - طناب نخاعیmacrophage inflammatory protein-2 - ماکروفاژ التهابی پروتئین -2SEM - مدل معادلات ساختاری / میکروسکوپ الکترونی روبشیpolymerase chain reaction - واکنش زنجیره ای پلیمرازPCR - واکنش زنجیرهٔ پلیمرازMonocyte chemotactic protein-1 - پروتئین chemotactic monocyte-1mitogen-activated protein kinase - پروتئین کیناز فعال با mitogenextracellular signal-regulated kinase - کیناز تنظیم شده سیگنال خارج سلولیdorsal root ganglia - گانگلیس ریشه پشتی
موضوعات مرتبط
علوم زیستی و بیوفناوری
علم عصب شناسی
علوم اعصاب (عمومی)
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The mechanism underlying neuropathic pain (NP) is complex and has not been fully elucidated. The TWIK-related spinal cord K+ (TRESK) is the major background potassium current in dorsal root ganglia (DRG), we found that mitogen-activated protein kinase (MAPK) signal pathway were activated in spinal cord accompanied by TRESK down regulation in response to NP. Therefore, we investigated whether TRESK mediates inflammation and apoptosis by MAPK pathway in the spinal cord of NP rats. SNI rats exhibited reduced TRESK expression in DRG and spinal cord and higher sensitivity to mechanical stimuli but no effect on thermal stimuli. Intrathecal injections of TRESK overexpressing adenovirus alleviated mechanical allodynia, inhibited phosphorylation of extracellular signal-regulated kinase (ERK) and p38, and decreased inflammatory reactions and apoptosis in the spinal cords of SNI rats. Down regulation of TRESK in DRG and spinal cord was detected in normal rats after intrathecal TRESK shRNA lentivirus injection, which induced mechanical allodynia but had no effect on pain thresholds for heat stimulation. Phosphorylated ERK and p38 were increased in the spinal cord. Intrathecal injection of an ERK antagonist (PD98059) and p38 antagonist (SB203580) prevented ERK and p38 activation in the spinal cord and mechanical allodynia induced by TRESK shRNA lentivirus. In conclusion, our study clearly demonstrated an important role for TRESK in NP and that TRESK regulation contributes to pain sensitivity mediates inflammation and apoptosis by ERK and p38 MAPK signaling in the spinal cord.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Neuroscience - Volume 339, 17 December 2016, Pages 622-633
Journal: Neuroscience - Volume 339, 17 December 2016, Pages 622-633
نویسندگان
Jun Zhou, Wenjing Lin, Hongtao Chen, Youling Fan, Chengxiang Yang,