کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8350960 | 1541860 | 2014 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
The inhibitor of calcium/calmodulin-dependent protein kinase II KN93 attenuates bone cancer pain via inhibition of KIF17/NR2B trafficking in mice
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کلمات کلیدی
NMDARPWMTKN93p-CaMKIINR2BCaMKIICREBpaw withdrawal mechanical threshold - آستانه مکانیکی برداشتن پاi.t - آی تیintrathecal - اینتراکتالanalysis of variance - تحلیل واریانسANOVA - تحلیل واریانس Analysis of variancelong-term potentiation - تقویت درازمدتLTP - تقویت طولانی مدت یا LTP bone cancer pain - درد سرطان استخوانsubstantia gelatinosa - محرک ژلاتینوزاcAMP-response element-binding protein - پروتئین متصل به عنصر cAMP-responsecalcium/calmodulin-dependent protein kinase II - پروتئین کیناز II وابسته به کلسیم / کالودولینN-methyl-d-aspartate receptor - گیرنده N-methyl-d-aspartate
موضوعات مرتبط
علوم زیستی و بیوفناوری
بیوشیمی، ژنتیک و زیست شناسی مولکولی
زیست شیمی
پیش نمایش صفحه اول مقاله
چکیده انگلیسی
The N-methyl-d-aspartate receptor (NMDAR) containing subunit 2B (NR2B) is critical for the regulation of nociception in bone cancer pain, although the precise molecular mechanisms remain unclear. KIF17, a kinesin motor, plays a key role in the dendritic transport of NR2B. The up-regulation of NR2B and KIF17 transcription results from an increase in phosphorylated cAMP-response element-binding protein (CREB), which is activated by calcium/calmodulin-dependent protein kinase II (CaMKII). In this study, we hypothesized that CaMKII-mediated KIF17/NR2B trafficking may contribute to bone cancer pain. Osteosarcoma cells were implanted into the intramedullary space of the right femurs of C3H/HeJ mice to induce progressive bone cancer-related pain behaviors. The expression of spinal t-CaMKII, p-CaMKII, NR2B and KIF17 after inoculation was also evaluated. These results showed that inoculation of osteosarcoma cells induced progressive bone cancer pain and resulted in a significant up-regulation of p-CaMKII, NR2B and KIF17 expression after inoculation. Intrathecal administration of KN93, a CaMKII inhibitor, down-regulated these three proteins and attenuated bone cancer pain in a dose- and time-dependent manner. These findings indicated that CaMKII-mediated KIF17/NR2B trafficking may contribute to bone cancer pain, and inhibition of CaMKII may be a useful alternative or adjunct therapy for relieving cancer pain.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Pharmacology Biochemistry and Behavior - Volume 124, September 2014, Pages 19-26
Journal: Pharmacology Biochemistry and Behavior - Volume 124, September 2014, Pages 19-26
نویسندگان
Yue Liu, Ying Liang, Bailing Hou, Ming Liu, Xuli Yang, Chenglong Liu, Juan Zhang, Wei Zhang, Zhengliang Ma, Xiaoping Gu,