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学科主题基础医学
Potentiation of the P2X3 ATP receptor by PAR-2 in rat dorsal root ganglia neurons, through protein kinase-dependent mechanisms, contributes to inflammatory pain
Wang, Shenglan1,2,3; Dai, Yi1,3; Kobayashi, Kimiko1,3; Zhu, Wanjun3; Kogure, Yoko1,3; Yamanaka, Hiroki3; Wan, You4; Zhang, Wensheng2; Noguchi, Koichi3
关键词inflammatory pain protease-activated receptor 2 protein kinase A protein kinase C P2X3
刊名EUROPEAN JOURNAL OF NEUROSCIENCE
2012-08-01
DOI10.1111/j.1460-9568.2012.08142.x
36期:3页:2293-2301
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Neurosciences
研究领域[WOS]Neurosciences & Neurology
关键词[WOS]ACTIVATED RECEPTOR-2 ; P2X(3) RECEPTORS ; PROTEASE-ACTIVATED-RECEPTOR-2 SENSITIZES ; SENSORY NEURONS ; HYPERALGESIA ; NOCICEPTION ; MICE ; PHOSPHORYLATION ; PEPTIDES ; CURRENTS
英文摘要

Proinflammatory agents trypsin and mast cell tryptase cleave and activate protease-activated receptor-2 (PAR-2), which is expressed on sensory nerves and causes neurogenic inflammation. P2X3 is a subtype of the ionotropic receptors for adenosine 5′-triphosphate (ATP), and is mainly localized on nociceptors. Here, we show that a functional interaction of the PAR-2 and P2X3 in primary sensory neurons could contribute to inflammatory pain. PAR-2 activation increased the P2X3 currents evoked by a, beta, methylene ATP in dorsal root ganglia (DRG) neurons. Application of inhibitors of either protein kinase C (PKC) or protein kinase A (PKA) suppressed this potentiation. Consistent with this, a PKC or PKA activator mimicked the PAR-2-mediated potentiation of P2X3 currents. In the in vitro phosphorylation experiments, application of a PAR-2 agonist failed to establish phosphorylation of the P2X3 either on the serine or the threonine site. In contrast, application of a PAR-2 agonist induced trafficking of the P2X3 from the cytoplasm to the plasma membrane. These findings indicate that PAR-2 agonists may potentiate the P2X3, and the mechanism of this potentiation is likely to be a result of translocation, but not phosphorylation. The functional interaction between P2X3 and PAR-2 was also confirmed by detection of the a, beta, methylene-ATP-evoked extracellular signal-regulated kinases (ERK) activation, a marker of neuronal signal transduction in DRG neurons, and pain behavior. These results demonstrate a functional interaction of the protease signal with the ATP signal, and a novel mechanism through which protease released in response to tissue inflammation might trigger the sensation to pain through P2X3 activation.

语种英语
WOS记录号WOS:000307167400003
项目编号20602017 ; 22S014 ; S0901048 ; 2012ZX09103-201
资助机构KAKENHI ; Hyogo Science and Technology Association ; Research Basis Formation Supporting Project for Private University ; State Key Laboratory of Earth Surface Processes and Resource Ecology ; Key New Drug Creation and Development Programme of China
引用统计
被引频次:13[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
版本出版稿
条目标识符http://ir.bjmu.edu.cn/handle/400002259/59492
专题北京大学基础医学院_神经生物学系
北京大学基础医学院
作者单位1.Hyogo Univ Hlth Sci, Sch Pharm, Dept Pharm, Kobe, Hyogo 6508530, Japan
2.Beijing Normal Univ, State Key Lab Earth Surface Proc & Resource Ecol, Beijing 100088, Peoples R China
3.Hyogo Coll Med, Dept Anat & Neurosci, Nishinomiya, Hyogo 6638501, Japan
4.Peking Univ, Neurosci Res Inst, Sch Basic Med Sci, Beijing 100083, Peoples R China
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Wang, Shenglan,Dai, Yi,Kobayashi, Kimiko,et al. Potentiation of the P2X3 ATP receptor by PAR-2 in rat dorsal root ganglia neurons, through protein kinase-dependent mechanisms, contributes to inflammatory pain[J]. EUROPEAN JOURNAL OF NEUROSCIENCE,2012,36(3):2293-2301.
APA Wang, Shenglan.,Dai, Yi.,Kobayashi, Kimiko.,Zhu, Wanjun.,Kogure, Yoko.,...&Noguchi, Koichi.(2012).Potentiation of the P2X3 ATP receptor by PAR-2 in rat dorsal root ganglia neurons, through protein kinase-dependent mechanisms, contributes to inflammatory pain.EUROPEAN JOURNAL OF NEUROSCIENCE,36(3),2293-2301.
MLA Wang, Shenglan,et al."Potentiation of the P2X3 ATP receptor by PAR-2 in rat dorsal root ganglia neurons, through protein kinase-dependent mechanisms, contributes to inflammatory pain".EUROPEAN JOURNAL OF NEUROSCIENCE 36.3(2012):2293-2301.
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