Sensitization of ASIC3 by proteinase-activated receptor 2 signaling contributes to acidosis-induced nociception
作者: Jing WuTing-Ting LiuYi-Mei ZhouChun-Yu QiuPing RenMing JiaoWang-Ping Hu
作者单位: 1Hubei University of Science and Technology
刊名: Journal of Neuroinflammation, 2017, Vol.14 (1)
来源数据库: Springer Nature Journal
DOI: 10.1186/s12974-017-0916-4
关键词: Proteinase-activated receptor 2Acid-sensing ion channel 3Proton-gated currentNociceptionDorsal root ganglion neuron
英文摘要: Tissue acidosis and inflammatory mediators play critical roles in pain. Pro-inflammatory agents trypsin and tryptase cleave and activate proteinase-activated receptor 2 (PAR2) expressed on sensory nerves, which is involved in peripheral mechanisms of inflammation and pain. Extracellular acidosis activates acid-sensing ion channel 3 (ASIC3) to trigger pain sensation. Here, we show that a functional interaction of PAR2 and ASIC3 could contribute to acidosis-induced nociception.
原始语种摘要: Tissue acidosis and inflammatory mediators play critical roles in pain. Pro-inflammatory agents trypsin and tryptase cleave and activate proteinase-activated receptor 2 (PAR2) expressed on sensory nerves, which is involved in peripheral mechanisms of inflammation and pain. Extracellular acidosis activates acid-sensing ion channel 3 (ASIC3) to trigger pain sensation. Here, we show that a functional interaction of PAR2 and ASIC3 could contribute to acidosis-induced nociception.
全文获取路径: Springer Nature  (合作)
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影响因子:4.351 (2012)

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关键词翻译
关键词翻译
  • nociception 伤害感受
  • proteinase 朊酶
  • induced 感应的
  • receptor 接受体
  • acidosis 酸中毒
  • activated 激化了的
  • ASIC application specific integrated circuit
  • inflammatory 激怒的
  • signaling 发信号
  • contribute 贡献