論文

査読有り
2015年3月

Involvement of TRPM2 in a wide range of inflammatory and neuropathic pain mouse models

JOURNAL OF PHARMACOLOGICAL SCIENCES
  • Kanako So
  • ,
  • Kayo Haraguchi
  • ,
  • Kayoko Asakura
  • ,
  • Koichi Isami
  • ,
  • Shinya Sakimoto
  • ,
  • Hisashi Shirakawa
  • ,
  • Yasuo Mori
  • ,
  • Takayuki Nakagawa
  • ,
  • Shuji Kaneko

127
3
開始ページ
237
終了ページ
243
記述言語
英語
掲載種別
研究論文(学術雑誌)
DOI
10.1016/j.jphs.2014.10.003
出版者・発行元
JAPANESE PHARMACOLOGICAL SOC

Recent evidence suggests a role of transient receptor potential melastatin 2 (TRPM2) in immune and inflammatory responses. We previously reported that TRPM2 deficiency attenuated inflammatory and neuropathic pain in some pain mouse models, including formalin-or carrageenan-induced inflammatory pain, and peripheral nerve injury-induced neuropathic pain models, while it had no effect on the basal mechanical and thermal nociceptive sensitivities. In this study, we further explored the involvement of TRPM2 in various pain models using TRPM2-knockout mice. There were no differences in the chemo-nociceptive behaviors evoked by intraplantar injection of capsaicin or hydrogen peroxide between wildtype and TRPM2-knockout mice, while acetic acid-induced writhing behavior was significantly attenuated in TRPM2-knockout mice. In the postoperative incisional pain model, no difference in mechanical allodynia was observed between the two genotypes. By contrast, mechanical allodynia in the monosodium iodoacetate-induced osteoarthritis pain model and the experimental autoimmune encephalomyelitis model were significantly attenuated in TRPM2-knockout mice. Furthermore, mechanical allodynia in paclitaxel-induced peripheral neuropathy and streptozotocin-induced painful diabetic neuropathy models were significantly attenuated in TRPM2-knockout mice. Taken together, these results suggest that TRPM2 plays roles in a wide range of pathological pain models based on peripheral and central neuroinflammation, rather than physiological nociceptive pain. (C) 2015 The Authors. Production and hosting by Elsevier B.V. on behalf of Japanese Pharmacological Society. This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).

リンク情報
DOI
https://doi.org/10.1016/j.jphs.2014.10.003
PubMed
https://www.ncbi.nlm.nih.gov/pubmed/25837919
Web of Science
https://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=JSTA_CEL&SrcApp=J_Gate_JST&DestLinkType=FullRecord&KeyUT=WOS:000353118900001&DestApp=WOS_CPL
ID情報
  • DOI : 10.1016/j.jphs.2014.10.003
  • ISSN : 1347-8613
  • eISSN : 1347-8648
  • PubMed ID : 25837919
  • Web of Science ID : WOS:000353118900001

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