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Title: TRPM2 Contributes to Inflammatory and Neuropathic Pain through the Aggravation of Pronociceptive Inflammatory Responses in Mice.
Authors: Haraguchi, Kayo
Kawamoto, Ai
Isami, Kouichi
Maeda, Sanae
Kusano, Ayaka
Asakura, Kayoko
Shirakawa, Hisashi  kyouindb  KAKEN_id
Mori, Yasuo  kyouindb  KAKEN_id
Nakagawa, Takayuki  kyouindb  KAKEN_id
Kaneko, Shuji  kyouindb  KAKEN_id
Author's alias: 中川, 貴之
金子, 周司
原口, 佳代
Issue Date: 14-Mar-2012
Publisher: Society for Neuroscience
Citation: Haraguchi K, Kawamoto A, Isami K, Maeda S, Kusano A, Asakura K, Shirakawa H, Mori Y, Nakagawa T, Kaneko S. TRPM2 Contributes to Inflammatory and Neuropathic Pain through the Aggravation of Pronociceptive Inflammatory Responses in Mice. J Neurosci. 2012 Mar 14;32(11):3931-41.
Journal title: The Journal of neuroscience : the official journal of the Society for Neuroscience
Volume: 32
Issue: 11
Start page: 3931
End page: 3941
Abstract: Accumulating evidence suggests that neuroimmune interactions contribute to pathological pain. Transient receptor potential melastatin 2 (TRPM2) is a nonselective Ca(2+)-permeable cation channel that acts as a sensor for reactive oxygen species. TRPM2 is expressed abundantly in immune cells and is important in inflammatory processes. The results of the present study show that TRPM2 plays a crucial role in inflammatory and neuropathic pain. While wild-type and TRPM2 knock-out mice showed no difference in their basal sensitivity to mechanical and thermal stimulation, nocifensive behaviors in the formalin test were reduced in TRPM2 knock-out mice. In carrageenan-induced inflammatory pain and sciatic nerve injury-induced neuropathic pain models, mechanical allodynia and thermal hyperalgesia were attenuated in TRPM2 knock-out mice. Carrageenan-induced inflammation and sciatic nerve injury increased the expression of TRPM2 mRNA in the inflamed paw and around the injured sciatic nerve, respectively. TRPM2 deficiency diminished the infiltration of neutrophils and the production of chemokine (C-X-C motif) ligand-2 (CXCL2), a major chemokine that recruits neutrophils, but did not alter the recruitment of F4/80-positive macrophages in the inflamed paw or around the injured sciatic nerve. Microglial activation after nerve injury was suppressed in the spinal cord of TRPM2 knock-out mice. Furthermore, CXCL2 production and inducible nitric oxide synthase induction were diminished in cultured macrophages and microglia derived from TRPM2 knock-out mice. Together, these results suggest that TRPM2 expressed in macrophages and microglia aggravates peripheral and spinal pronociceptive inflammatory responses and contributes to the pathogenesis of inflammatory and neuropathic pain.
Description: 慢性痛の原因となる神経炎症応答の増悪機構を解明-新しい鎮痛薬開発の可能性-. 京都大学プレスリリース. 2012-03-15.
Rights: Copyright © 2012 the authors
許諾条件により本文は2012-09-14に公開.
URL: http://www.jneurosci.org/content/32/11/3931.abstract
URI: http://hdl.handle.net/2433/154291
DOI(Published Version): 10.1523/JNEUROSCI.4703-11.2012
PubMed ID: 22423113
Related Link: http://www.kyoto-u.ac.jp/ja/news_data/h/h1/news6/2011/120315_3.htm
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