Roles of TRP channels expressed in immune and glial cells in chronic pain
Roles of TRP channels expressed in immune and glial cells in chronic pain
批准号:
23790641
负责人:
NAKAGAWA Takayuki
金额:
$2.75万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Young Scientists (B)
财政年份:
2011
资助国家:
日本
项目状态:
已结题
起止时间:
2011 至 2012
中文摘要
慢性疼痛,如外周神经损伤引起的神经性疼痛,是基于外周和中枢致敏,这是由外周/脊髓神经元和免疫/胶质细胞相互作用介导的神经炎症引起的。在本研究中,我们发现免疫/胶质细胞中表达的瞬时受体电位(TRP)通道在慢性疼痛中起重要作用。特别是,我们研究了TRPM2在小鼠炎症性和神经性疼痛中的作用,TRPM2在巨噬细胞和小胶质细胞中作为活性氧(ROS)的传感器
英文摘要
Chronic pain, such as peripheral nerve injury-induced neuropathic pain, is based on both peripheral and central sensitization, which is caused by neuroinflammation mediated by the interaction between peripheral/spinal neurons and immune/glial cells. In this research, we found that transient receptor potential (TRP) channels expressed in immune/glial cells play an important role in chronic pain. Especially, we examined the roles of TRPM2, which acts as a sensor for reactive oxygen species (ROS) in macrophages and microglia, in inflammatory and neuropathic pain in mice
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Involvement of ROS-mediated TRPA1 activation in oxaliplatin-induced acute peripheral neuropathy
ROS 介导的 TRPA1 激活参与奥沙利铂诱导的急性周围神经病变
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[趙 萌, 三宅崇仁, 中村彩希, 浜野 智, 高橋重成, 白川久志, 中川貴之, 森 泰生, 金子周司]
通讯作者:
金子周司
DOI:
10.1371/journal.pone.0066410
发表时间:
2013
期刊:
PloS one
影响因子:
3.7
作者:
[Isami K, Haraguchi K, So K, Asakura K, Shirakawa H, Mori Y, Nakagawa T, Kaneko S]
通讯作者:
Kaneko S
DOI:
10.1371/journal.pone.0054788
发表时间:
2013
期刊:
PloS one
影响因子:
3.7
作者:
[Sakai H, Sagara A, Matsumoto K, Hasegawa S, Sato K, Nishizaki M, Shoji T, Horie S, Nakagawa T, Tokuyama S, Narita M]
通讯作者:
Narita M
A pathophysiological role of TRPM2 in ischemic injury after transient focal cerebral ischemia in mice.
TRPM2 在小鼠短暂局灶性脑缺血后缺血性损伤中的病理生理学作用。
DOI:
--
发表时间:
2011
期刊:
影响因子:
--
作者:
[Sakimoto, S., Munakata, M., Shirakawa, H., Nakagawa, T., Kaneko, S.]
通讯作者:
S.
ミクログリアおける TRPV1チャネルの遊走能および貪食作用への関与
TRPV1通道参与小胶质细胞迁移能力和吞噬作用
DOI:
--
发表时间:
2013
期刊:
影响因子:
--
作者:
[三宅崇仁, 白川久志, 宮之原 遵, 中川貴之, 金子周司]
通讯作者:
金子周司
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