IR@PKUHSC  > 北京大学公共卫生学院
学科主题公共卫生
Ultrafine carbon black induces glutamate and ATP release by activating connexin and pannexin hemichannels in cultured astrocytes
Wei, Hongying; Deng, Furong; Chen, Yiyong; Qin, Yu; Hao, Yu; Guo, Xinbiao
关键词Ultrafine carbon black Ultrafine particles Glutamate ATP Hemichannel Neurotoxicity
刊名TOXICOLOGY
2014-09-02
DOI10.1016/j.tox.2014.06.005
323页:32-41
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Pharmacology & Pharmacy ; Toxicology
研究领域[WOS]Pharmacology & Pharmacy ; Toxicology
关键词[WOS]GAP-JUNCTION HEMICHANNELS ; BLOOD-BRAIN-BARRIER ; PARTICULATE MATTER ; P2X(7) RECEPTOR ; OXIDATIVE STRESS ; NERVOUS-SYSTEM ; AIR-POLLUTION ; METAL-OXIDE ; MECHANISMS ; PARTICLES
英文摘要

Ultrafine particles could enter central nervous system and were associated with brain damage. The underlying mechanisms have not been fully elucidated. Glutamate and ATP are important signaling molecules in brain physiology and pathology. We investigated whether ultrafine carbon black (ufCB) could regulate the release of glutamate and ATP from cultured cortical astrocytes and the involvement of hemichannels in the release mechanism. Our results showed that ufCB dose-dependently increased glutamate and ATP release and activated hemichannels in astrocytes. ufCB-activated hemichannels were attributed to the activation of both connexin 43 (Cx43) and pannexin1 (Panx1) hemichannels, which was based on the finding of increased protein expression and distribution on cell surface of Cx43 and Panx1, and the inhibiting effects of hemichannel inhibitor carbenoxolone, Cx43 hemichannel inhibitor (43)Gap27 and Panx1 hemichannel inhibitor (10)Panx1 on hemichannel activation. Furthermore, ufCB-induced glutamate and ATP release were dependent on Cx43 and Panx1 hemichannels, because carbenoxolone and (43)Gap27 inhibited ufCB-induced glutamate and ATP release, and (10)Panx1 inhibited ufCB-induced ATP release. Taken together, we demonstrated, for the first time, that ufCB could induce glutamate and ATP release by activating Cx43 and Panx1 hemchannels in astrocytes. Our findings suggest a novel mechanism for neurotoxicity caused by ultrafine particles. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

语种英语
WOS记录号WOS:000340308000005
项目编号2012AA062804 ; 21077006
资助机构National High Technology Research and Development Program of China ; National Natural Science Foundation of China
引用统计
被引频次:18[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/66262
专题北京大学公共卫生学院
北京大学公共卫生学院_劳动卫生与环境卫生学系
北京大学公共卫生学院_公共卫生学院
作者单位Peking Univ, Sch Publ Hlth, Dept Occupat & Environm Hlth Sci, Beijing 100191, Peoples R China
推荐引用方式
GB/T 7714
Wei, Hongying,Deng, Furong,Chen, Yiyong,et al. Ultrafine carbon black induces glutamate and ATP release by activating connexin and pannexin hemichannels in cultured astrocytes[J]. TOXICOLOGY,2014,323:32-41.
APA Wei, Hongying,Deng, Furong,Chen, Yiyong,Qin, Yu,Hao, Yu,&Guo, Xinbiao.(2014).Ultrafine carbon black induces glutamate and ATP release by activating connexin and pannexin hemichannels in cultured astrocytes.TOXICOLOGY,323,32-41.
MLA Wei, Hongying,et al."Ultrafine carbon black induces glutamate and ATP release by activating connexin and pannexin hemichannels in cultured astrocytes".TOXICOLOGY 323(2014):32-41.
条目包含的文件
条目无相关文件。
个性服务
推荐该条目
保存到收藏夹
查看访问统计
导出为Endnote文件
谷歌学术
谷歌学术中相似的文章
[Wei, Hongying]的文章
[Deng, Furong]的文章
[Chen, Yiyong]的文章
百度学术
百度学术中相似的文章
[Wei, Hongying]的文章
[Deng, Furong]的文章
[Chen, Yiyong]的文章
必应学术
必应学术中相似的文章
[Wei, Hongying]的文章
[Deng, Furong]的文章
[Chen, Yiyong]的文章
相关权益政策
暂无数据
收藏/分享
所有评论 (0)
暂无评论
 

除非特别说明,本系统中所有内容都受版权保护,并保留所有权利。