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H. pylori related proinflammatory cytokines contribute to the induction of miR-146a in human gastric epithelial cells. Mol Biol Rep. 2012 Apr;39(4):4655-61 因无法登陆web of science，求SCI文章检索号，填表用，谢谢！ |
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linda831223: 金币+5, ★★★★★最佳答案, 谢谢版主！ 2014-08-20 12:13:54
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H. pylori related proinflammatory cytokines contribute to the induction of miR-146a in human gastric epithelial cells 作者:Li, N (Li, Na)[ 1 ] ; Xu, X (Xu, Xiang)[ 2 ] ; Xiao, B (Xiao, Bin)[ 1 ] ; Zhu, ED (Zhu, En-Dong)[ 1 ] ; Li, BS (Li, Bo-sheng)[ 1 ] ; Liu, Z (Liu, Zhen)[ 1 ] ; Tang, B (Tang, Bin)[ 1 ] ; Zou, QM (Zou, Quan-Ming)[ 1 ] ; Liang, HP (Liang, Hua-Ping)[ 2 ] ; Mao, XH (Mao, Xu-Hu)[ 1 ] MOLECULAR BIOLOGY REPORTS 卷: 39 期: 4 页: 4655-4661 DOI: 10.1007/s11033-011-1257-5 出版年: APR 2012 查看期刊信息 摘要 MicroRNAs have been implicated as a central regulator of the immune system. We have previously reported that Helicobacter pylori (H. pylori) was able to increase the expression of miR-146a, and miR-146a may negatively regulate H. pylori-induced inflammation, but the exact mechanism of how H. pylori contribute the induction of miR-146a is not clear. Here, we attempted to assess the role of H. pylori related proinflammatory cytokines including interleukin (IL)-8, tumor necrosis factor (TNF)-alpha, and interleukin (IL)-1 beta, and cytotoxin-associated gene A (CagA) virulence factor on the induction of miR-146a. We found that IL-8, TNF-alpha, and IL-1 beta could contribute to the induction of miR-146a in gastric epithelial cell HGC-27 in NF-kappa B-dependent manner, while the induction of miR-146a upon H. pylori stimulation was independent of above proinflammatory cytokines. Furthermore, overexpression of miR-146a reduced H. pylori-induced IL-8, TNF-alpha, and IL-1 beta. However, CagA had no effect on the miR-146a induction. Taken together, our study suggest that proinflammatory cytokines IL-8, TNF-alpha, and IL-1 beta could contribute to the induction of miR-146a during H. pylori infection, while CagA is not necessarily required for miR-146a induction. miR-146a may function as novel negative regulators to modulate the inflammation. 关键词 作者关键词:miR-146a; H. pylori; Proinflammatory cytokines; CagA KeyWords Plus:NORMAL IMMUNE FUNCTION; HELICOBACTER-PYLORI; INFLAMMATORY RESPONSE; RHEUMATOID-ARTHRITIS; T-CELLS; MICRORNAS; ACTIVATION; EXPRESSION; PHOSPHORYLATION; MECHANISM 作者信息 通讯作者地址: Xiao, B (通讯作者) 显示增强组织信息的名称 Third Mil Med Univ, Dept Clin Microbiol & Immunol, Coll Med Lab Sci, Chongqing 400038, Peoples R China. 地址: 显示增强组织信息的名称 [ 1 ] Third Mil Med Univ, Dept Clin Microbiol & Immunol, Coll Med Lab Sci, Chongqing 400038, Peoples R China 显示增强组织信息的名称 [ 2 ] Third Mil Med Univ, State Key Lab Trauma Burns & Combined Injury, Dept 1, Inst Surg Res,Daping Hosp, Chongqing 400042, Peoples R China 电子邮件地址:binxiaotmmu@163.com; huaping_liang@yahoo.com.cn; xhmaotmmu@yeah.net 基金资助致谢 基金资助机构 授权号 Scientific Innovation Research Foundation of Third Military Medical University 2009XQN20 Chinese National Natural Science Foundation 30770113 State Key Laboratory of Trauma, Burns, and Combined Injury SKF201012 查看基金资助信息 出版商 SPRINGER, VAN GODEWIJCKSTRAAT 30, 3311 GZ DORDRECHT, NETHERLANDS 类别 / 分类 研究方向:Biochemistry & Molecular Biology Web of Science 类别:Biochemistry & Molecular Biology 文献信息 文献类型:Article 语种:English 入藏号: WOS:000301108500147 ISSN: 0301-4851 期刊信息 Impact Factor (影响因子): Journal Citation Reports® 其他信息 IDS 号: 903HZ Web of Science 核心合集中的 "引用的参考文献": 25 Web of Science 核心合集中的 "被引频次": 7 |
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