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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

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linda831223: 金币+5, ★★★★★最佳答案, 谢谢版主! 2014-08-20 12:13:54
jssxh: 金币+5, 检索EPI+1, 谢谢参与,请继续关注本版块! 2014-08-21 21:25:48
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
非淡泊无以明志,非宁静无以致远
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