NF-κB-mediated inhibition of microRNA-149-5p regulates Chitinase-3-like 1 expression in human airway epithelial cells.

Abstract:
:Lower respiratory tract infections are among the most common causes of death worldwide. Main pathogens leading to these severe infections are viruses and gram-positive bacteria that activate toll-like receptor (TLR)-mediated immune responses via pathogen-associated molecular patterns. One protective factor induced during infection is Chitinase-3-like 1 (CHI3L1), which exerts various functions, e.g. in host cell proliferation and bacterial counteraction, and has been proposed as a biomarker in several acute and chronic inflammatory conditions. MicroRNAs (miR) have become important regulators of inflammation and infection and are considered therapeutic targets in recent years. However, it is not known whether microRNAs play a role in the regulation of CHI3L1 expression in TLR-mediated respiratory epithelial cell inflammation. In this study, we analysed the pre- and post-transcriptional regulation of CHI3L1 by TLRs in bronchial epithelial cells. Therefore, we stimulated BEAS-2B cells with the bacterial TLR2-ligand lipoteichoic acid or the viral dsRNA analogue poly(I:C). We observed an increase in the expression of CHI3L1, which was dependent on TNF-α-mediated NF-κB activation in TLR2- and TLR3-activated cells. Moreover, TLR2 and - 3 stimulation caused downregulation of the microRNA miR-149-5p, an effect that could be suppressed by inhibiting NF-κB translocation into the nucleus. Luciferase reporter assays identified a direct interaction of miR-149-5p with the CHI3L1 3´untranslated region. This interaction was confirmed by inhibition and overexpression of miR-149-5p in BEAS-2B cells, which altered the expression levels of CHI3L1 mRNA. In summary, miR-149-5p directly regulates CHI3L1 in context of TLR-mediated airway epithelial cell inflammation and may be a potential therapeutic target in inflammation and other diseases.
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CELLULAR SIGNALLING
CELL SIGNAL
最新影响因子:4.85 | 期刊ISSN:0898-6568 | CiteScore:3.91 |
出版周期:Monthly | 是否OA:YES | 出版年份:1989 |
期刊官方网址:http://www.journals.elsevier.com/cellular-signalling/
自引率:2.50% | 研究方向:生物-细胞生物学 |
出版地区:UNITED STATES |
SCI期刊coverage:Science Citation Index Expanded(科学引文索引扩展)
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CELLULAR SIGNALLING 期刊简介
英文简介:
Cellular Signalling publishes original research describing fundamental and clinical findings on the mechanisms, actions and structural components of cellular signalling systems in vitro and in vivo. Cellular Signalling aims at full length research papers defining signalling systems ranging from microorganisms to cells, tissues and higher organisms. Cellular Signalling strives to offer a fair and fast peer-review process with a single round of revisions. Reviews are by invitation-only. Short Reports are not accepted.
中文简介:(来自Google、百度翻译)
《细胞信号》发表了关于细胞信号系统在体内和体外的机制、作用和结构组成的基础和临床研究成果。 《细胞信号》的目标是完整的研究论文,定义从微生物到细胞、组织和高等生物体的信号系统。 蜂窝信号努力提供一个公平和快速的同行审查过程,只需一轮修订。 评论只接受邀请。简短的报告不被接受。
CELLULAR SIGNALLING 期刊中科院评价数据
最新中科院分区
大类(学科) | 小类(学科) | 学科排名 |
生物 |
CELL BIOLOGY(细胞生物学) 3区 |
90/190 |
最新公布的期刊年发文量
年度总发文量 | 年度论文发表量 | 年度综述发表量 |
234 | 197 | 37 |
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引文计数(2018)
文献(2015-2017)
3104次引用
793篇文献
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序号 | 类别 | 排名 | 百分位 |
1 |
大类(学科):Biochemistry, Genetics and Molecular Biology
小类(学科):Cell Biology
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#73/264
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