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IR@PKUHSC  > 北京大学第二临床医学院  > 心血管内科  > 期刊论文
学科主题: 临床医学
题名:
MicroRNA-223 inhibits tissue factor expression in vascular endothelial cells
作者: Li, Sufang1; Chen, Hong1; Ren, Jingyi1; Geng, Qiang1; Song, Junxian1; Lee, Chongyou1; Cao, Chengfu1; Zhang, Jing1; Xu, Ning2
关键词: Tissue factor ; microRNA-223 ; TNF-alpha ; Atherosclerosis ; Thrombogenesis
刊名: ATHEROSCLEROSIS
发表日期: 2014-12-01
DOI: 10.1016/j.atherosclerosis.2014.09.033
卷: 237, 期:2, 页:514-520
收录类别: SCI
文章类型: Article
WOS标题词: Science & Technology
类目[WOS]: Peripheral Vascular Disease
研究领域[WOS]: Cardiovascular System & Cardiology
关键词[WOS]: MYOCARDIAL-INFARCTION ; CORONARY SYNDROMES ; MECHANISMS ; ATHEROSCLEROSIS ; DISEASE ; PROTEIN ; PLAQUE ; INFLAMMATION ; BIOLOGY ; BINDING
英文摘要:

Objective: Atherosclerosis is a chronic inflammatory process, in which vascular endothelial cells (ECs) become dysfunctional owing to the effects of chemical substances, such as inflammatory factor and growth factors. Tissue factor (TF) expression is induced by the above chemical substances in activated ECs. TF initiates thrombosis on disrupted atherosclerotic plaques which plays an essential role during the onset of acute coronary syndromes (ACS). Increasing evidences suggest the important role of microRNAs as epigenetic regulators of atherosclerotic disease. The aim of our study is to identify if microRNA-223 (miR-223) targets TF in ECs. Methods and results: Bioinformatic analysis showed that TF is a target candidate of miR-223. Western blotting analysis revealed that tumor necrosis factor alpha (TNF-alpha) increased TF expression in aorta of C57BL/6J mice and cultured ECs (EA.hy926 cells and HUVEC) after 4 h treatment. In TNF-alpha treated ECs, TF mRNA was also increased measured by real-time PCR. Real-time PCR results showed that miR-223 levels were downregulated in TNF-alpha-treated aorta of C57BL/6J mice and cultured ECs. Transfection of ECs with miR-223 mimic or miR-223 inhibitor modified TF expression both in mRNA and protein levels. Luciferase assays confirmed that miR-223 suppressed TF expression by binding to the sequence of TF 3′-untranslated regions (3′UTR). TF procoagulant activity was inhibited by overexpressing miR-223 with or without TNF-alpha stimulation. Conclusions: MiR-223-mediated suppression of TF expression provides a novel molecular mechanism for the regulation of coagulation cascade, and suggests a clue against thrombogenesis during the process of atherosclerotic plaque rupture. (C) 2014 Elsevier Ireland Ltd. All rights reserved.

语种: 英语
所属项目编号: 2012ZX09303019 ; D141100003014002 ; 501100001809 ; 81270274 ; 81270276 ; 7132225 ; 7122198
项目资助者: National Science and Technology "Creation of Major New Dugs" ; Beijing Science and Technology Project ; National Natural Science Foundation of China ; Beijing Natural Science Foundation
WOS记录号: WOS:000346066600052
Citation statistics:
内容类型: 期刊论文
URI标识: http://ir.bjmu.edu.cn/handle/400002259/59449
Appears in Collections:北京大学第二临床医学院_心血管内科_期刊论文

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作者单位: 1.Karolinska Inst, Dept Med, Stockholm, Sweden
2.Peking Univ, Peoples Hosp, Dept Cardiol, Beijing 100044, Peoples R China

Recommended Citation:
Li, Sufang,Chen, Hong,Ren, Jingyi,et al. MicroRNA-223 inhibits tissue factor expression in vascular endothelial cells[J]. ATHEROSCLEROSIS,2014,237(2):514-520.
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