Kruppel-like factor 4 inhibits the expression of interleukin-1 beta in lipopolysaccharide-induced RAW264.7 macrophages

被引：16
|
作者：
Liu, Junwen [1 ,2 ]
Yang, Tao [2 ,3 ]
Liu, Ying [1 ]
Zhang, Huali [1 ]
Wang, Kangkai [1 ]
Liu, Meidong [1 ]
Chen, Guangwen [1 ]
Xiao, Xianzhong [1 ]
机构：
[1] Cent S Univ, Sch Basic Med Sci, Dept Pathophysiol, Lab Shock, Changsha 410008, Hunan, Peoples R China
[2] Cent S Univ, Sch Basic Med Sci, Dept Histol & Embryol, Changsha 410013, Hunan, Peoples R China
[3] Changsha Univ Sci & Technol, Coll Chem & Bioengn, Changsha 410076, Hunan, Peoples R China
来源：
FEBS LETTERS | 2012年 / 586卷 / 06期
基金：
中国国家自然科学基金;
关键词：
Kruppel-like factor 4; Interleukin; 1; beta; Inflammation; Gene regulation; TRANSCRIPTION FACTORS; GENE; ACTIVATION; IL-1-BETA; INDUCTION; KLF4; KRUPPEL-LIKE-FACTOR-4; INVOLVEMENT; PROMOTES; MEDIATOR;
D O I：
10.1016/j.febslet.2012.02.003
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
RAW264.7 macrophages and human peripheral blood mononuclear cells were treated with LPS to determine the expression of KLF4 and release of IL-1 beta. A full-length cDNA or short interference RNA of KLF4 was transfected into RAW264.7 macrophages; the expression and release of IL-1 beta were analyzed. The transcription and DNA binding activities of KLF4 to the IL-1 beta promoter were detected further. The results showed LPS treatment resulted in the increase of KLF4 level and IL-1 beta release; KLF4 overexpression decreased the expression of IL-1 beta, while KLF4 inhibition increased the expression of IL-1 beta; overexpression of KLF4 promoted the DNA binding activity of KLF4 to the IL-1 beta promoter and attenuated the transcription of IL-1 beta promoter, indicating an important role of KLF4 in regulating expression of IL-1 beta. (C) 2012 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码：834 / 840
页数：7
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