C-reactive protein induces G2/M phase cell cycle arrest and apoptosis in monocytes through the upregulation of B-cell translocation gene 2 expression

被引:25
|
作者
Kim, Yuna [1 ]
Ryu, Jewon [1 ]
Ryu, Min Sook [3 ]
Lim, Sunny [1 ]
Han, Ki Ok [2 ]
Lim, In Kyoung [3 ]
Han, Ki Hoon [1 ]
机构
[1] Univ Ulsan, Coll Med, Asan Med Ctr, Dept Cardiol, Seoul, South Korea
[2] Kwandong Univ, Sch Med, Dept Endocrinol & Metab, Seoul, South Korea
[3] Ajou Univ, Sch Med, Div Cell Transformat & Restorat BK21, Dept Biochem & Mol Biol, Suwon 443721, South Korea
基金
新加坡国家研究基金会;
关键词
C-reactive protein; Monocytes; p53; B-cell translocation gene 2; Apoptosis; Atherogenesis; P53; ATHEROSCLEROSIS; RESPONSES; BINDING; CANCER;
D O I
10.1016/j.febslet.2014.01.008
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
We hypothesized that C-reactive protein (CRP) may affect the cell cycle and induce apoptotic changes of monocytes. CRP (similar to 25 mu g/ml) significantly increased expressions of B-cell translocation gene 2 (BTG2) mRNA and protein in human monocytes through pathways involving CD32/NADPH oxidase 2/p53, which eventually induced G2/M phase arrest and apoptotic cell death. Such pro-apoptotic effect of CRP was not found in thioglycollate-elicited intraperitoneal monocytes/macrophages harvested from BTG2-knockout male C57BL/6 mice (n = 5). Within atheromatous plaques obtained from CRP-transgenic male LDLR (/) C57BL/6 mice (n = 5) and human coronary arteries, BTG2 co-localized with CRP, p53 and monocytes/macrophages. Therefore the pro-apoptotic pathway of CRP-CD32-Nox2-p53-BTG2 may contribute to the retardation of the atherogenic process. (C) 2014 Published by Elsevier B.V. on behalf of the Federation of European Biochemical Societies.
引用
收藏
页码:625 / 631
页数:7
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