期刊
FEBS LETTERS
卷 588, 期 4, 页码 625-631出版社
WILEY
DOI: 10.1016/j.febslet.2014.01.008
关键词
C-reactive protein; Monocytes; p53; B-cell translocation gene 2; Apoptosis; Atherogenesis
资金
- Korean Ministry of Health and Welfare [A050020]
- Asan Institute for Life Sciences [2011-288]
- Korea Science and Engineering Foundation (KOSEF) [C00058, M10748000263-07N4800-26310]
- Korea government (MOST)
- Dong-a research fund
- Ministry for Health, Welfare and Family Affairs, Republic of Korea [A080016]
- Basic Science Research Program through the National Research Foundation of Korea (NRF)
- Ministry of Education, Science and Technology [2009-0072141]
- NRF, MEST, Korea [20110027584]
- Korea Health Promotion Institute [A080016, A050020] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
- National Research Foundation of Korea [2009-0072141] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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.
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