TRB3, upregulated by ox-LDL, mediates human monocyte-derived macrophage apoptosis

被引：31
作者：
Shang, Yuan-yuan [1 ,2 ]
Wang, Zhi-hao [1 ,2 ]
Zhang, Li-ping [3 ]
Zhong, Ming [1 ,2 ]
Zhang, Yun [1 ,2 ]
Deng, Jing-ti [3 ]
Zhang, Wei [1 ,2 ]
机构：
[1] Shandong Univ, Qilu Hosp, Dept Cardiol, Chinese Minist Publ Hlth, Jinan 250012, Peoples R China
[2] Shandong Univ, Qilu Hosp, Chinese Minist Educ, Key Lab Cardiovasc Remodeling & Funct Res, Jinan 250012, Peoples R China
[3] Shandong Univ, Sch Med, Dept Anat, Jinan 250012, Peoples R China
来源：
FEBS JOURNAL | 2009年 / 276卷 / 10期
基金：
中国国家自然科学基金;
关键词：
apoptosis; atherosclerosis; macrophage; ox-LDL; TRB3; LOW-DENSITY-LIPOPROTEIN; OXIDIZED LDL; TRIBBLES HOMOLOG; ACTIVATION; EXPRESSION; INSULIN; CELLS; ATHEROSCLEROSIS; MORPHOGENESIS; DROSOPHILA;
D O I：
10.1111/j.1742-4658.2009.06998.x
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：
Tribble3 (TRB3), a mammalian homolog of Drosophila tribbles, slows cell-cycle progression, and its expression is increased in response to various stresses. The aim of this study was to investigate the role of the TRB3 gene in macrophage apoptosis induced by oxidized low-density lipoprotein (ox-LDL). We found that, in human monocyte-derived macrophages, TRB3 is upregulated by ox-LDL in a dose- and time-dependent manner. The cell viability of TRB3-overexpressing macrophages was decreased, but apoptosis was increased and the level of activated caspase-3 increased. Factorial analyses revealed no significant interaction between TRB3 overexpression and ox-LDL stimulation with respect to macrophage apoptosis. Furthermore, TRB3-silenced macrophages showed decreased apoptosis, and TRB3-silenced cells treated with ox-LDL showed significantly increased apoptosis. Silencing of TRB3 and ox-LDL stimulation showed significant interaction for macrophage apoptosis, suggesting that TRB3 knockdown resisted the macrophage apoptosis induced by ox-LDL. Therefore, TRB3 in part mediates the macrophage apoptosis induced by ox-LDL, which suggests that TRB3 might be involved in vulnerable atherosclerotic plaque progression.
引用
收藏
页码：2752 / 2761
页数：10
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