Delayed liver injury and impaired hepatocyte proliferation after carbon tetrachloride exposure in BPOZ2-deficient mice

被引:3
作者
Zhang, Feng [1 ,2 ,3 ,6 ]
Shu, Runzhe [1 ,2 ,3 ,6 ]
Wu, Xiaolin [3 ]
Zhao, Xiaoping [3 ]
Feng, Dechun [1 ,2 ,6 ]
Wang, Long [4 ,5 ]
Lu, Shunyuan [4 ,5 ]
Liu, Qiaoling [5 ]
Xiang, Yougui [5 ]
Fei, Jian [5 ]
Huang, Lei [3 ]
Wang, Zhugang [1 ,2 ,3 ,4 ,5 ]
机构
[1] Chinese Acad Sci, Inst Hlth Sci, Shanghai Inst Biol Sci, Shanghai 200031, Peoples R China
[2] Shanghai Jiao Tong Univ, Sch Med, Shanghai 200031, Peoples R China
[3] SJTUSM, Inst Shanghai Univ E, Model Organism Div, Dept Med Genet, Shanghai 200025, Peoples R China
[4] SJTUSM, Rui Jin Hosp, State Key Lab Med Genom, Shanghai 200025, Peoples R China
[5] Shanghai Res Ctr Model Organisms, Shanghai 201210, Peoples R China
[6] Chinese Acad Sci, Grad Sch, Shanghai 200031, Peoples R China
基金
中国国家自然科学基金;
关键词
Carbon tetrachloride; BPOZ2; Liver injury; Hepatocyte proliferation; Cyclin D1; ERK; CYCLIN D1; SIGNALING PATHWAY; ANKYRIN REPEAT; INTERLEUKIN-6-DEFICIENT MICE; FACTOR RECEPTOR; REGENERATION; GROWTH; PROTEIN; GENE; EXPRESSION;
D O I
10.1016/j.toxlet.2009.04.009
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
BPOZ2 is a tumor suppressive mediator in PTEN signaling pathway and plays an important role in cell proliferation. In this study, we investigated the physiology functions of BPOZ2 in CCl4-induced liver injury and hepatocyte proliferation afterwards. After acute CCl4 administration, BPOZ2 null mice exhibited delayed liver injury and impaired hepatocyte proliferation, which was accompanied by altered kinetics of CYP2E1 protein expression, compromised cyclin D1 expression and shortened duration of ERK activation. These results for the first time define that BPOZ2 is an important regulator involved in the injury and repair process induced by acute CCl4 administration in mouse liver. (C) 2009 Elsevier Ireland Ltd. All rights reserved.
引用
收藏
页码:201 / 207
页数:7
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