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

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• 作者：Feng Zhang ; Runzhe Shu ; Xiaolin Wu ; Xiaoping Zhao ; Dechun Feng ; Long Wang ; Shunyuan Lu ; Qiaoling Liu ; Yougui Xiang ; Jian Fei ; Lei Huang ; Zhugang Wang
• 关键词：Carbon tetrachloride ; BPOZ2 ; Liver injury ; Hepatocyte proliferation ; Cyclin D1 ; ERK
• 刊名：Toxicology Letters
• 出版年：2009
• 出版时间：10 August 2009
• 年：2009
• 卷：188
• 期：3
• 页码：201-207
• 全文大小：2068 K

文摘

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 CC1₄ administration in mouse liver.