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

Feng Zhang, Runzhe Shu, Xiaolin Wu, Xiaoping Zhao, Dechun Feng, Long Wang, Shunyuan Lu, Qiaoling Liu, Yougui Xiang, Jian Fei, Lei Huang, Zhugang Wang

Research output: Contribution to journalArticle

2 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)201-207
Number of pages7
JournalToxicology Letters
Issue number3
Publication statusPublished - Aug 10 2009



  • BPOZ2
  • Carbon tetrachloride
  • Cyclin D1
  • ERK
  • Hepatocyte proliferation
  • Liver injury

ASJC Scopus subject areas

  • Toxicology

Cite this