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

doi:10.1016/j.toxlet.2009.04.009

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

Molecular Biology

Research output: Contribution to journal › Article › peer-review

2 Scopus citations

Abstract

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 language	English (US)
Pages (from-to)	201-207
Number of pages	7
Journal	Toxicology Letters
Volume	188
Issue number	3
DOIs	https://doi.org/10.1016/j.toxlet.2009.04.009
State	Published - Aug 10 2009

Keywords

BPOZ2
Carbon tetrachloride
Cyclin D1
ERK
Hepatocyte proliferation
Liver injury

ASJC Scopus subject areas

Toxicology

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10.1016/j.toxlet.2009.04.009

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

abstract = "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.",

keywords = "BPOZ2, Carbon tetrachloride, Cyclin D1, ERK, Hepatocyte proliferation, Liver injury",

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

note = "Funding Information: This work is partially supported by the grants of National Natural Science Foundation of China (39925023, 30370793), Ministry of Science and Technology of China (2006BAI23B02), Ministry of Education of China (00TPJS111), and the grants from Science and Technology Commission of Shanghai Municipality (07DZ22929, 06DZ05907), E-Institutes of Shanghai Municipal Education Commission (E03003). ",

year = "2009",

month = aug,

day = "10",

doi = "10.1016/j.toxlet.2009.04.009",

language = "English (US)",

volume = "188",

pages = "201--207",

journal = "Toxicology Letters",

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T1 - Delayed liver injury and impaired hepatocyte proliferation after carbon tetrachloride exposure in BPOZ2-deficient mice

AU - Zhang, Feng

AU - Shu, Runzhe

AU - Wu, Xiaolin

AU - Zhao, Xiaoping

AU - Feng, Dechun

AU - Wang, Long

AU - Lu, Shunyuan

AU - Liu, Qiaoling

AU - Xiang, Yougui

AU - Fei, Jian

AU - Huang, Lei

AU - Wang, Zhugang

N1 - Funding Information: This work is partially supported by the grants of National Natural Science Foundation of China (39925023, 30370793), Ministry of Science and Technology of China (2006BAI23B02), Ministry of Education of China (00TPJS111), and the grants from Science and Technology Commission of Shanghai Municipality (07DZ22929, 06DZ05907), E-Institutes of Shanghai Municipal Education Commission (E03003).

PY - 2009/8/10

Y1 - 2009/8/10

N2 - 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.

AB - 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.

KW - BPOZ2

KW - Carbon tetrachloride

KW - Cyclin D1

KW - ERK

KW - Hepatocyte proliferation

KW - Liver injury

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

Abstract

Keywords

ASJC Scopus subject areas

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