Deficiency of BPOZ2 decreases liver fibrosis after chronic carbon tetrachloride administration in mice

Feng Zhang, Suying Dang, Runzhe Shu, Yougui Xiang, Ying Kuang, Jian Fei, Zhugang Wang

Research output: Contribution to journalArticle

Abstract

Bood POZ containing gene type 2 (BPOZ2), a Broad-Complex, Tramtrack, and Bric a brac domain containing protein, is an adaptor protein for the E3 ubiquitin ligase scaffold protein CUL3. It plays an important role in acute carbon tetrachloride (CCl4)-induced liver injury and regeneration in mice. In this study, we investigated the role of BPOZ2 in the process of liver fibrosis induced by chronic CCl4 treatment. The results indicate that BPOZ2 deficiency decreases sustained activation of hepatic stellate cells, attenuates collagen αI(I) and tissue inhibitor of matrix metalloprotease 1 expression, and decreases liver fibrosis after repeated CCl4 administration. These findings suggest BPOZ2 as a new therapeutic target for the prevention and treatment of hepatic fibrosis in chronic liver disease.

Original languageEnglish (US)
Pages (from-to)204-210
Number of pages7
JournalInternational Journal of Toxicology
Volume34
Issue number2
DOIs
StatePublished - Mar 10 2015

Keywords

  • BPOZ2
  • carbon tetrachloride
  • HSC
  • liver fibrosis
  • TIMP-1

ASJC Scopus subject areas

  • Toxicology

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