Foxl1 promotes liver repair following cholestatic injury in mice

Sara D. Sackett, Yan Gao, Soona Shin, Yonah B. Esterson, Akivaga Tsingalia, Reginald S. Hurtt, Karrie Brondell, Klaus H. Kaestner, Linda E. Greenbaum

Research output: Contribution to journalArticlepeer-review

Abstract

Cholangiocyte proliferation is one of the hallmarks of the response to cholestatic injury. We previously reported that the winged helix transcription factor Foxl1 is dramatically induced in cholangiocytes following bile duct ligation. In this study, we investigated the function of Foxl1 in the bile duct ligation model of cholestatic liver injury in Foxl1 / and control mice. We found that Foxl1 / livers exhibit an increase in parenchymal necrosis, significantly impaired cholangiocyte and hepatocyte proliferation, and failure to expand bile ductular mass. Wnt3a and Wnt7b expression was decreased in the livers of Foxl1 / mice along with reduced expression of the Β-catenin target gene Cyclin D1 in Foxl1 / cholangiocytes. These results show that Foxl1 promotes liver repair after bile-duct-ligation-induced liver injury through activation of the canonical wnt/Β-catenin pathway.

Original languageEnglish (US)
Pages (from-to)1387-1396
Number of pages10
JournalLaboratory Investigation
Volume89
Issue number12
DOIs
StatePublished - Dec 2009
Externally publishedYes

Keywords

  • B-catenin
  • Bile duct ligation
  • Cholangiocyte
  • Cyclin D1
  • Wnt

ASJC Scopus subject areas

  • Pathology and Forensic Medicine
  • Molecular Biology
  • Cell Biology

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