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Liver-specific loss of beta-catenin results in delayed hepatocyte proliferation after partial hepatectomy.

Publication ,  Journal Article
Sekine, S; Gutiérrez, PJA; Lan, BY-A; Feng, S; Hebrok, M
Published in: Hepatology
February 2007

UNLABELLED: Recent studies have suggested that beta-catenin is involved in the regulation of hepatocyte proliferation in multiple contexts, including organ development and tumorigenesis. We explored the role of beta-catenin during liver regeneration using T cell factor/lymphoid enhancer factor (TCF/LEF)-reporter mice (TOPGal mice) and liver-specific beta-catenin knockout mice. Liver-specific beta-catenin knockout mice showed a delayed onset of DNA synthesis after hepatectomy, whereas recovery of liver mass was not affected. Among putative beta-catenin target genes examined, the induction of Ccnd1 expression was reduced, whereas the expression of Myc and Egfr was unaffected. Furthermore, cyclin D1 protein levels were not induced, and the expression of cyclins A, E, and proliferating cell nuclear antigen was delayed. Intriguingly, the analysis of TOPGal mice showed that hepatocytes with active TCF/LEF transcription are confined to the pericentral zone and are not increased in number during regeneration, indicating an uncoupling between beta-catenin/TCF signaling activity and hepatocyte proliferation. CONCLUSION: Our results indicate that beta-catenin is critical for the proper regulation of hepatocyte proliferation during liver regeneration; however, the activity of beta-catenin/TCF signaling does not correlate with hepatocyte proliferation, suggesting that this regulation might be indirect/secondary.

Duke Scholars

Published In

Hepatology

DOI

ISSN

0270-9139

Publication Date

February 2007

Volume

45

Issue

2

Start / End Page

361 / 368

Location

United States

Related Subject Headings

  • beta Catenin
  • TCF Transcription Factors
  • Signal Transduction
  • Models, Animal
  • Mice, Knockout
  • Mice
  • Male
  • Liver Regeneration
  • Liver
  • Hepatocytes
 

Citation

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ICMJE
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Sekine, S., Gutiérrez, P. J. A., Lan, B.-A., Feng, S., & Hebrok, M. (2007). Liver-specific loss of beta-catenin results in delayed hepatocyte proliferation after partial hepatectomy. Hepatology, 45(2), 361–368. https://doi.org/10.1002/hep.21523
Sekine, Shigeki, Pedro J. A. Gutiérrez, Billy Yu-Ang Lan, Sandy Feng, and Matthias Hebrok. “Liver-specific loss of beta-catenin results in delayed hepatocyte proliferation after partial hepatectomy.Hepatology 45, no. 2 (February 2007): 361–68. https://doi.org/10.1002/hep.21523.
Sekine S, Gutiérrez PJA, Lan BY-A, Feng S, Hebrok M. Liver-specific loss of beta-catenin results in delayed hepatocyte proliferation after partial hepatectomy. Hepatology. 2007 Feb;45(2):361–8.
Sekine, Shigeki, et al. “Liver-specific loss of beta-catenin results in delayed hepatocyte proliferation after partial hepatectomy.Hepatology, vol. 45, no. 2, Feb. 2007, pp. 361–68. Pubmed, doi:10.1002/hep.21523.
Sekine S, Gutiérrez PJA, Lan BY-A, Feng S, Hebrok M. Liver-specific loss of beta-catenin results in delayed hepatocyte proliferation after partial hepatectomy. Hepatology. 2007 Feb;45(2):361–368.
Journal cover image

Published In

Hepatology

DOI

ISSN

0270-9139

Publication Date

February 2007

Volume

45

Issue

2

Start / End Page

361 / 368

Location

United States

Related Subject Headings

  • beta Catenin
  • TCF Transcription Factors
  • Signal Transduction
  • Models, Animal
  • Mice, Knockout
  • Mice
  • Male
  • Liver Regeneration
  • Liver
  • Hepatocytes