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Depletion of [Beta]-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development

Depletion of β-catenin impairs regeneration of the rapid turn-over gut epithelial cells, but appears dispensable for that of the slow turn-over mature hepatocytes in mice until 1 y of age. As the life span of mature murine hepatocytes is about 400 d, we studied conditional β-catenin knockout mice (.... Full description

Journal Title: Proceedings of the National Academy of Sciences of the United States of America Nov 8, 2011, Vol.108(45), p.18384
Main Author: Wang, Er-Yea
Other Authors: Yeh, Shiou-Hwei , Tsai, Ting-Fen , Huang, Hsiang-Po , Jeng, Yung-Ming , Lin, Wei-Hsiang , Chen, Wei-Chih , Yeh, Kun-Huei , Chen, Pei-Jer , Chen, Ding-Shinn
Format: Electronic Article Electronic Article
Language: English
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ID: ISSN: 00278424 ; E-ISSN: 10916490
Link: http://search.proquest.com/docview/903510869/?pq-origsite=primo
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title: Depletion of [Beta]-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development
format: Article
creator:
  • Wang, Er-Yea
  • Yeh, Shiou-Hwei
  • Tsai, Ting-Fen
  • Huang, Hsiang-Po
  • Jeng, Yung-Ming
  • Lin, Wei-Hsiang
  • Chen, Wei-Chih
  • Yeh, Kun-Huei
  • Chen, Pei-Jer
  • Chen, Ding-Shinn
subjects:
  • Cells
  • Rodents
  • Tumors
  • Liver
  • Biomarkers
ispartof: Proceedings of the National Academy of Sciences of the United States of America, Nov 8, 2011, Vol.108(45), p.18384
description: Depletion of β-catenin impairs regeneration of the rapid turn-over gut epithelial cells, but appears dispensable for that of the slow turn-over mature hepatocytes in mice until 1 y of age. As the life span of mature murine hepatocytes is about 400 d, we studied conditional β-catenin knockout mice (...) until 20 mo of age to determine the function of β-catenin in the postnatal liver. β-catenin was absent from the hepatocytes of β-catenin knockout mice 4 wk after delivery. From 9 mo of age, hepatocytes were gradually replaced by newly formed β-catenin-positive hepatocytes, which constituted about 90% of hepatocytes at 18-20 mo of age. This process was accompanied by active proliferation of bile duct/ductule cells. β-catenin-positive hepatocytes exhibited elevated proliferation activity and expression of progenitor cell markers, but lower albumin and Cre. This might explain their intact β-catenin protein, and suggest their origins from hepatic progenitor cells. Liver tumors arose spontaneously from β-catenin-positive cells, and tumorigenesis was accelerated by hepatitis B X protein. These results indicate β-catenin critical for the regeneration of mature hepatocytes. Failure to regenerate mature hepatocytes results in proliferation of hepatic progenitor cells that are able to maintain liver function but are predisposed to form liver tumors. (ProQuest: ... denotes formulae/symbols omitted.)
language: eng
source:
identifier: ISSN: 00278424 ; E-ISSN: 10916490
fulltext: fulltext
issn:
  • 00278424
  • 0027-8424
  • 10916490
  • 1091-6490
url: Link


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titleDepletion of [Beta]-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development
creatorWang, Er-Yea ; Yeh, Shiou-Hwei ; Tsai, Ting-Fen ; Huang, Hsiang-Po ; Jeng, Yung-Ming ; Lin, Wei-Hsiang ; Chen, Wei-Chih ; Yeh, Kun-Huei ; Chen, Pei-Jer ; Chen, Ding-Shinn
ispartofProceedings of the National Academy of Sciences of the United States of America, Nov 8, 2011, Vol.108(45), p.18384
identifierISSN: 00278424 ; E-ISSN: 10916490
subjectCells ; Rodents ; Tumors ; Liver ; Biomarkers
descriptionDepletion of β-catenin impairs regeneration of the rapid turn-over gut epithelial cells, but appears dispensable for that of the slow turn-over mature hepatocytes in mice until 1 y of age. As the life span of mature murine hepatocytes is about 400 d, we studied conditional β-catenin knockout mice (...) until 20 mo of age to determine the function of β-catenin in the postnatal liver. β-catenin was absent from the hepatocytes of β-catenin knockout mice 4 wk after delivery. From 9 mo of age, hepatocytes were gradually replaced by newly formed β-catenin-positive hepatocytes, which constituted about 90% of hepatocytes at 18-20 mo of age. This process was accompanied by active proliferation of bile duct/ductule cells. β-catenin-positive hepatocytes exhibited elevated proliferation activity and expression of progenitor cell markers, but lower albumin and Cre. This might explain their intact β-catenin protein, and suggest their origins from hepatic progenitor cells. Liver tumors arose spontaneously from β-catenin-positive cells, and tumorigenesis was accelerated by hepatitis B X protein. These results indicate β-catenin critical for the regeneration of mature hepatocytes. Failure to regenerate mature hepatocytes results in proliferation of hepatic progenitor cells that are able to maintain liver function but are predisposed to form liver tumors. (ProQuest: ... denotes formulae/symbols omitted.)
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titleDepletion of [Beta]-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development
descriptionDepletion of β-catenin impairs regeneration of the rapid turn-over gut epithelial cells, but appears dispensable for that of the slow turn-over mature hepatocytes in mice until 1 y of age. As the life span of mature murine hepatocytes is about 400 d, we studied conditional β-catenin knockout mice (...) until 20 mo of age to determine the function of β-catenin in the postnatal liver. β-catenin was absent from the hepatocytes of β-catenin knockout mice 4 wk after delivery. From 9 mo of age, hepatocytes were gradually replaced by newly formed β-catenin-positive hepatocytes, which constituted about 90% of hepatocytes at 18-20 mo of age. This process was accompanied by active proliferation of bile duct/ductule cells. β-catenin-positive hepatocytes exhibited elevated proliferation activity and expression of progenitor cell markers, but lower albumin and Cre. This might explain their intact β-catenin protein, and suggest their origins from hepatic progenitor cells. Liver tumors arose spontaneously from β-catenin-positive cells, and tumorigenesis was accelerated by hepatitis B X protein. These results indicate β-catenin critical for the regeneration of mature hepatocytes. Failure to regenerate mature hepatocytes results in proliferation of hepatic progenitor cells that are able to maintain liver function but are predisposed to form liver tumors. (ProQuest: ... denotes formulae/symbols omitted.)
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titleDepletion of [Beta]-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development
authorWang, Er-Yea ; Yeh, Shiou-Hwei ; Tsai, Ting-Fen ; Huang, Hsiang-Po ; Jeng, Yung-Ming ; Lin, Wei-Hsiang ; Chen, Wei-Chih ; Yeh, Kun-Huei ; Chen, Pei-Jer ; Chen, Ding-Shinn
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abstractDepletion of β-catenin impairs regeneration of the rapid turn-over gut epithelial cells, but appears dispensable for that of the slow turn-over mature hepatocytes in mice until 1 y of age. As the life span of mature murine hepatocytes is about 400 d, we studied conditional β-catenin knockout mice (...) until 20 mo of age to determine the function of β-catenin in the postnatal liver. β-catenin was absent from the hepatocytes of β-catenin knockout mice 4 wk after delivery. From 9 mo of age, hepatocytes were gradually replaced by newly formed β-catenin-positive hepatocytes, which constituted about 90% of hepatocytes at 18-20 mo of age. This process was accompanied by active proliferation of bile duct/ductule cells. β-catenin-positive hepatocytes exhibited elevated proliferation activity and expression of progenitor cell markers, but lower albumin and Cre. This might explain their intact β-catenin protein, and suggest their origins from hepatic progenitor cells. Liver tumors arose spontaneously from β-catenin-positive cells, and tumorigenesis was accelerated by hepatitis B X protein. These results indicate β-catenin critical for the regeneration of mature hepatocytes. Failure to regenerate mature hepatocytes results in proliferation of hepatic progenitor cells that are able to maintain liver function but are predisposed to form liver tumors. (ProQuest: ... denotes formulae/symbols omitted.)
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urlhttp://search.proquest.com/docview/903510869/
pages18384-18389
doi10.1073/pnas.1116386108
date2011-11-08