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Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology
Most cells in mammalian tissues usually contain a diploid complement of chromosomes. However, numerous studies have demonstrated a major role of “diploid-polyploid conversion” during physiopathological processes in several tissues. In the liver parenchyma, progressive polyploidization of hepatocytes...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2012
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485502/ https://www.ncbi.nlm.nih.gov/pubmed/23150829 http://dx.doi.org/10.1155/2012/282430 |
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author | Gentric, Géraldine Desdouets, Chantal Celton-Morizur, Séverine |
author_facet | Gentric, Géraldine Desdouets, Chantal Celton-Morizur, Séverine |
author_sort | Gentric, Géraldine |
collection | PubMed |
description | Most cells in mammalian tissues usually contain a diploid complement of chromosomes. However, numerous studies have demonstrated a major role of “diploid-polyploid conversion” during physiopathological processes in several tissues. In the liver parenchyma, progressive polyploidization of hepatocytes takes place during postnatal growth. Indeed, at the suckling-weaning transition, cytokinesis failure events induce the genesis of binucleated tetraploid liver cells. Insulin signalling, through regulation of the PI3K/Akt signalling pathway, is essential in the establishment of liver tetraploidization by controlling cytoskeletal organisation and consequently mitosis progression. Liver cell polyploidy is generally considered to indicate terminal differentiation and senescence, and both lead to a progressive loss of cell pluripotency associated to a markedly decreased replication capacity. Although adult liver is a quiescent organ, it retains a capacity to proliferate and to modulate its ploidy in response to various stimuli or aggression (partial hepatectomy, metabolic overload (i.e., high copper and iron hepatic levels), oxidative stress, toxic insult, and chronic hepatitis etc.). Here we review the mechanisms and functional consequences of hepatocytes polyploidization during normal and pathological liver growth. |
format | Online Article Text |
id | pubmed-3485502 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2012 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-34855022012-11-13 Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology Gentric, Géraldine Desdouets, Chantal Celton-Morizur, Séverine Int J Hepatol Review Article Most cells in mammalian tissues usually contain a diploid complement of chromosomes. However, numerous studies have demonstrated a major role of “diploid-polyploid conversion” during physiopathological processes in several tissues. In the liver parenchyma, progressive polyploidization of hepatocytes takes place during postnatal growth. Indeed, at the suckling-weaning transition, cytokinesis failure events induce the genesis of binucleated tetraploid liver cells. Insulin signalling, through regulation of the PI3K/Akt signalling pathway, is essential in the establishment of liver tetraploidization by controlling cytoskeletal organisation and consequently mitosis progression. Liver cell polyploidy is generally considered to indicate terminal differentiation and senescence, and both lead to a progressive loss of cell pluripotency associated to a markedly decreased replication capacity. Although adult liver is a quiescent organ, it retains a capacity to proliferate and to modulate its ploidy in response to various stimuli or aggression (partial hepatectomy, metabolic overload (i.e., high copper and iron hepatic levels), oxidative stress, toxic insult, and chronic hepatitis etc.). Here we review the mechanisms and functional consequences of hepatocytes polyploidization during normal and pathological liver growth. Hindawi Publishing Corporation 2012 2012-10-22 /pmc/articles/PMC3485502/ /pubmed/23150829 http://dx.doi.org/10.1155/2012/282430 Text en Copyright © 2012 Géraldine Gentric et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Article Gentric, Géraldine Desdouets, Chantal Celton-Morizur, Séverine Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology |
title | Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology |
title_full | Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology |
title_fullStr | Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology |
title_full_unstemmed | Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology |
title_short | Hepatocytes Polyploidization and Cell Cycle Control in Liver Physiopathology |
title_sort | hepatocytes polyploidization and cell cycle control in liver physiopathology |
topic | Review Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3485502/ https://www.ncbi.nlm.nih.gov/pubmed/23150829 http://dx.doi.org/10.1155/2012/282430 |
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