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Calcium Signalling and Liver Regeneration

After partial hepatectomy (PH) the initial mass of the organ is restored through a complex network of cellular interactions that orchestrate both proliferative and hepatoprotective signalling cascades. Among agonists involved in this network many of them drive Ca(2+) movements. During liver regenera...

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Detalles Bibliográficos
Autores principales: Garcin, Isabelle, Tordjmann, Thierry
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2012
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3479951/
https://www.ncbi.nlm.nih.gov/pubmed/23119169
http://dx.doi.org/10.1155/2012/630670
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author Garcin, Isabelle
Tordjmann, Thierry
author_facet Garcin, Isabelle
Tordjmann, Thierry
author_sort Garcin, Isabelle
collection PubMed
description After partial hepatectomy (PH) the initial mass of the organ is restored through a complex network of cellular interactions that orchestrate both proliferative and hepatoprotective signalling cascades. Among agonists involved in this network many of them drive Ca(2+) movements. During liver regeneration in the rat, hepatocyte cytosolic Ca(2+) signalling has been shown on the one hand to be deeply remodelled and on the other hand to enhance progression of hepatocytes through the cell cycle. Mechanisms through which cytosolic Ca(2+) signals impact on hepatocyte cell cycle early after PH are not completely understood, but at least they include regulation of immediate early gene transcription and ERK and CREB phosphorylation. In addition to cytosolic Ca(2+), there is also evidence that mitochondrial Ca(2+) and also nuclear Ca(2+) may be critical for the regulation of liver regeneration. Finally, Ca(2+) movements in hepatocytes, and possibly in other liver cells, not only impact hepatocyte progression in the cell cycle but more generally may regulate cellular homeostasis after PH.
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spelling pubmed-34799512012-11-01 Calcium Signalling and Liver Regeneration Garcin, Isabelle Tordjmann, Thierry Int J Hepatol Review Article After partial hepatectomy (PH) the initial mass of the organ is restored through a complex network of cellular interactions that orchestrate both proliferative and hepatoprotective signalling cascades. Among agonists involved in this network many of them drive Ca(2+) movements. During liver regeneration in the rat, hepatocyte cytosolic Ca(2+) signalling has been shown on the one hand to be deeply remodelled and on the other hand to enhance progression of hepatocytes through the cell cycle. Mechanisms through which cytosolic Ca(2+) signals impact on hepatocyte cell cycle early after PH are not completely understood, but at least they include regulation of immediate early gene transcription and ERK and CREB phosphorylation. In addition to cytosolic Ca(2+), there is also evidence that mitochondrial Ca(2+) and also nuclear Ca(2+) may be critical for the regulation of liver regeneration. Finally, Ca(2+) movements in hepatocytes, and possibly in other liver cells, not only impact hepatocyte progression in the cell cycle but more generally may regulate cellular homeostasis after PH. Hindawi Publishing Corporation 2012 2012-10-16 /pmc/articles/PMC3479951/ /pubmed/23119169 http://dx.doi.org/10.1155/2012/630670 Text en Copyright © 2012 I. Garcin and T. Tordjmann. 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
Garcin, Isabelle
Tordjmann, Thierry
Calcium Signalling and Liver Regeneration
title Calcium Signalling and Liver Regeneration
title_full Calcium Signalling and Liver Regeneration
title_fullStr Calcium Signalling and Liver Regeneration
title_full_unstemmed Calcium Signalling and Liver Regeneration
title_short Calcium Signalling and Liver Regeneration
title_sort calcium signalling and liver regeneration
topic Review Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3479951/
https://www.ncbi.nlm.nih.gov/pubmed/23119169
http://dx.doi.org/10.1155/2012/630670
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