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International Journal of Hepatology
Volume 2012 (2012), Article ID 328372, 13 pages
Review Article

The MAPK MEK1/2-ERK1/2 Pathway and Its Implication in Hepatocyte Cell Cycle Control

1Inserm, U1085, Institut de Recherche sur la Santé l’Environnement et le Travail (IRSET), Université de Rennes 1, SFR Biosit, 35043 Rennes, France
2IRSET, Université de Rennes 1, Campus de Villejean, CS 34317, 35043 Rennes, France
3Institut de Recherche en Immunologie et Cancérologie, Université de Montréal, P.O. Box 6128, Montreal, QC, Canada H3C 3J7

Received 29 May 2012; Revised 6 September 2012; Accepted 10 September 2012

Academic Editor: Chantal Desdouets

Copyright © 2012 Jean-Philippe Guégan et al. 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.


Primary cultures of hepatocytes are powerful models in studying the sequence of events that are necessary for cell progression from a G0-like state to S phase. The models mimic the physiological process of hepatic regeneration after liver injury or partial hepatectomy. Many reports suggest that the mitogen-activated protein kinase (MAPK) ERK1/2 can support hepatocyte proliferation in vitro and in vivo and the MEK/ERK cascade acts as an essential element in hepatocyte responses induced by the EGF. Moreover, its disregulation has been associated with the promotion of tumor cell growth of a variety of tumors, including hepatocellular carcinoma. Whereas the strict specificity of action of ERK1 and ERK2 is still debated, the MAPKs may have specific biological functions under certain contexts and according to the differentiation status of the cells, notably hepatocytes. In this paper, we will focus on MEK1/2-ERK1/2 activations and roles in normal rodent hepatocytes in vitro and in vivo after partial hepatectomy and in human hepatocarcinoma cells. The possible specificity of ERK1 and ERK2 in normal and transformed hepatocyte will be discussed in regard to other differentiated and undifferentiated cellular models.