NDLI: p38 deficiency and oxidative stress cause cytokinesis failure in hepatocytes.

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p38 deficiency and oxidative stress cause cytokinesis failure in hepatocytes.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Tormos Ana, M. Taléns-Visconti, Raquel Jorques, María Pérez-Garrido, Salvador Bonora-Centelles, Ana Nebreda Ángel, R. Sastre, Juan
Description	Country affiliation: Spain Author Affiliation: Tormos Ana M ( University of Valencia (Faculty of Pharmacy), Department of Pharmacy and Pharmaceutical Technology, Spain.); Taléns-Visconti R ( University of Valencia (Faculty of Pharmacy), Department of Pharmacy and Pharmaceutical Technology, Spain.); Jorques M ( University of Valencia (Faculty of Pharmacy), Department of Pharmacy and Pharmaceutical Technology, Spain.); Pérez-Garrido S ( University of Valencia (Faculty of Pharmacy), Department of Pharmacy and Pharmaceutical Technology, Spain.); Bonora-Centelles A ( University of Valencia (Faculty of Pharmacy), Department of Pharmacy and Pharmaceutical Technology, Spain.); Nebreda Ángel R ( Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona, Spain.); Sastre J ( University of Valencia (Faculty of Pharmacy), Department of Pharmacy and Pharmaceutical Technology, Spain.)
Abstract	Cytokinesis is the last step in mitosis and it implies re-organization of the actin cytoskeleton. Its failure is one of the major mechanisms of polyploidy and binucleation in mammals. Our aims were 1) to assess the role of redox-sensitive p38 MAPK in cytokinesis by studying the liver of wild type mice or liver-specific p38 knock-out mice; 2) to assess the role of oxidative stress associated with hepatocyte isolation on cytokinesis. When p38 was down-regulated in hepatocytes, MK2 phosphorylation on threonine 334 was completely abrogated. Activation of MNK-1, required for abscission of the intercellular bridge, was diminished. Key proteins of the RhoA pathway (phospho-PRK2, nuclear phosphorylated cofilin, and cytosolic p27) were assessed confirming the impairment of this pathway. The absence of p38 in aging liver also led to a decrease in HSP27 phosphorylation, which is required for actin polymerization. Indeed, a severe impairment in the F-actin filamentous structure was found in the liver of old mice upon p38 deficiency. Consequently, long-term p38 MAPK down-regulation markedly affects the RhoA pathway and actin cytoskeleton dynamics inducing actin disassembly and cytokinesis failure upon aging. On the other hand, hepatocyte isolation caused marked glutathione depletion, increased generation of reactive oxygen species, and activated cell cycle entry. Addition of N-acetyl cysteine to isolation media prevented glutathione depletion, restrained the cell cycle entry, and abrogated defective cytokinesis and the formation of binucleated hepatocytes during isolation. Our results show that hepatocytes do enter into S phase but they do not complete cell division with age upon p38 deficiency or upon oxidative stress associated with isolation leading in both cases to cytokinesis failure and binucleation.
File Format	HTM / HTML
ISSN	08915849
Issue Number	Suppl 1
Journal	Free Radical Biology and Medicine
Volume Number	75
e-ISSN	18734596
Language	English
Publisher	Elsevier
Publisher Date	2014-10-01
Publisher Place	United States
Access Restriction	One Nation One Subscription (ONOS)
Content Type	Text
Resource Type	Article
Subject	Physiology (medical) Biochemistry

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