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Involvement of nuclear phosphatidylinositol‐dependent phospholipases c in cell cycle progression during rat liver regeneration
Author(s) -
Albi Elisabetta,
Rossi Graziella,
Maraldi Nadir Mario,
Magni Mariapia Viola,
Cataldi Samuela,
Solimando Liliana,
Zini Nicoletta
Publication year - 2003
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.10292
Subject(s) - biology , cell cycle , microbiology and biotechnology , dna replication , lamin , liver regeneration , chromatin , phospholipase c , nuclear membrane , dna synthesis , cell , regeneration (biology) , dna , signal transduction , biochemistry , nucleus
Abstract Nuclear lipid metabolism is involved in the regulation of cell proliferation. Modulation of the expression and activity of nuclear PI‐phospholipase C (PI‐PLC) has been reported during liver regeneration after partial hepatectomy, although it has not been determined whether different PLC isoforms play specific roles in the regulation of cell cycle progression. Here, we report evidence that the increased activity of nuclear PLCs in regenerating rat liver occurs before the peak of DNA replication and involves the enzyme activity associated to the chromatin and not that associated to the nuclear membrane. Immunocytochemical analyses indicate that PI‐PLC β 1 isoform is exclusively localized at the chromatin level, PI‐PLC β 1 co‐localizes with DNA replication sites much more than PI‐PLC γ 1 , which is also present at the nuclear envelope. These findings and the increased amount of PI‐PLC γ 1 occurring after the peak of DNA replication suggest that PI‐PLC β 1 and γ 1 play different roles in cell cycle progression during regenerating liver. The increased activity of PI‐PLC β 1 constitutively present within the hepatocyte nucleus, should trigger DNA replication, whereas PI‐PLC γ 1 should be involved in G2/M phase transition through lamin phosphorylation. J. Cell. Physiol. 197: 181–188, 2003. © 2003 Wiley‐Liss, Inc.