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14-3-3 epsilon Plays a Role in Cardiac Ventricular Compaction by Regulating the Cardiomyocyte Cell Cycle
Journal article   Open access   Peer reviewed

14-3-3 epsilon Plays a Role in Cardiac Ventricular Compaction by Regulating the Cardiomyocyte Cell Cycle

Yasuhiro Kosaka, Katarzyna A. Cieslik, Ling Li, George Lezin, Colin T. Maguire, Yukio Saijoh, Kazuhito Toyo-oka, Michael J. Gambello, Matteo Vatta, Anthony Wynshaw-Boris, …
Molecular and cellular biology, v 32(24), pp 5089-5102
01 Dec 2012
PMID: 23071090
url
https://doi.org/10.1128/mcb.00829-12View
Published, Version of Record (VoR)Maybe Open Access (Publisher Bronze) Open
url
https://doi.org/10.1128/MCB.00829-12View
Published, Version of Record (VoR) Open

Abstract

Biochemistry & Molecular Biology Cell Biology Life Sciences & Biomedicine Science & Technology
Trabecular myocardium accounts for the majority of the ventricles during early cardiogenesis, but compact myocardium is the primary component at later developmental stages. Elucidation of the genes regulating compact myocardium development is essential to increase our understanding of left ventricular noncompaction (LVNC), a cardiomyopathy characterized by increased ratios of trabecular to compact myocardium. 14-3-3 epsilon is an adapter protein expressed in the lateral plate mesoderm, but its in vivo cardiac functions remain to be defined. Here we show that 14-3-3 epsilon is expressed in the developing mouse heart as well as in cardiomyocytes. 14-3-3 epsilon deletion did not appear to induce compensation by other 14-3-3 isoforms but led to ventricular noncompaction, with features similar to LVNC, resulting from a selective reduction in compact myocardium thickness. Abnormal compaction derived from a 50% decrease in cardiac proliferation as a result of a reduced number of cardiomyocytes in G(2)/M and the accumulation of cardiomyocytes in the G(0)/G(1) phase of the cell cycle. These defects originated from downregulation of cyclin E1 and upregulation of p27(Kip1), possibly through both transcriptional and posttranslational mechanisms. Our work shows that 14-3-3 epsilon regulates cardiogenesis and growth of the compact ventricular myocardium by modulating the cardiomyocyte cell cycle via both cyclin E1 and p27(Kip1). These data are consistent with the long-held view that human LVNC may result from compaction arrest, and they implicate 14-3-3 epsilon as a new candidate gene in congenital human cardiomyopathies.

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Collaboration types
Domestic collaboration
International collaboration
Web of Science research areas
Biochemistry & Molecular Biology
Cell Biology
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