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Over expression of Plk1 does not induce cell division in rat cardiac myocytes in vitro

Coxon, C. H., Bicknell, K. A. ORCID: https://orcid.org/0000-0002-5888-1424, Moseley, F. L. and Brooks, G. (2009) Over expression of Plk1 does not induce cell division in rat cardiac myocytes in vitro. PLoS ONE, 4 (8). e6752. ISSN 1932-6203

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To link to this item DOI: 10.1371/journal.pone.0006752

Abstract/Summary

BACKGROUND: Mammalian cardiac myocytes withdraw from the cell cycle during post-natal development, resulting in a non-proliferating, fully differentiated adult phenotype that is unable to repair damage to the myocardium, such as occurs following a myocardial infarction. We and others previously have shown that forced expression of certain cell cycle molecules in adult cardiac myocytes can promote cell cycle progression and division in these cells. The mitotic serine/threonine kinase, Polo-like kinase-1 (Plk1), is known to phosphorylate and activate a number of mitotic targets, including Cdc2/Cyclin B1, and to promote cell division. PRINCIPAL FINDINGS: The mammalian Plk family are all differentially regulated during the development of rat cardiac myocytes, with Plk1 showing the most dramatic decrease in both mRNA, protein and activity in the adult. We determined the potential of Plk1 to induce cell cycle progression and division in cultured rat cardiac myocytes. A persistent and progressive loss of Plk1 expression was observed during myocyte development that correlated with the withdrawal of adult rat cardiac myocytes from the cell cycle. Interestingly, when Plk1 was over-expressed in cardiac myocytes by adenovirus infection, it was not able to promote cell cycle progression, as determined by cell number and percent binucleation. CONCLUSIONS: We conclude that, in contrast to Cdc2/Cyclin B1 over-expression, the forced expression of Plk1 in adult cardiac myocytes is not sufficient to induce cell division and myocardial repair.

Item Type:Article
Refereed:Yes
Divisions:Life Sciences > School of Biological Sciences
Life Sciences > School of Chemistry, Food and Pharmacy > School of Pharmacy > Division of Pharmacology
Interdisciplinary centres and themes > Institute for Cardiovascular and Metabolic Research (ICMR)
ID Code:1985
Publisher:Public Library of Science
Publisher Statement:The Public Library of Science (PLoS) applies the Creative Commons Attribution License (CCAL) to all works we publish. Under the CCAL, authors retain ownership of the copyright for their article, but authors allow anyone to download, reuse, reprint, modify, distribute, and/or copy articles in PLoS journals, so long as the original authors and source are cited. No permission is required from the authors or the publishers.

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