Stabilised beta-catenin in postnatal ventricular myocardium leads to dilated cardiomyopathy and premature death.
Details
Serval ID
serval:BIB_B1DC71F5CCDC
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
Stabilised beta-catenin in postnatal ventricular myocardium leads to dilated cardiomyopathy and premature death.
Journal
Basic Research in Cardiology
ISSN
1435-1803[electronic], 0300-8428[linking]
Publication state
Published
Issued date
2010
Volume
105
Number
5
Pages
597-608
Language
english
Abstract
Beta-catenin is a component of the intercalated disc in cardiomyocytes, but can also be involved in signalling and activation of gene transcription. We wanted to determine how long-term changes in beta-catenin expression levels would affect mature cardiomyocytes. Conditional transgenic mice that either lacked beta-catenin or that expressed a non-degradable form of beta-catenin in the adult ventricle were created. While mice lacking beta-catenin in the ventricle do not have an overt phenotype, mice expressing a non-degradable form develop dilated cardiomyopathy and do not survive beyond 5 months. A detailed analysis could reveal that this phenotype is correlated with a distinct localisation of beta-catenin in adult cardiomyocytes, which cannot be detected in the nucleus, no matter how much protein is present. Our report is the first study that addresses long-term effects of either the absence of beta-catenin or its stabilisation on ventricular cardiomyocytes and it suggests that beta-catenin's role in the nucleus may be of little significance in the healthy adult heart.
Keywords
myocyte-specific excision, cardiac-hypertrophy, intercalated disc, signaling pathway, mouse development, nuclear-membrane, progenitor cells, protein emerin, cancer cells, gene, Beta-catenin, Hypertrophy, Intercalated disc, Canonical Wnt signalling, Dilated cardiomyopathy
Pubmed
Web of science
Create date
25/08/2010 11:36
Last modification date
20/08/2019 16:20