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  In vivo cardiac role of migfilin during experimental pressure overload

Haubner, B. J., Moik, D., Schuetz, T., Reiner, M. F., Voelkl, J. G., Streil, K., et al. (2015). In vivo cardiac role of migfilin during experimental pressure overload. CARDIOVASCULAR RESEARCH, 106(3), 398-407. doi:10.1093/cvr/cvv125.

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 Creators:
Haubner, Bernhard Johannes1, Author
Moik, Daniel2, Author              
Schuetz, Thomas1, Author
Reiner, Martin F.1, Author
Voelkl, Jakob G.1, Author
Streil, Katrin1, Author
Bader, Kerstin1, Author
Zhao, Lei1, Author
Scheu, Claudia1, Author
Mair, Johannes1, Author
Pachinger, Otmar1, Author
Metzler, Bernhard1, Author
Affiliations:
1external, ou_persistent22              
2Fässler, Reinhard / Molecular Medicine, Max Planck Institute of Biochemistry, Max Planck Society, ou_1565147              

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Free keywords: LIPOMA-PREFERRED-PARTNER; NF-KAPPA-B; LIM PROTEIN; HEART-FAILURE; TARGETED DISRUPTION; GENE; HYPERTROPHY; ASSOCIATION; ACTIVATION; ZYXINMigfilin; Cardiac hypertrophy; Cardiac function; Pressure overload; Myocardial remodelling;
 Abstract: Aims Increased myocardial wall strain triggers the cardiac hypertrophic response by increasing cardiomyocyte size, reprogramming gene expression, and enhancing contractile protein synthesis. The LIM protein, migfilin, is a cytoskeleton-associated protein that was found to translocate in vitro into the nucleus in a Ca2+-dependent manner, where it co-activates the pivotal cardiac transcription factor Csx/Nkx2.5. However, the in vivo role of migfilin in cardiac function and stress response is unclear. Methods and results To define the role of migfilin in cardiac hypertrophy, we induced hypertension by transverse aortic constriction (TAC) and compared cardiac morphology and function of migfilin knockout (KO) with wild-type (WT) hearts. Heart size and myocardial contractility were comparable in untreated migfilin KO and WT hearts, but migfilin-null hearts presented a reduced extent of hypertrophic remodelling in response to chronic hypertensile stress. Migfilin KO mice maintained their cardiac function for a longer time period compared with WT mice, which presented extensive fibrosis and death due to heart failure. Migfilin translocated into the nucleus of TAC-treated cardiomyocytes, and migfilin KO hearts showed reduced Akt activation during the early response to pressure overload. Conclusions Our findings indicate an important role of migfilin in the regulation of cardiac hypertrophy upon experimental TAC.

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Language(s): eng - English
 Dates: 2015
 Publication Status: Published in print
 Pages: 10
 Publishing info: -
 Table of Contents: -
 Rev. Type: Peer
 Identifiers: ISI: 000359088400008
DOI: 10.1093/cvr/cvv125
 Degree: -

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Title: CARDIOVASCULAR RESEARCH
Source Genre: Journal
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Publ. Info: GREAT CLARENDON ST, OXFORD OX2 6DP, ENGLAND : OXFORD UNIV PRESS
Pages: - Volume / Issue: 106 (3) Sequence Number: - Start / End Page: 398 - 407 Identifier: ISSN: 0008-6363