Adenoviral Expression of Calmodulin Antisense Reduces Hypertrophy in Cultured Cardiomyocytes

:  Sustained myocardial hypertrophy is associated with an increased risk of sudden death and progression to heart failure. Multiple signal pathways are involved in cardiac hypertrophy and understanding their interaction may point to new therapeutic targets. In this work, we tested the hypothesis tha...

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Published in:Artificial organs 2007-04, Vol.31 (4), p.274-277
Main Authors: Arruda, Ligia H., Cestari, Idágene A., Leirner, Adolfo A., Cestari, Ismar N.
Format: Article
Language:English
Subjects:
Adenoviridae - genetics
Adenovirus
Angiotensin II - pharmacology
Animals
Animals, Newborn
Antisense
Calmodulin
Calmodulin - biosynthesis
Calmodulin - genetics
Cardiac myocytes
Cell Enlargement - drug effects
Cells, Cultured
Genetic Vectors
Heart Ventricles - cytology
Hypertrophy
Myocytes, Cardiac - metabolism
Myocytes, Cardiac - pathology
Oligonucleotides, Antisense - pharmacology
Phenylephrine - pharmacology
Rats
Vasoconstrictor Agents - pharmacology
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Summary::  Sustained myocardial hypertrophy is associated with an increased risk of sudden death and progression to heart failure. Multiple signal pathways are involved in cardiac hypertrophy and understanding their interaction may point to new therapeutic targets. In this work, we tested the hypothesis that adenovirus‐mediated calmodulin (CaM) antisense expression will reduce the intracellular availability of CaM and inhibit the hypertrophic response. Three recombinant adenoviruses were constructed: AdASCaM, containing the AntiSense sequence of CaM and the enhanced green fluorescent protein (GFP) coding sequence; AdCaM, containing the coding sequence of CaM and the GFP sequence; and the AdGFP, containing the GFP coding sequence. Neonatal rat ventricular cardiomyocytes were infected with AdASCaM, AdCaM, or AdGFP and stimulated with phenylephrine (PE, 50 µM) or angiotensin II (AngII, 10 µM) for 48 h and cell surface area measured with planimetry. After PE treatment, the surface areas of cardiomyocytes infected with AdASCaM or AdGFP were 411 ± 174.3 µ2 and 832.6 ± 372.3 µ2, respectively (P 
ISSN:0160-564X
1525-1594
DOI:10.1111/j.1525-1594.2007.00375.x