Restoration of calcium handling properties of adult cardiac myocytes from hypertrophied hearts

Reductions in cardiac sarcoplasmic reticulum calcium-ATPase (Serca2a) levels are thought to underlie the prolonged calcium (Ca2+) transients and consequent reduced contractile performance seen in human cardiac hypertrophy and heart failure. In freshly isolated cardiac myocytes from rats with monocro...

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Bibliographic Details
Published in:Cell calcium (Edinburgh) 2001-07, Vol.30 (1), p.59-66
Main Authors: Reilly, A.M., Petrou, S., Pancha, R.G., Williams, D.A.
Format: Article
Language:English
Subjects:
Adenoviridae Infections - enzymology
Adenoviridae Infections - metabolism
Adenoviridae Infections - pathology
Animals
Calcium - metabolism
Calcium - physiology
Calcium-Transporting ATPases - metabolism
Cardiomegaly - enzymology
Cardiomegaly - metabolism
Cardiomegaly - pathology
Cells, Cultured
Genetic Vectors - chemical synthesis
Heart Ventricles - drug effects
Heart Ventricles - metabolism
Heart Ventricles - pathology
Humans
Injections, Intraperitoneal
Male
Monocrotaline - administration & dosage
Myocardium - enzymology
Myocardium - metabolism
Myocardium - pathology
Rats
Rats, Sprague-Dawley
Sarcoplasmic Reticulum Calcium-Transporting ATPases
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Summary:Reductions in cardiac sarcoplasmic reticulum calcium-ATPase (Serca2a) levels are thought to underlie the prolonged calcium (Ca2+) transients and consequent reduced contractile performance seen in human cardiac hypertrophy and heart failure. In freshly isolated cardiac myocytes from rats with monocrotaline-induced right ventricular hypertrophy we found reduced sarcoplasmic reticulum Serca2a expression and prolonged Ca2+transients, characteristic of hypertrophic cardiac disease. Modulation of intracellular Ca2+levels, Ca2+kinetics or Ca2+sensitivity is the focus of many current therapeutic approaches to improve contractile performance in the hypertrophic or failing heart. However, the functional effects of increasing Serca2a expression on Ca2+handling properties in myocytes from an animal model of cardiac hypertrophy are largely unknown. Here, we describe enhancement of the deficient Ca2+handling properties evident in myocytes from hypertrophied hearts following adenoviral-mediated transfer of the human Serca2a gene to these myocytes. These results highlight the importance of Serca2a deficiencies in the hypertrophic phenotype of cardiac muscle and suggest a simple, effective approach for manipulation of normal cardiac function.
ISSN:0143-4160
1532-1991
DOI:10.1054/ceca.2001.0213