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Molecular characterisation of neonatal cardiac hypertrophy and its regression

Published online by Cambridge University Press:  21 January 2005

Bamini Gopinath
Affiliation:
Department of Molecular and Clinical Genetics, Royal Prince Alfred Hospital, and Central Clinical School, The University of Sydney, Australia
Ronald J. Trent
Affiliation:
Department of Molecular and Clinical Genetics, Royal Prince Alfred Hospital, and Central Clinical School, The University of Sydney, Australia
Bing Yu
Affiliation:
Department of Molecular and Clinical Genetics, Royal Prince Alfred Hospital, and Central Clinical School, The University of Sydney, Australia

Abstract

Neonatal cardiac hypertrophy associated with diabetic pregnancy is transient and regresses naturally, but is associated with increased morbidity and mortality.

This study was undertaken to analyse the changes in expression of 5 cardiac genes, including atrial natriuretic peptide, α- and β-myosin heavy chain, and cardiac and skeletal α-actin genes, using a rat neonatal model, in which cardiac hypertrophy was induced via maternal diabetes.

In the hypertrophied left ventricle of neonates from diabetic mothers, the levels of mRNA from all the above genes except skeletal α-actin were increased by between 1.8- and 12-fold compared with the controls at birth (p < 0.05). In the first 28 days, the level of mRNA for α-myosin heavy chain increased slightly, while that for atrial natriuretic peptide and β-myosin heavy chain decreased continuously similar to the controls, but at a significantly faster rate. No significant difference between the two groups of neonates was observed in all 5 genes after 1 month, indicating complete regression.

Expression of 5 cardiac genes in the neonatal cardiac hypertrophy was characterised in both hypertrophic and regressive phases. Hypertrophic regression provides a unique model for the testing of new drugs or genetic modifying factors in cardiac hypertrophy.

Type
Original Article
Copyright
© 2004 Cambridge University Press

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