Cross talk between corticosteroids and alpha-adrenergic signalling augments cardiomyocyte hypertrophy: a possible role for SGK1

Cardiovascular Research
Kerrie ListerKaren E Sheppard

Abstract

Mineralocorticoids and glucocorticoids have been implicated in the pathogenesis of cardiac diseases; however, both in vivo and in vitro studies indicate that changes in the cellular milieu of either the cardiomyocyte and/or cells of the vasculature is required for corticosteroid signalling to be pathological. The aim of the current study was to directly address whether signalling pathways that are activated during myocyte hypertrophy alter corticosteroid signalling and thus enable these steroids to significantly impact on the hypertrophic response. Neonatal rat ventricular cardiomyocytes were treated with phenylephrine or phorbol ester for 48 h to induce myocyte hypertrophy. Following treatment, the expression of glucocorticoid receptor, mineralocorticoid receptor, and 11beta-hydroxysteroid dehydrogenase were determined by ribonuclease protection assay. In addition, the activity of 11beta-hydroxysteroid dehydrogenase and the ability of glucocorticoid and mineralocorticoid receptors to induce serum- and glucocorticoid-induced kinase 1 (SGK1) gene transcription were assessed. Corticosteroid effects on phenylephrine and phorbol ester-induced hypertrophy were determined by measuring atrial natriuretic peptide (ANP) mRNA expression,...Continue Reading

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