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Titolo:
PREREQUISITE FOR CARDIAC ALDOSTERONE ACTION - MINERALOCORTICOID RECEPTOR AND 11-BETA-HYDROXYSTEROID DEHYDROGENASE IN THE HUMAN HEART
Autore:
LOMBES M; ALFAIDY N; EUGENE E; LESSANA A; FARMAN N; BONVALET JP;
Indirizzi:
UNIV PARIS 07,INST FEDERAT RECH CELLULES EPITHELIALES,INSERM,U246,16 RUE H HUCHARD F-75870 PARIS 18 FRANCE
Titolo Testata:
Circulation
fascicolo: 2, volume: 92, anno: 1995,
pagine: 175 - 182
SICI:
0009-7322(1995)92:2<175:PFCAA->2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
ANTI-IDIOTYPIC ANTIBODY; MYOCARDIAL FIBROSIS; DEPENDENT ISOFORM; GENE-EXPRESSION; INTERNAL IMAGE; BINDING-SITES; TARGET-CELLS; RAT; LOCALIZATION; HORMONES;
Keywords:
ADRENAL CORTEX HORMONES; GLUCOCORTICOIDS TRANSPLANTATION; ANTIBODIES; ENZYMES;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
40
Recensione:
Indirizzi per estratti:
Citazione:
M. Lombes et al., "PREREQUISITE FOR CARDIAC ALDOSTERONE ACTION - MINERALOCORTICOID RECEPTOR AND 11-BETA-HYDROXYSTEROID DEHYDROGENASE IN THE HUMAN HEART", Circulation, 92(2), 1995, pp. 175-182

Abstract

Background It has been proposed that aldosterone exerts direct effects on heart function, most notably on the development of myocardial fibrosis during ventricular hypertrophy in rat. Initial events in aldosterone action entail its binding to mineralocorticoid receptor (MR). Because MR displays similar affinities for aldosterone and glucocorticoids, the in vivo aldosterone selectivity of MR requires the presence of an enzyme, 11 beta-hydroxysteroid dehydrogenase (11-HSD), which metabolizes glucocorticoids into inactive derivatives. Although evidence exists for the presence of MR in rodent heart, no data are available for humans; moreover, the existence of cardiac 11-HSD is controversial. Methods and Results The heart samples used originated from tissue removed during cardiac surgery in nontransplant patients or from endocavitary biopsies done for the follow-up of heart transplantation. The expression of MR was examined at the mRNA and protein level by in situ hybridization with cRNA probes specific for human MR mRNA and by immuno-detection with two specific anti-MR antibodies. 11-HSD catalytic activitywas determined by measurement of the metabolic rate of tritiated corticosteroids by cardiac samples. In nontransplanted hearts, an in situ hybridization signal equivalent to that found in the whole kidney was present on cardiomyocytes. Specific immunolabeling of cardiomyocytes with anti-MR antibodies demonstrated the presence of the MR protein. Cardiac 11-HSD activity was detected (243+/-26 fmol . 30 min(-1) . mg protein(-1)) and was dependent on the cofactor NAD, not NADP, suggestingthat it corresponds to the form of the enzyme specifically responsible for MR protection. In transplanted hearts that presented severe alterations, MR immunodetection was weaker and irregular, with no specifichybridization signal. Conclusions Our results demonstrate that MR is coexpressed with 11-HSD in human heart, which thus possesses the cellular machinery required for direct aldosterone action.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 21:44:31