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Titolo:
Mineralocorticoid receptor affects AP-1 and nuclear factor-kappa B activation in angiotensin II-Induced cardiac injury
Autore:
Fiebeler, A; Schmidt, F; Muller, DN; Park, JK; Dechend, R; Bieringer, M; Shagdarsuren, E; Breu, V; Haller, H; Luft, FC;
Indirizzi:
Franz Volhard Clin, D-13125 Berlin, Germany Franz Volhard Clin Berlin Germany D-13125 Clin, D-13125 Berlin, Germany Humboldt Univ, Charite, Fac Med, Max Delbruck Ctr Mol Med, Berlin, GermanyHumboldt Univ Berlin Germany Max Delbruck Ctr Mol Med, Berlin, Germany F Hoffmann La Roche & Co Ltd, Dept Med Nephrol, CH-4002 Basel, SwitzerlandF Hoffmann La Roche & Co Ltd Basel Switzerland CH-4002 asel, Switzerland Univ Hannover, Hannover Med Sch, D-30167 Hannover, Germany Univ Hannover Hannover Germany D-30167 ed Sch, D-30167 Hannover, Germany
Titolo Testata:
HYPERTENSION
fascicolo: 2, volume: 37, anno: 2001,
parte:, 2 supplemento:, S
pagine: 787 - 793
SICI:
0194-911X(200102)37:2<787:MRAAAN>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
CONGESTIVE-HEART-FAILURE; SMOOTH-MUSCLE CELLS; PROTEIN-KINASE; ALDOSTERONE PRODUCTION; MEDIATED REGULATION; HYPERTENSIVE RATS; GENE-EXPRESSION; SPIRONOLACTONE; FIBROSIS; MECHANISMS;
Keywords:
angiotensin; nuclear factors; receptors, mineralocorticoid; spironolactone;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Luft, FC Franz Volhard Clin, Wiltberg Str 50, D-13125 Berlin, Germany Franz Volhard Clin Wiltberg Str 50 Berlin Germany D-13125 ermany
Citazione:
A. Fiebeler et al., "Mineralocorticoid receptor affects AP-1 and nuclear factor-kappa B activation in angiotensin II-Induced cardiac injury", HYPERTENSIO, 37(2), 2001, pp. 787-793

Abstract

Aldosterone is implicated in cardiac hypertrophy and fibrosis. We tested the role of the mineralocorticoid receptor in a model of angiotensin II-induced cardiac injury. We administered spironolactone (SPIRO; 20 mg . kg(-1) .d(-1)), valsartan (VAL; 10 mg . kg(-1) . d(-1)), or vehicle to rats doubletransgenic for the human renin and angiotensinogen genes (dTGR). We investigated basic fibroblast growth factor (bFGF), platelet-derived growth factor, transforming growth factor-beta (1), and the transcription factors AP-1 and nuclear factor (NF)-kappaB. We used immunohistochemistry, electrophoretic mobility shift assays, and TaqMan RT-PCR. Untreated dTGR developed hypertension, cardiac hypertrophy, vasculopathy, and fibrosis with a 50% mortality rates at 7 weeks. SPIRO and VAL prevented death and reversed cardiac hypertrophy, while only VAL normalized blood pressure. Both drugs prevented vasculopathy. bFGF was markedly upregulated in dTGR, whereas platelet-derivedgrowth factor-B and transforming growth factor-beta (1) were little changed. VAL and SPIRO suppressed this upregulation. Both AP-1 and NF-kappaB wereactivated in dTGR compared with controls. VAL and SPIRO reduced both transcription factors and reduced bFGF, collagen I, fibronectin, and laminin in the interstitium. These findings show that aldosterone promotes hypertrophy, cardiac remodeling, and fibrosis, independent of blood pressure. The effects involve AP-1, NF-kappaB, and bFGF. Mineralocorticoid receptor blockade downregulates these effecters and reduces angiotensin II-induced cardiac damage.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 16:28:34