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Titolo:
Inhibition of endogenous nitric oxide synthase potentiates ischemia-reperfusion-induced myocardial apoptosis via a caspase-3 dependent pathway
Autore:
Weiland, U; Haendeler, J; Ihling, C; Albus, U; Scholz, W; Ruetten, H; Zeiher, AM; Dimmeler, S;
Indirizzi:
Univ Frankfurt, Dept Internal Med 4, D-60596 Frankfurt, Germany Univ Frankfurt Frankfurt Germany D-60596 d 4, D-60596 Frankfurt, Germany Univ Freiburg, Inst Pathol, D-7800 Freiburg, Germany Univ Freiburg Freiburg Germany D-7800 t Pathol, D-7800 Freiburg, Germany Hoechst AG, D-6230 Frankfurt, Germany Hoechst AG Frankfurt Germany D-6230 oechst AG, D-6230 Frankfurt, Germany
Titolo Testata:
CARDIOVASCULAR RESEARCH
fascicolo: 3, volume: 45, anno: 2000,
pagine: 671 - 678
SICI:
0008-6363(200002)45:3<671:IOENOS>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROGRAMMED CELL-DEATH; ISOLATED RAT HEARTS; L-ARGININE; IN-VIVO; BCL-2; CARDIOMYOCYTES; INJURY; BAX; IDENTIFICATION; PROTEINS;
Keywords:
apoptosis; ischemia; nitric oxide; reperfusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Dimmeler, S Univ Frankfurt, Dept Internal Med 4, Theodor SternKai 7, D-60596 Frankfurt, Germany Univ Frankfurt Theodor SternKai 7 Frankfurt Germany D-60596 y
Citazione:
U. Weiland et al., "Inhibition of endogenous nitric oxide synthase potentiates ischemia-reperfusion-induced myocardial apoptosis via a caspase-3 dependent pathway", CARDIO RES, 45(3), 2000, pp. 671-678

Abstract

Objective: Apoptosis of cardiomyocytes may contribute to ischemia-reperfusion injury. The rule of nitric oxide (NO) in apoptosis is controversial. Therefore, we investigated the effect of NO synthase inhibition on apoptosis of cardiomyocytes during ischemia and reperfusion and elucidated the underlying mechanisms. Methods and results: Isolated perfused rat hearts (n=6/group) were subjected to ischemia (30 min) and reperfusion (30 min) in the presence or absence of the NO synthase inhibitor N-G-mono-methyl-L-arginine. Reperfusion induced cardiomyocyte apoptosis as assessed by immunohistochemistry (TUNEL-staining) and the demonstration of the typical DNA laddering. Apoptosis during reperfusion was associated with the cleavage of caspase-3, the final down-stream executioner caspase, whereas the protein levels of theanti-apoptotic protein Bcl-2 and the pro-apoptotic protein Bar were unchanged. Inhibition of the NO synthase drastically increased ischemia and reperfusion-induced apoptosis of cardiomyocytes. Moreover, the NO synthase inhibitor enhanced the activation of caspase-3, suggesting that NO interferes with the activation of caspases in ischemia-reperfusion. Conclusion: The results of the present study demonstrate that inhibition of endogenous NO synthesis during ischemia and reperfusion leads to an enhanced induction of apoptosis, suggesting that the endogenous NO synthesis protects against apoptotic cell death. Inhibition of NO synthesis thereby activates the caspase cascade, whereas the Bcl-2/Bax protein levels remained unchanged. (C) 2000 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 10/07/20 alle ore 12:55:02