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Titolo:
Tumor necrosis factor-alpha induces apoptosis via inducible nitric oxide synthase in neonatal mouse cardiomyocytes
Autore:
Song, W; Lu, XR; Feng, QP;
Indirizzi:
Univ Western Ontario, Cardiol Res Lab, London Hlth Sci Ctr, Dep Med,Cardiol Div,Dept Pharmacol & Toxicol, London, ON N6A 4G5, Canada Univ Western Ontario London ON Canada N6A 4G5 London, ON N6A 4G5, Canada
Titolo Testata:
CARDIOVASCULAR RESEARCH
fascicolo: 3, volume: 45, anno: 2000,
pagine: 595 - 602
SICI:
0008-6363(200002)45:3<595:TNFIAV>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; CARDIAC MYOCYTES; EXPRESSION; DEATH; PHARMACOLOGY; CYTOTOXICITY; PHYSIOLOGY; DISEASE; NO;
Keywords:
apoptosis; myocytes; nitric oxide;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
32
Recensione:
Indirizzi per estratti:
Indirizzo: Feng, QP Univ Western Ontario, Cardiol Res Lab, London Hlth Sci Ctr, Dep Med,Cardiol Div,Dept Pharmacol & Toxicol, London, ON N6A 4G5, Canada Univ Western Ontario London ON Canada N6A 4G5 ON N6A 4G5, Canada
Citazione:
W. Song et al., "Tumor necrosis factor-alpha induces apoptosis via inducible nitric oxide synthase in neonatal mouse cardiomyocytes", CARDIO RES, 45(3), 2000, pp. 595-602

Abstract

Objective: It has been demonstrated that tumor necrosis factor-alpha (TNF alpha) induces apoptosis in cardiac myocytes. However, its mechanism of action is still not well understood. In the present study, we hypothesized that TNFa induces myocardial apoptosis by induction of inducible nitric oxide synthase (iNOS). Methods: Neonatal cardiac myocytes were isolated from iNOS(-/-) mutant and C57BL6 wild type mice. Cells were cultured for 3 days before treatment with an NO donor or TNF alpha. Following treatment with S-nitroso-N-acetyl-penicillamine (SNAP) or TNF-alpha, cells were tested for apoptosis by terminal deoxynucleotidyl transfer-mediated end labeling (TUNEL) staining and cell death detection ELISA. NO production was measured by nitrite concentration in the culture medium. Cardiomyocyte expression of iNOS and TNF type 1 receptor (TNFR1) mRNA was determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: SNAP (0.01-100 mu M) induced apoptosis of cardiac myocytes in a concentration-dependent manner in the wild type mice (n=5, P<0.01). TNFR1 mRNA was expressed in neonatal cardiomyocytes from both wild type and iNOS (-/-) mutant mice. TNF alpha induced a concentration-dependent increase in iNOS mRNA expression and nitrite production as well as significant apoptosis of cardiomyocytes in the wild type mice (n=4, P<0.01). However, without iNOS expression, the apoptotic effects of TNF-alpha were significantly attenuated in cardiomyocytes from iNOS (-/-) mutant mice (n=4, P<0.05). Conclusion: TNF alpha induces apoptosis via iNOS expression and NO production in neonatal mouse cardiomyocytes. (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 14/07/20 alle ore 12:11:37