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Titolo:
GENETIC DISRUPTION OF POLY (ADP-RIBOSE) SYNTHETASE INHIBITS THE EXPRESSION OF P-SELECTIN AND INTERCELLULAR-ADHESION MOLECULE-1 IN MYOCARDIAL ISCHEMIA REPERFUSION INJURY/
Autore:
ZINGARELLI B; SALZMAN AL; SZABO C;
Indirizzi:
CHILDRENS HOSP,MED CTR,DIV CRIT CARE,3333 BURNET AVE CINCINNATI OH 45229
Titolo Testata:
Circulation research
fascicolo: 1, volume: 83, anno: 1998,
pagine: 85 - 94
SICI:
0009-7330(1998)83:1<85:GDOP(S>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
ISCHEMIA-REPERFUSION INJURY; CELLULAR-ENERGY DEPLETION; PEROXIDE-INDUCED INJURY; DNA STRAND BREAKAGE; POLY(ADP-RIBOSE) SYNTHETASE; ICAM-1 EXPRESSION; CANINE MYOCARDIUM; HYDROGEN-PEROXIDE; MONOCLONAL-ANTIBODY; NEUTROPHIL ADHESION;
Keywords:
NITRIC OXIDE; PEROXYNITRITE; CELL ADHESION MOLECULE; NEUTROPHIL; 3-AMINOBENZAMIDE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
56
Recensione:
Indirizzi per estratti:
Citazione:
B. Zingarelli et al., "GENETIC DISRUPTION OF POLY (ADP-RIBOSE) SYNTHETASE INHIBITS THE EXPRESSION OF P-SELECTIN AND INTERCELLULAR-ADHESION MOLECULE-1 IN MYOCARDIAL ISCHEMIA REPERFUSION INJURY/", Circulation research, 83(1), 1998, pp. 85-94

Abstract

The nuclear enzyme poly (ADP-ribose) synthetase (PARS) has been shownto play an important role in the pathogenesis of ischemia/reperfusioninjury and circulatory shock. The aim of this study was to investigate whether PARS activity may modulate endothelial-neutrophil interaction. We present evidence that genetic disruption of PARS provides protection against myocardial ischemia and reperfusion injury by inhibiting the expression of P-selectin and intercellular adhesion molecule-1 (ICAM-1) and, consequently, by inhibiting the recruitment of neutrophils into the jeopardized tissue. Furthermore, using in vitro studies, we demonstrate that in fibroblasts lacking a functional gene for PARS, cytokine-stimulated expression of ICAM-1 is significantly reduced compared with fibroblasts from animals with a normal genotype, Similarly, in cultured human endothelial cells, oxidative- or cytokine-dependent expression of P-selectin and ICAM-1 is reduced by pharmacological inhibition of PARS by 3-aminobenzamide. These findings provide the first direct evidence that PARS activation participates in neutrophil-mediated myocardial damage by regulating the expression of P-selectin and ICAM-1in ischemic and reperfused myocardium, and they also provide the basis for a novel therapeutic approach for the treatment of reperfusion injury.

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Documento generato il 09/04/20 alle ore 10:58:02