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Titolo:
ISCHEMIC PRECONDITIONING ATTENUATES APOPTOTIC CELL-DEATH ASSOCIATED WITH ISCHEMIA REPERFUSION/
Autore:
MAULIK N; YOSHIDA T; ENGELMAN RM; DEATON D; FLACK JE; ROUSOU JA; DAS DK;
Indirizzi:
UNIV CONNECTICUT,SCH MED,DEPT SURG,DIV CARDIOVASC FARMINGTON CT 06030 BAYSTATE MED CTR,DEPT SURG SPRINGFIELD MA 01107
Titolo Testata:
Molecular and cellular biochemistry
fascicolo: 1-2, volume: 186, anno: 1998,
pagine: 139 - 145
SICI:
0300-8177(1998)186:1-2<139:IPAACA>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
REPERFUSION ARRHYTHMIAS; FREE-RADICALS; HEART; INJURY; CARDIOMYOCYTES; TISSUE;
Keywords:
APOPTOSIS; DNA FRAGMENTATION; ISCHEMIA/REPERFUSION; ISCHEMIC PRECONDITIONING; MYOCARDIAL ADAPTATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
27
Recensione:
Indirizzi per estratti:
Citazione:
N. Maulik et al., "ISCHEMIC PRECONDITIONING ATTENUATES APOPTOTIC CELL-DEATH ASSOCIATED WITH ISCHEMIA REPERFUSION/", Molecular and cellular biochemistry, 186(1-2), 1998, pp. 139-145

Abstract

Apoptosis or programmed cell death is a genetically controlled response for cells to commit suicide and is associated with DNA fragmentation or laddering. The common inducers of apoptosis include oxygen free radicals/oxidative stress and Ca2+ which are also implicated in the pathogenesis of myocardial ischemic reperfusion injury. To examine whether ischemic reperfusion injury is mediated by apoptotic cell death, isolated perfused rat hearts were subjected to 15, 30 or 60 min of ischemia as well as 15 min of ischemia followed by 30, 60, 90 or 120 min of reperfusion. At the end of each experiment, the heart was processed for the evaluation of apoptosis and DNA laddering. Apoptosis was studiedby visualizing the apoptotic cardiomyocytes by direct fluorescence detection of digoxigenin-labeled genomic DNA using APOPTAG(R) in situ apoptosis detection kit. DNA laddering was evaluated by subjecting the DNA obtained from the hearts to 1.8% agarose gel electrophoresis and photographed under UV illumination. The results of our study revealed apoptotic cells only in the 90 and 120 min reperfused hearts as demonstrated by the intense fluorescence of the immunostained digoxigenin-labeled genomic DNA when observed under fluorescence microscopy. None of the ischemic hearts showed any evidence of apoptosis. These results were corroborated with the findings of DNA fragmentation which showed increased ladders of DNA bands in the same reperfused hearts representinginteger multiples of the internucleosomal DNA length (about 180 bp). The presence of apoptotic cells and DNA fragmentation in the myocardium were completely abolished by subjecting the myocardium to repeated short-term ischemia and reperfusion which also reduced the ischemic reperfusion injury as evidenced by better recovery of left ventricular performance in the preconditioned myocardium. The results of this study indicate that reperfusion of ischemic heart, but not ischemia, inducesapoptotic cell death and DNA fragmentation which can be inhibited by myocardial adaptation to ischemia.

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Documento generato il 20/09/20 alle ore 01:09:32