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Titolo:
Protection against ischemia/reperfusion injury and myocardial dysfunction by antisense-oligodeoxynucleotide directed at angiotensin-converting enzymemRNA
Autore:
Chen, H; Mohuczy, D; Li, D; Kimura, B; Phillips, MI; Mehta, P; Mehta, JL;
Indirizzi:
Univ Arkansas, Dept Med & Physiol, Little Rock, AR 72204 USA Univ Arkansas Little Rock AR USA 72204 Physiol, Little Rock, AR 72204 USA VA Med Ctr, Little Rock, AR USA VA Med Ctr Little Rock AR USAVA Med Ctr, Little Rock, AR USA Univ Florida, Coll Med, Dept Physiol, Gainesville, FL USA Univ Florida Gainesville FL USA l Med, Dept Physiol, Gainesville, FL USA
Titolo Testata:
GENE THERAPY
fascicolo: 10, volume: 8, anno: 2001,
pagine: 804 - 810
SICI:
0969-7128(200105)8:10<804:PAIIAM>2.0.ZU;2-1
Fonte:
ISI
Lingua:
ENG
Soggetto:
RECEPTOR MESSENGER-RNA; BRADYKININ ANTAGONIST; ISCHEMIA-REPERFUSION; ENDOTHELIAL-CELLS; BLOOD-PRESSURE; INFARCT SIZE; GENE-THERAPY; IN-VIVO; INHIBITION; HEART;
Keywords:
antisense; angiotensin-converting enzyme; captopril; cardioprotection; ischemia/reperfusion;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Mehta, JL Univ Arkansas Med Sci, 4301 W Markham,Mail Slot 532, Little Rock, AR 72205USA Univ Arkansas Med Sci 4301 W Markham,Mail Slot 532 Little Rock AR USA 72205
Citazione:
H. Chen et al., "Protection against ischemia/reperfusion injury and myocardial dysfunction by antisense-oligodeoxynucleotide directed at angiotensin-converting enzymemRNA", GENE THER, 8(10), 2001, pp. 804-810

Abstract

Angiotensin-converting enzyme (ACE) activity in the myocardium and angiotensin-II (Ang-II) levels in plasma increase after myocardial ischemia, whichlead to exacerbation of myocardial injury and cardiac dysfunction. We examined the protective role of no vel antisense-oligodeoxynucleotide (AS-ODN) directed at ACE mRNA in myocardial ischemic injury. Sprague-Dawley rats were treated with ACE-AS-ODN (200 mug per rat n = 8, i.v.) or inverted-ODN (IN-ODN, 200 mug per rat, n = 8, iv.), given with 600 mug per rat of liposome DOTAP/DOPE. Hearts from AS-ODN- or IN-ODN-treated rats were excised, perfused in vitro, and subjected to 25 min of global ischemia followed by 30 min of reperfusion. Parallel groups of rats were given ACE inhibitor captopril (5 mg/kg, n = 8) or saline (n = 8) before excising the hearts. Ischemia/reperfusion resulted in myocardial dysfunction (increase in coronary perfusionpressure and LV end-diastolic pressure and a decrease in developed LV pressure) in the saline-treated rats. Myocardial dysfunction was associated with evidence of lipid peroxidation and enzyme leakage (MDA and LDH levels in the myocardium) and up-regulation of ACE protein expression. Administrationof AS-ODN or captopril, but not IN-ODN, reduced Ang-II levels in the plasma, decreased ischemia/reperfusion-mediated cardiac functional deteriorationand lipid peroxidation, and preserved LDH in the myocardium (all P < 0.05 versus the saline group). AS-ODN and captopril had equipotent effects on cardiac dynamics. ACE protein expression (Western blot) was decreased in the hearts of the AS-ODN-treated group, but not in IN-ODN-treated rat hearts. In contrast, ACE protein expression was significantly increased in captopril-treated rat hearts. These observations suggest that AS-ODN directed at ACEmRNA can ameliorate myocardial dysfunction and injury after ischemia/reperfusion, and its use is associated with decreased expression of ACE protein in the ischemic myocardium.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/01/20 alle ore 17:14:05