Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Caveolin-1 peptide exerts cardioprotective effects in myocardial ischemia-reperfusion via nitric oxide mechanism
Autore:
Young, LH; Ikeda, Y; Lefer, AM;
Indirizzi:
Thomas Jefferson Univ, Jefferson Med Coll, Dept Physiol, Philadelphia, PA 19107 USA Thomas Jefferson Univ Philadelphia PA USA 19107 hiladelphia, PA 19107 USA
Titolo Testata:
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY
fascicolo: 6, volume: 280, anno: 2001,
pagine: H2489 - H2495
SICI:
0363-6135(200106)280:6<H2489:CPECEI>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
PROTEIN-KINASE-C; HUMAN ENDOTHELIAL-CELLS; P-SELECTIN EXPRESSION; TIME-COURSE; RAT HEARTS; SIGNAL-TRANSDUCTION; SYNTHASE ACTIVITY; RELEASE; INJURY; NEUTROPHILS;
Keywords:
contractile dysfunction; polymorphonuclear leukocytes; polymorphonuclear neutrophil adherence;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
33
Recensione:
Indirizzi per estratti:
Indirizzo: Lefer, AM Thomas Jefferson Univ, Jefferson Med Coll, Dept Physiol, 1020 Locust St, Philadelphia, PA 19107 USA Thomas Jefferson Univ 1020 Locust St Philadelphia PA USA 19107 A
Citazione:
L.H. Young et al., "Caveolin-1 peptide exerts cardioprotective effects in myocardial ischemia-reperfusion via nitric oxide mechanism", AM J P-HEAR, 280(6), 2001, pp. H2489-H2495

Abstract

Caveolin-1 is a protein constituent of cell membranes. The caveolin-1 scaffolding region (residues 82-101) is a known inhibitor of protein kinase C. Inhibition of protein kinase C results in maintained nitric oxide (NO) release from the endothelium, which attenuates cardiac dysfunction after ischemia-reperfusion (I/R). Therefore, we hypothesized that the caveolin-1 scaffolding region of the molecule, termed caveolin-1 peptide, might attenuate postischemia polymorphonuclear neutrophil (PMN)-induced cardiac dysfunction. We examined the effects of caveolin-1 peptide in isolated ischemic (20 min)and reperfused (45 min) rat hearts reperfused with PMNs. Caveolin-1 peptide (165 or 330 mug) given intravenously 1 h before I/R significantly attenuated postischemic PMN-induced cardiac dysfunction, as exemplified by left ventricular developed pressure (LVDP) (P< 0.01) and the maximal rate of develped pressure (+dP/dt(max))( P< 0.01), compared with I/R hearts obtained from rats given 0.9% NaCl. In addition, caveolin-1 peptide significantly reduced cardiac PMN infiltration from 195 +/- 5 PMNs/mm(2) in untreated hearts to 103 +/- 5 and 60 +/- 5 PMNs/mm(2) in hearts from 165 and 330 mg caveolin-1 peptide-treated rats, respectively (P< 0.01). PMN adherence to the rat coronary vasculature was also significantly reduced in rats given either 165 or 330 mg caveolin-1 peptide compared with rats given 0.9% NaCl (P< 0.01). Moreover, caveolin-1 peptide-treated rat aortas exhibited a 2.2-fold greater basal release of NO than vehicle-treated aortas (P< 0.01), and this was inhibited by N-G-nitro-L-arginine methyl ester. These results provide evidence that caveolin-1 peptide significantly attenuated PMN-induced post-I/R cardiac contractile dysfunction in the isolated perfused rat heart, probably via enhanced release of endothelium-derived NO.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:42:20