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Titolo:
L-arginine administration reduces neointima formation after stent injury in rats by a nitric oxide-mediated mechanism
Autore:
Vermeersch, P; Nong, Z; Stabile, E; Varenne, O; Gillijns, H; Pellens, M; Van Pelt, N; Hoylaerts, M; De Scheerder, I; Collen, D; Janssens, S;
Indirizzi:
Flanders Interuniv Inst Biotechnol, Ctr Transgene Technol & Gene Therapy, B-3000 Louvain, Belgium Flanders Interuniv Inst Biotechnol Louvain Belgium B-3000 uvain, Belgium Katholieke Univ Leuven, Dept Cardiol, Louvain, Belgium Katholieke Univ Leuven Louvain Belgium , Dept Cardiol, Louvain, Belgium
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 10, volume: 21, anno: 2001,
pagine: 1604 - 1609
SICI:
1079-5642(200110)21:10<1604:LARNFA>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
MUSCLE CELL-PROLIFERATION; PLASMINOGEN-ACTIVATOR INHIBITOR-1; SYNTHASE GENE-TRANSFER; BALLOON INJURY; INTIMAL HYPERPLASIA; ENDOTHELIAL DYSFUNCTION; CORONARY ANGIOPLASTY; ARTERIAL INJURY; CAROTID-ARTERY; IN-VIVO;
Keywords:
arginine; neointima formation; gene therapy; stents; nitric oxide synthase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
44
Recensione:
Indirizzi per estratti:
Indirizzo: Janssens, S Flanders Interuniv Inst Biotechnol, Ctr Transgene Technol & Gene Therapy, 49 Herestr, B-3000 Louvain, Belgium Flanders Interuniv Inst Biotechnol 49 Herestr Louvain Belgium B-3000
Citazione:
P. Vermeersch et al., "L-arginine administration reduces neointima formation after stent injury in rats by a nitric oxide-mediated mechanism", ART THROM V, 21(10), 2001, pp. 1604-1609

Abstract

The clinical outcome of vascular stenting is limited by in-stent stenosis. Increased nitric oxide (NO)/cGMP signaling by L-arginine (L-Arg) supplementation, the substrate for NO synthase (NOS), or NOS gene transfer may reduce in-stent neointima formation. After stenting, vascular cell proliferationin rat carotid arteries, as measured by 5'-bromodeoxyuridine (5'-BrdU) incorporation, indicated 15 +/-8%, 28 +/-5%, and 33 +/-7% 5'-BrdU-positive vascular cells at 4, 7, and 14 days, respectively. Reporter beta -galactosidase gene transfer efficacy was evidenced by 30% beta -galactosidase-expressing medial smooth muscle cells at 14 days. The intima-to-media ratio (I/M) progressively increased to 2.32 +/-0.24 at 14 days. To target in-stent neointima formation, animals were infected with adenoviral vectors (4x10(10) plaque-forming units per mL) expressing NOS2 (AdNOS2) or no transgene (AdRR5), or they received daily doses of L-Arg (500 mg.kg(-1).(d-1) IP). The neointima at 14 days was smaller in L-Arg-treated than in untreated rats (I/M 1.25+/-0.35 vs 2.32 +/-0.24, P<0.05, n=7 each) or in AdRR5- and AdNOS2-infected rats (I/M 2.57<plus/minus>0.43, n=7 and 1.82 +/-0.75, n= 8, respectively;P<0.05 for both). The effect of L-Arg was abolished by simultaneous administration of N-G-nitro L-arginine methyl ester, an NOS inhibitor (2.03<plus/minus>0.39, P<0.05, VS L-Arg). Inflammation was markedly less in L-Arg- andAdNOS2-treated than in AdRR5-infected rats. Supplemental L-Arg reduces neointima formation after stenting by way of an NOS-dependent mechanism and may be a valuable strategy to target in-stent stenosis.

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Documento generato il 06/07/20 alle ore 05:40:10