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Titolo:
Bolus endovascular PDGFR-beta antisense treatment suppressed intimal hyperplasia in a rat carotid injury model
Autore:
Noiseux, N; Boucher, CH; Cartier, R; Sirois, MG;
Indirizzi:
Montreal Heart Inst, Montreal, PQ H1T 1C8, Canada Montreal Heart Inst Montreal PQ Canada H1T 1C8 ntreal, PQ H1T 1C8, Canada Univ Montreal, Dept Pharmacol, Montreal, PQ H3C 3J7, Canada Univ MontrealMontreal PQ Canada H3C 3J7 ol, Montreal, PQ H3C 3J7, Canada
Titolo Testata:
CIRCULATION
fascicolo: 11, volume: 102, anno: 2000,
pagine: 1330 - 1336
SICI:
0009-7322(20000912)102:11<1330:BEPATS>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBROBLAST GROWTH-FACTOR; SMOOTH-MUSCLE MIGRATION; CORONARY ANGIOPLASTY; BALLOON ANGIOPLASTY; ARTERIAL INJURY; RECEPTOR; RESTENOSIS; INHIBITION; EXPRESSION; PROLIFERATION;
Keywords:
gene therapy; angioplasty; growth substances; restenosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
24
Recensione:
Indirizzi per estratti:
Indirizzo: Sirois, MG Montreal Heart Inst, 5000 Belanger St, Montreal, PQ H1T 1C8, Canada Montreal Heart Inst 5000 Belanger St Montreal PQ Canada H1T 1C8
Citazione:
N. Noiseux et al., "Bolus endovascular PDGFR-beta antisense treatment suppressed intimal hyperplasia in a rat carotid injury model", CIRCULATION, 102(11), 2000, pp. 1330-1336

Abstract

Background-Intimal thickening in accelerated arteriopathies relies on the migration of medial vascular smooth muscle cells (VSMCs) and their proliferation within the neointima. Activation of platelet-derived growth factor receptor-P (PDGFR-beta) expressed in injured VSMCs is responsible for the migration of medial VSMCs to the intima. In the present study, we wanted to assess whether a single local endovascular delivery of antisense PDGFR-beta in injured rat carotid arteries would be sufficient to prevent intimal hyperplasia and how it might contribute to the vascular healing process. Methods and Results-A bolus of antisense PDGFR-beta delivered into injuredrat carotid arteries reduced PDGFR-beta protein overexpression by >90% from day 3 to 28 after injury. At day 28 after injury, compared with injured untreated carotids, treatment with antisense PDGFR-beta reduced intimal hyperplasia by 58% and medial VSMC migration by 49% and improved vascular reendothelialization by 100% and vascular reactivity (EC50) to acetylcholine by 5-fold. Conclusions-A single-bolus luminal delivery of antisense PDGFR-beta to injured rat carotids reduced intimal hyperplasia, improved the reendothelialization process, and led to the recovery of endothelium-dependent regulation of vascular tone.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/04/20 alle ore 04:56:40