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Titolo:
Endothelial NO synthase overexpression inhibits lesion formation in mouse model of vascular remodeling
Autore:
Kawashima, S; Yamashita, T; Ozaki, M; Ohashi, Y; Azumi, H; Inoue, N; Hirata, K; Hayashi, Y; Itoh, H; Yokoyama, M;
Indirizzi:
Kobe Univ, Sch Med, Dept Internal Med 1, Chuo Ku, Kobe, Hyogo 6500017, Japan Kobe Univ Kobe Hyogo Japan 6500017 1, Chuo Ku, Kobe, Hyogo 6500017, Japan Kobe Univ, Sch Med, Dept Pathol 1, Kobe, Hyogo 650, Japan Kobe Univ Kobe Hyogo Japan 650 Med, Dept Pathol 1, Kobe, Hyogo 650, Japan
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 2, volume: 21, anno: 2001,
pagine: 201 - 207
SICI:
1079-5642(200102)21:2<201:ENSOIL>2.0.ZU;2-4
Fonte:
ISI
Lingua:
ENG
Soggetto:
NITRIC-OXIDE SYNTHASE; SMOOTH-MUSCLE CELLS; CAROTID-ARTERY; BLOOD-FLOW; BALLOON ANGIOPLASTY; INTIMAL HYPERPLASIA; DEFICIENT MICE; IN-VIVO; GENE; VASORELAXATION;
Keywords:
nitric oxide; endothelial nitric oxide synthase; transgenic mouse; vascular remodeling; intimal thickening;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
30
Recensione:
Indirizzi per estratti:
Indirizzo: Kawashima, S Kobe Univ, Sch Med, Dept Internal Med 1, Chuo Ku, 7-5-1 Kusunoki Cho, Kobe, Hyogo 6500017, Japan Kobe Univ 7-5-1 Kusunoki Cho Kobe HyogoJapan 6500017 , Japan
Citazione:
S. Kawashima et al., "Endothelial NO synthase overexpression inhibits lesion formation in mouse model of vascular remodeling", ART THROM V, 21(2), 2001, pp. 201-207

Abstract

NO produced by endothelial NO synthase (eNOS) plays important roles in theregulation of vascular tone and structure. The purpose of this study was to clarify the role of eNOS-derived NO on vascular remodeling by use of eNOS-transgenic (eNOS-Tg) mice. The common carotid artery was ligated just proximal to the carotid bifurcation. Four weeks later, the proximal carotid artery of the ligation site was histologically examined. In this vascular remodeling model, the endothelium remains uninjured, but neointimal and medial thickening occurs in combination with a reduction in vascular diameter at the proximal portion of the ligation. At 4 weeks after ligation, the respective neointimal and medial areas in wild-type mice were 17 200 +/- 1100 and 24 300 +/- 1500 mum(2), whereas both were reduced to 8000 +/- 1900 (P<0.01)and 18 400<plus/minus>700 mum(2) (P<0.01) in eNOS-Tg mice (n=8). Total vascular area was not different between the 2 genotypes. N-G-Nitro-L-arginine methyl ester treatment increased neointimal and medial areas to the same extent in both genotypes. Leukocyte infiltration was observed in the luminal side of the vessel, but the number of infiltrating cells was significantly attenuated in eNOS-Tg mice compared with wild-type mice. This reduction of leukocyte infiltration in eNOS-Tg mice was associated with reduced expressions of intracellular adhesion molecule-1 and vascular cellular adhesion molecule-1 on the endothelium, In conclusion, chronic eNOS overexpression in the endothelium reduced leukocyte infiltration and inhibited neointimal formation and medial thickening. Our data provide the evidence for the regulatory role of NO from the endothelium on vascular structure integrity.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 29/09/20 alle ore 04:36:30