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Titolo:
NATIVE ATHEROSCLEROSIS AND VEIN GRAFT ARTERIALIZATION - ASSOCIATION WITH INCREASED UROKINASE RECEPTOR EXPRESSION IN-VITRO AND IN-VIVO
Autore:
OKADA SS; GOLDEN MA; RAGHUNATH PN; TOMASZEWSKI JE; DAVID ML; KUO A; KARIKO K; BARNATHAN ES;
Indirizzi:
GEORGETOWN UNIV,MED CTR,DIV CARDIOL,BLDG D ROOM 396B,4000 RESERVOIR RD NW WASHINGTON DC 20007 UNIV PENN,SCH MED,DEPT MED PHILADELPHIA PA 19104 UNIV PENN,SCH MED,DEPT SURG PHILADELPHIA PA 19104 UNIV PENN,SCH MED,DEPT NEUROSURG PHILADELPHIA PA 19104 UNIV PENN,SCH MED,DEPT PATHOL PHILADELPHIA PA 19104 UNIV PENN,SCH MED,DEPT LAB MED PHILADELPHIA PA 19104 CENTOCOR INC MALVERN PA 00000
Titolo Testata:
Thrombosis and haemostasis
fascicolo: 1, volume: 80, anno: 1998,
pagine: 140 - 147
SICI:
0340-6245(1998)80:1<140:NAAVGA>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
VASCULAR SMOOTH-MUSCLE; PLASMINOGEN-ACTIVATOR; ENDOTHELIAL-CELLS; IN-VITRO; MIGRATION; INVASION; PROLIFERATION; HYBRIDIZATION; ADHESION; BINDING;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
32
Recensione:
Indirizzi per estratti:
Citazione:
S.S. Okada et al., "NATIVE ATHEROSCLEROSIS AND VEIN GRAFT ARTERIALIZATION - ASSOCIATION WITH INCREASED UROKINASE RECEPTOR EXPRESSION IN-VITRO AND IN-VIVO", Thrombosis and haemostasis, 80(1), 1998, pp. 140-147

Abstract

Interaction of proteases with cell surface receptors may modulate cell adhesion, migration, invasion, and matric degradation. Since the plasminogen activator system has been hypothesized to play a role in intimal thickening after various types of vascular injury. We first studied the expression of urokinase receptor(u-PAR) protein and mRNA by smooth muscle cells (SMC) grown in explant cultures from normal and diseased vessels. Using equilibrium binding studies with radiolabeled I-125-labeled single chain urokinase-type plasminogen activator (scu-PA), wedetermined that SMC cultured from atherosclerotic arteries expressed a higher maximal number of binding sites/cell (3.6 +/- 0.4 x 10(5) sites/cell vs. 2.1 +/- 0.3 x 10(5), +/- SEM. p < 0.05) with a similar affinity (Kd = 1.5 +/- 0.1 vs. 1.2 +/- 0.2 nM, p = ns). However, SMC subcultured from diseased saphenous vein grafts expressed the highest levels of u-PAR compared to SMC from normal saphenous vein (4.8 +/- 0.6 x 10(5) sites/cell vs. 1.6 +/- 0.9 x 10(5). +/- SEM p <0.05). Using binding studies and Northern analysis, we demonstrated a dose and time dependent upregulation of u-PAR protein and mRNA expression respectively in human SMC in response to serum stimulation. Using a rabbit specificu-PAR cDNA probe, we demonstrated a similar upregulation of u-PAR mRNA both in rabbit aortic SMC in culture in response to serum stimulation and up to a 20 fold increase in u-PAR mRNA in rabbit jugular veins in response to implantation as arterial grafts in vivo. Finally, to confirm that u-PAR mRNA is upregulated in human vessels after injury, we performed immunohistochemistry and in situ hybridization studies on coronary arteries. normal saphenous veins and saphenous veins from 10 weeks to 13 years after implantation as grafts. u-PAR mRNA was found mainly in the periadventitial microcirculation in normal veins, but was found to be upregulated in the neointima and media of thickened veins in both macrophages and smooth muscle cells. SMC near the internal elastic laminae in diseased coronary arteries appeared to express increased u-PAR mRNA. These data suggest that this increased expression of u-PAR may contribute to early lesion development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 22/10/20 alle ore 12:40:40