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Titolo:
HYPOXIA PRIMES ENDOTOXIN-INDUCED TISSUE FACTOR EXPRESSION IN HUMAN MONOCYTES AND ENDOTHELIAL-CELLS BY A PAF-DEPENDENT MECHANISM
Autore:
HERBERT JM; CORSEAUX D; LALE A; BERNAT A;
Indirizzi:
SANOFI RECH,HAEMOBIOL RES DEPT,195 ROUTE ESPAGNE F-31036 TOULOUSE FRANCE
Titolo Testata:
Journal of cellular physiology
fascicolo: 2, volume: 169, anno: 1996,
pagine: 290 - 299
SICI:
0021-9541(1996)169:2<290:HPETFE>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLATELET-ACTIVATING-FACTOR; MACROPHAGE PROCOAGULANT ACTIVITY; ISCHEMIA-REPERFUSION INJURY; MYOCARDIAL-ISCHEMIA; IN-VITRO; THROMBOSIS; ANTAGONIST; ADHERENCE; MODELS; RATS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
42
Recensione:
Indirizzi per estratti:
Citazione:
J.M. Herbert et al., "HYPOXIA PRIMES ENDOTOXIN-INDUCED TISSUE FACTOR EXPRESSION IN HUMAN MONOCYTES AND ENDOTHELIAL-CELLS BY A PAF-DEPENDENT MECHANISM", Journal of cellular physiology, 169(2), 1996, pp. 290-299

Abstract

Tissue factor (TF) is a glycoprotein which acts as a trigger of the coagulation cascade. TF expression may be induced at the surface of monocytes and endothelial cells by several stimuli including bacterial endotoxin (LPS) and cytokines (IL1 beta, TNF alpha) and there is a largebody of evidence for the involvement of hypoxia as a primaring factorin the process leading to thrombosis. To define the molecular basis underlying this phenomenon, we evaluated the relative role of platelet activating factor (PAF). PAF primed human monocytes and human umbilical vein endothelial cells (HUVEC) for TF expression following exposure to E. coli LPS but was unable to enhance the induction of TF expression by IL1 beta. The priming effect of PAF with regard to LPS occurred in a time- and dose-dependent manner and was inhibited by the PAF receptor antagonist SR 27417. When HUVEC or monocytes were exposed to an hypoxic environment, a significant rise in LPS-induced TF expression wasobserved. Hypoxia had no effect on IL1-induced TF expression. The enhanced LPS-induced TF expression in both cell types was mediated by PAFas indicated by the inhibition obtained with SR 27417, added during hypoxia. Although the importance of hypoxia in the etiology of venous thrombosis has been acknowledged for a long time, evaluation of the relative importance of PAF in the process leading to thrombus formation is still lacking. Stasis-induced thrombosis performed in the rabbit jugular vein was enhanced in a dose-dependent manner by the prior i.v. administration of LPS (0.05 to 100 mu g/kg, i.v.). SR 27417 administeredsimultaneously with LPS prevented thrombus formation with an ED50 value of 0.1 +/- 0.04 mg/kg. These results therefore show that hypoxia promotes LPS-induced TF expression in HUVEC and human monocytes through a PAF-dependent mechanism in vitro and in vivo. (C) 1996 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/09/20 alle ore 16:44:22