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Titolo:
LOSS OF ATP-DIPHOSPHOHYDROLASE ACTIVITY WITH ENDOTHELIAL-CELL ACTIVATION
Autore:
ROBSON SC; KACZMAREK E; SIEGEL JB; CANDINAS D; KOZIAK K; MILLAN M; HANCOCK WW; BACH FH;
Indirizzi:
HARVARD UNIV,SCH MED,BETH ISRAEL DEACONESS MED CTR,RM 370 99 BROOKLINE AVE BOSTON MA 02215 HARVARD UNIV,SCH MED,NEW ENGLAND DEACONESS HOSP,SANDOZ CTR IMMUNOBIOLBOSTON MA 02215 HARVARD UNIV,SCH MED,NEW ENGLAND DEACONESS HOSP,DEPT MED BOSTON MA 02215 HARVARD UNIV,SCH MED,NEW ENGLAND DEACONESS HOSP,DEPT PATHOL BOSTON MA02215 HARVARD UNIV,SCH MED,NEW ENGLAND DEACONESS HOSP,DEPT SURG BOSTON MA 02215 UNIV CAPE TOWN,MRC,CTR LIVER,SCH MED,GROOTE SCHUUR HOSP ZA-7925 CAPE TOWN SOUTH AFRICA
Titolo Testata:
The Journal of experimental medicine
fascicolo: 1, volume: 185, anno: 1997,
pagine: 153 - 163
SICI:
0022-1007(1997)185:1<153:LOAAWE>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
EXTRACELLULAR ADENINE-NUCLEOTIDES; PLATELET REACTIVITY; HEPARAN-SULFATE; INHIBITION; INJURY; THROMBOREGULATION; SURFACE; BLOOD; THROMBOMODULIN; PURIFICATION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
47
Recensione:
Indirizzi per estratti:
Citazione:
S.C. Robson et al., "LOSS OF ATP-DIPHOSPHOHYDROLASE ACTIVITY WITH ENDOTHELIAL-CELL ACTIVATION", The Journal of experimental medicine, 185(1), 1997, pp. 153-163

Abstract

Quiescent endothelial cells (EC) regulate blood flow and prevent intravascular thrombosis. This latter effect is mediated in a number of ways, including expression by EC of thrombomodulin and heparan sulfate, both of which are lost from the EC surface as part of the activation response to proinflammatory cytokines. Loss of these anticoagulant molecules potentiates the procoagulant properties of the injured vasculature. An additional thromboregulatory factor, ATP diphosphohydrolase (ATPDase; designated as EC 3.6.1.5) is also expressed by quiescent EC, and has the capacity to degrade the extracellular inflammatory mediatorsATP and ADP to AMP, thereby inhibiting platelet activation and modulating vascular thrombosis. We describe here that the antithrombotic effects of the ATPDase, like heparan sulfate and thrombomodulin, are lostafter EC activation, both in vitro and in vivo. Because platelet activation and aggregation are important components of the hemostatic changes that accompany inflammatory diseases, we suggest that the loss of vascular ATPDase may be crucial for the progression of vascular injury.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 26/11/20 alle ore 14:23:06