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Titolo:
Platelet activation by sustained exposure to low-dose plasmin
Autore:
Ervin, AL; Peerschke, EIB;
Indirizzi:
Mem Sloan Kettering Canc Ctr, Dept Pediat Oncol, New York, NY 10021 USA Mem Sloan Kettering Canc Ctr New York NY USA 10021 New York, NY 10021 USA Cornell Univ, Weill Med Coll, Dept Pathol, New York, NY USA Cornell Univ New York NY USA ill Med Coll, Dept Pathol, New York, NY USA
Titolo Testata:
BLOOD COAGULATION & FIBRINOLYSIS
fascicolo: 6, volume: 12, anno: 2001,
pagine: 415 - 425
SICI:
0957-5235(200109)12:6<415:PABSET>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
MURINE MONOCLONAL-ANTIBODY; GLYCOPROTEIN-IIB/IIIA; CARDIOPULMONARY BYPASS; VONWILLEBRAND-FACTOR; FIBRINOGEN RECEPTOR; THROMBIN RECEPTOR; TYROSINE KINASES; AGGREGATION; INHIBITION; MECHANISM;
Keywords:
plasmin; platelets; platelet aggregation; fibrinogen;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
50
Recensione:
Indirizzi per estratti:
Indirizzo: Peerschke, EIB New York Presbyterian Hosp, 525 E 68th St,F 707, New York, NY 10021 USA New York Presbyterian Hosp 525 E 68th St,F 707 New York NY USA10021
Citazione:
A.L. Ervin e E.I.B. Peerschke, "Platelet activation by sustained exposure to low-dose plasmin", BL COAG FIB, 12(6), 2001, pp. 415-425

Abstract

Plasmin has been reported to activate and inhibit platelet function depending on dose and exposure temperature. The present study examines the induction of fibrinogen-dependent platelet aggregation following prolonged (60 min) platelet exposure to very low doses of plasmin (0.05 CU/ml) at either 22or 37 degreesC. Maximum aggregation [mean +/- SD, 60 +/- 19 light transmission units (LTU); n=43] occurred following platelet exposure to plasmin at 22 degreesC, but significant platelet aggregation (28 +/- 4 LTU, n=3) also occurred following plasmin treatment at 37 degreesC. Plasmin-induced platelet aggregates appeared microscopically larger than aggregates of adenosine diphosphate (ADP)-activated platelets, and were less reversible. Aggregatedplasmin-treated platelets also expressed more procoagulant activity than platelets aggregated with ADP, as reflected by shortening of the plasma kaolin recalcification time. Aggregation of platelets exposed to very low dosesof plasmin was not accompanied by dense or alpha-granule secretion, and was unaffected by ADP antagonists or aspirin. Partial inhibition of platelet aggregation, however, was achieved with metabolic inhibitors, PGE(1), and inhibitors of phosphoinositide 3-kinase or protein kinase C. Although fibrinogen was required for plasmin-treated platelet aggregation, [I-125]-fibrinogen binding comprised only 58 +/- 3% (n=3) of fibrinogen binding associatedwith ADP aggregated platelets. This was consistent with observed decreasesin reptilase-induced fibrin clot retraction. Taken together, these data suggest that sustained exposure of platelets to very low plasmin doses leads to platelet activation and thus may contribute to thrombotic complications in vivo. (C) 2001 Lippincott Williams & Wilkins.

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Documento generato il 01/12/20 alle ore 21:16:30