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Titolo:
The effect of argatroban on injured endothelial cells by thrombin
Autore:
Ueshima, S; Fukao, H; Okada, K; Matsuo, O;
Indirizzi:
Kinki Univ, Sch Med, Dept Physiol, Osakasayama 5898511, Japan Kinki Univ Osakasayama Japan 5898511 Physiol, Osakasayama 5898511, Japan
Titolo Testata:
BLOOD COAGULATION & FIBRINOLYSIS
fascicolo: 7, volume: 11, anno: 2000,
pagine: 631 - 639
SICI:
0957-5235(200010)11:7<631:TEOAOI>2.0.ZU;2-7
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; PLASMINOGEN-ACTIVATOR-INHIBITOR; HUMAN-PLASMA; STAPHYLOKINASE; UROKINASE; RECEPTOR; PROTEIN; IDENTIFICATION; PURIFICATION; EXPRESSION;
Keywords:
endothelial cell; thrombin; argatroban; thrombolytic agents;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Ueshima, S Kinki Univ, Sch Med, Dept Physiol, Ohnohigashi 377-2, Osakasayama 5898511,Japan Kinki Univ Ohnohigashi 377-2 Osakasayama Japan 5898511 1,Japan
Citazione:
S. Ueshima et al., "The effect of argatroban on injured endothelial cells by thrombin", BL COAG FIB, 11(7), 2000, pp. 631-639

Abstract

When endothelial cells are exposed to thrombin, they become perturbed and acquire thrombogenic properties. Argatroban is an arginine derivative, synthetic small molecule that binds to the active site of thrombin and inhibitsits catalytic activity. Therefore, the effects of argatroban on endothelial cells, which had been injured by thrombin, were investigated. The established endothelial cell line, TKM-33, which had been cloned from human umbilical vein endothelial cells, was used. Endothelial cells produce plasminogenactivator (PA) to prevent thrombosis and maintain the blood flow. When theendothelial cells were injured by thrombin, secretion of plasminogen activator inhibitor-1 (PAI-1) increased and then the PA activity proportionally decreased. The treatment of endothelial cells with argatroban after thrombin injury did not restore their reduced PA activity. However, the treatment of endothelial cells with argatroban prior to thrombin injury resulted in inhibiting the induction of PAI-1 secretion. Thus, pretreatment of endothelial cells with argatroban suppresses the inhibition of their PA activity by thrombin. Since the effect of thrombolytic agent may be modified by the fibrinolytic factors produced by the endothelial cells, the activity of staphylokinase (SAK) was measured in the presence of endothelial cells that had been injured by thrombin. SAK is a newly developed thrombolytic agent. SAK activity in the presence of injured endothelial cells by thrombin was lower than that in the presence of endothelial cells without thrombin injury. However, treatment of endothelial cells with argatroban prior to thrombin injury revealed higher SAK activity than that after thrombin injury. These findings indicate that argatroban pretreatment prevents thrombin injury of endothelial cells, which may then maintain their physiological function. Blood Coagul Fibrinolysis 11:631-639 (C) 2000 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:37:52