HEPARIN-LIKE GLYCOSAMINOGLYCAN IS A RECEPTOR FOR ANTITHROMBIN-III-DEPENDENT BUT NOT FOR THROMBIN-DEPENDENT PROSTACYCLIN PRODUCTION IN HUMAN ENDOTHELIAL-CELLS

被引：115

作者：

HORIE, S ^{[1
]}

ISHII, H ^{[1
]}

KAZAMA, M ^{[1
]}

机构：

[1] TEIKYO UNIV,FAC PHARMACEUT SCI,SAGAMIKO,KANAGAWA 19901,JAPAN

来源：

THROMBOSIS RESEARCH | 1990年 / 59卷 / 06期

关键词：

Antithrombin III; Endothelial cell; Heparin; Prostacyclin; Thrombin; Thrombomodulin;

D O I：

10.1016/0049-3848(90)90113-Q

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Antithrombin III (ATIII) induced a marked increase in prostacyclin (PGI2) release from cultured human umbilical vein endothelial cells (HUVEC) after incubation for more than 2 hr and the induction continued for 8 hr, while thrombin induced the increase within 10 min. ATIII-dependent production of PGI2 was abolished by addition of heparin, but pretreatment of HUVEC with polyclonal antibody against thrombomodulin could not prevent the PGI2 productions by ATIII and thrombin. ATIII-dependent PGI2 production was significantly inhibited by pretreatment of HUVEC with β-d-xylosides or heparitinase, though neither pretreatment affected thrombin-induced PGI2 production. After treatment of HUVEC with 1 μg/ml cycloheximide, ATIII-dependent PGI2 production was completely abolished. These results indicate that the mechanism of the induction of PGI2 production by ATIII involves heparin-like glycosaminoglycans on HUVEC and the stimulation of synthesis of a protein related to PGI2 production. The ATIII-induced PGI2 production is very different from that induced by thrombin. © 1990.

引用

页码：895 / 904

页数：10

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