Hepatic stellate cell damage may lead to decreased plasma ADAMTS13 activity in rats

被引:34
作者
Kume, Yukio
Ikeda, Hitoshi
Inoue, Morihiro
Tejima, Kazuaki
Tomiya, Tomoaki
Nishikawa, Takako
Watanabe, Naoko
Ichikawa, Tatsuya
Kaneko, Makoto
Okubo, Shigeo
Yokota, Hiromitsu
Omata, Masao
Fujiwara, Kenji
Yatomi, Yutaka
机构
[1] Univ Tokyo, Grad Sch Med, Dept Lab Med, Bunkyo Ku, Tokyo 1138655, Japan
[2] Univ Tokyo, Grad Sch Med, Dept Gastroenterol, Bunkyo Ku, Tokyo 1138655, Japan
[3] Yokohama Rohsai Hosp, Kohoku Ku, Yokohama, Kanagawa 2220036, Japan
关键词
ADAMTS; 13; hepatic stellate cell; dimethylnitrosamine; hepatectomy;
D O I
10.1016/j.febslet.2007.03.029
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
ADAMTS13 is gaining attention, because its deficiency causes thrombotic thrombocytopenic purpura. Although its regulatory mechanism is not fully understood, we wondered if hepatic stellate cells (HSCs) play a role, because ADAMTS13 mRNA is exclusively expressed in the liver and primarily in HSCs. Plasma ADAMTS13 activity was markedly reduced in dimethylnitrosamine-treated rats, where HSC apoptosis is an essential event, but not in carbon tetrachloride- or thioacetamide-treated rats without HSC apoptosis. Furthermore, plasma ADAMTS13 activity was also reduced in 70% hepatectomized rats, where HSC loss occurs. These results suggest that HSC may be involved in the regulation of plasma ADAMTS13 activity. (c) 2007 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1631 / 1634
页数:4
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