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

Edited by Beat Imhof

Received 13 February 2007; received in revised form 2 March 2007; accepted 9 March 2007. published online 22 March 2007.

Abstract

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.

Keywords: ADAMTS13, Hepatic stellate cell, Dimethylnitrosamine, Hepatectomy

a Department of Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

b Department of Gastroenterology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan

c Yokohama Rohsai Hospital, 3211 Kodukue-chou, Koh-hoku-ku, Yokohama, Kanagawa 222-0036, Japan

Corresponding author. Address: Department of Laboratory Medicine, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-8655, Japan. Fax: +81 3 5689 0495.

PII: S0014-5793(07)00289-X

doi:10.1016/j.febslet.2007.03.029

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