Skip Navigation

Cardiovascular Research 2003 57(1):232-237; doi:10.1016/S0008-6363(02)00612-0
© 2003 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Marutsuka, K.
Right arrow Articles by Asada, Y.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Marutsuka, K.
Right arrow Articles by Asada, Y.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Adrenomedullin augments the release and production of tissue factor pathway inhibitor in human aortic endothelial cells

Kousuke Marutsuka*, Kinta Hatakeyama, Atsushi Yamashita, Yuichiro Sato, Akinobu Sumiyoshi and Yujiro Asada

First Department of Pathology, Miyazaki Medical College, 5200 Kihara, Kiyotake, Miyazaki 889-1692, Japan

* Corresponding author. Tel.: +81-985-852-810; fax: +81-985-857-614 kmaru{at}post.miyazaki-med.ac.jp

Objectives: Adrenomedullin (AM) is a hypotensive and vasodilative peptide. It has been reported that AM plays several biological roles in cardiovascular and endocrine systems, however, effects on the blood coagulation system have not been examined. In this study, we examined its effect on tissue factor pathway inhibitor (TFPI), which is a potent inhibitor of tissue factor/factor VIIa complex-induced coagulation cascade, and is synthesized and constitutively secreted by endothelial cells (ECs). The aim of this study was to elucidate the effects of AM on release and production of TFPI in ECs. Methods: Cultured human aortic ECs were incubated with AM (10–14–10–6 M), and the antigen levels and activity of the free and total form of TFPI after AM exposure were measured in culture media using ELISA. Furthermore, receptor interaction and cellular signaling of AM were investigated. Results: AM augmented TFPI release and production in a dose-dependent manner. The effect on TFPI production was inhibited by AM receptor antagonist (AM22–52), the monoclonal antibody against C-terminal region of AM, MAPKK inhibitor, and cAMP antagonist. Conclusion: These findings indicate that AM might play an important role in the modulation of anticoagulant properties in blood circulation.

KEYWORDS Anticoagulants; Arteries; Cell culture/isolation; Endothelial function; Hemostasis


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.