SEARCH:   Advanced

Blood, 15 November 2003, Vol. 102, No. 10, pp. 3621-3628. Prepublished online as a Blood First Edition Paper on July 31, 2003; DOI 10.1182/blood-2003-03-0700. This Article Full Text Full Text (PDF) All Versions of this Article: 2003-03-0700v1 102/10/3621    most recent Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Rights and Permissions Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Matsuno, H. Articles by Kozawa, O. Search for Related Content PubMed PubMed Citation Articles by Matsuno, H. Articles by Kozawa, O. Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Lack of 2-antiplasmin promotes re-endothelialization via over-release of VEGF after vascular injury in mice Hiroyuki Matsuno, Akira Ishisaki, Keiichi Nakajima, Kiyotaka Okada, Shigeru Ueshima, Osamu Matsuo, and Osamu Kozawa From the Department of Pharmacology, Gifu University School of Medicine, Gifu, Japan; Department of Physiology II, Kinki University School of Medicine, Osakasayama City, Japan. We here report that the arterial blood flow after endothelial injury in mice deficient in 2-antiplasmin (2-AP-/- mice) was well maintained compared with that of wild-type mice. Moreover, the development of neointima 4 weeks after injury in 2-AP-/- mice was significantly decreased. Histologic observations showed a prompt recovery of endothelial cells with a much higher proliferating index in repaired endothelium in 2-AP-/- mice. The amount of secreted vascular endothelial growth factor (VEGF) by explanted vascular smooth muscle cells (SMCs) from 2-AP-/- mice was significantly increased. In separate experiments using a human endothelial cell (EC) line, we could demonstrate that plasminogen binds to ECs and that this binding can be prevented by 2-AP. Finally, an injection of either an anti-VEGF receptor-1 antibody or 2-AP reduced the prompt endothelial healing. 2-AP is the main inactivator of plasmin, which cleaves extracellular matrix-bound VEGF to release a diffusible proteolytic fragment. Lack of 2-AP, therefore, could lead to a local over-release of VEGF by the continuously active plasmin in the injured area, which could result in a prompt re-endothelialization after vascular injury. Our results provide new insight into the role of 2-AP and VEGF in the pathogenesis of re-endothelialization following vascular injury. (Blood. 2003;102: 3621-3628) CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. Hou, K. Okada, C. Okamoto, S. Ueshima, and O. Matsuo Alpha2-Antiplasmin Is a Critical Regulator of Angiotensin II-Mediated Vascular Remodeling Arterioscler. Thromb. Vasc. Biol., July 1, 2008; 28(7): 1257 - 1262. [Abstract] [Full Text] [PDF]

	Copyright © 2003 by American Society of Hematology         Online ISSN: 1528-0020