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Blood, 15 October 2004, Vol. 104, No. 8, pp. 2385-2393. Prepublished online as a Blood First Edition Paper on July 20, 2004; DOI 10.1182/blood-2004-02-0665. This Article Full Text (PDF) All Versions of this Article: 2004-02-0665v1 104/8/2385    most recent Alert me when this article is cited Alert me if a correction is posted 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 Deem, T. L Articles by Cook-Mills, J. M Search for Related Content PubMed PubMed Citation Articles by Deem, T. L Articles by Cook-Mills, J. M Social Bookmarking                   What's this?  Previous Article  |  Next Article  Submitted February 23, 2004 Accepted July 7, 2004 Vascular Cell Adhesion Molecule-1 (VCAM-1) Activation of Endothelial Cell Matrix Metalloproteinases: Role of Reactive Oxygen Species Tracy L Deem and Joan M Cook-Mills* Department of Pathology and Laboratory Medicine, University of Cincinnati, Cincinnati, Ohio, USA * Corresponding author; email: joan.cook{at}uc.edu. Lymphocytes bound at endothelial cell junctions extravasate within minutes. Lymphocyte-endothelial cell binding is mediated by receptors such as VCAM-1. VCAM-1 activates endothelial cell NADPH oxidase in minutes and this activity is required for VCAM-1-dependent lymphocyte migration. In this report, we examined mechanisms for activation of matrix metalloproteinases (MMPs) during VCAM-1-dependent lymphocyte migration. Lymphocyte binding to VCAM-1 rapidly activated endothelial cell-associated MMPs. Furthermore, inhibition of MMPs on the endothelial cells but not on the lymphocytes blocked VCAM-1-dependent lymphocyte migration across endothelial cells. The activation of endothelial cell MMPs required VCAM-1-stimulated endothelial cell NADPH oxidase activity as determined by scavenging of reactive oxygen species (ROS) and by pharmacologic or antisense inhibition of NADPH oxidase. Exogenous addition of 1 µM H2O2, the level of H2O2 generated by VCAM-1-stimulated endothelial cells, rapidly activated endothelial cell-associated MMPs. In contrast, activation of lymphocyte-associated MMPs was delayed by hours after lymphocyte binding to VCAM-1 and this activation was blocked by inhibition of endothelial cell ROS generation. There was also a delay in H2O2-induced decrease in lymphocyte-associated TIMPs, resulting in an increase in MMP/TIMP ratio. In summary, this is the first report of a mechanism for ROS function in VCAM-1 activation of endothelial cell MMPs during VCAM-1-dependent lymphocyte migration. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: S. Berdnikovs, H. Abdala-Valencia, C. McCary, M. Somand, R. Cole, A. Garcia, P. Bryce, and J. M. Cook-Mills Isoforms of Vitamin E Have Opposing Immunoregulatory Functions during Inflammation by Regulating Leukocyte Recruitment J. Immunol., April 1, 2009; 182(7): 4395 - 4405. [Abstract] [Full Text] [PDF] R. Martinelli, M. Gegg, R. Longbottom, P. Adamson, P. Turowski, and J. Greenwood ICAM-1-mediated Endothelial Nitric Oxide Synthase Activation via Calcium and AMP-activated Protein Kinase Is Required for Transendothelial Lymphocyte Migration Mol. Biol. Cell, February 1, 2009; 20(3): 995 - 1005. [Abstract] [Full Text] [PDF] M.-C. Lauzier, G. A. Robitaille, D. A. Chan, A. J. Giaccia, and D. E. 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