SEARCH:   Advanced

Prepublished online as a Blood First Edition Paper on July 12, 2002; DOI 10.1182/blood-2002-03-0778. This Article Full Text Full Text (PDF) All Versions of this Article: 2002-03-0778v1 100/10/3611    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 May, A. E. Articles by Neumann, F.-J. Search for Related Content PubMed PubMed Citation Articles by May, A. E. Articles by Neumann, F.-J. Related Collections Hemostasis, Thrombosis, and Vascular Biology Social Bookmarking                   What's this?  Previous Article  |  Table of Contents  |  Next Article  Blood, 15 November 2002, Vol. 100, No. 10, pp. 3611-3617 HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY Urokinase receptor surface expression regulates monocyte adhesion in acute myocardial infarction Andreas E. May, Roland Schmidt, Sandip M. Kanse, Triantafyllos Chavakis, Ross W. Stephens, Albert Schömig, Klaus T. Preissner, and Franz-Josef Neumann From Medizinische Klinik des Klinikums Rechts der Isar und Deutsches Herzzentrum, Technische Universität München, Munich, Germany; Institut für Biochemie, Fachbereich Humanmedizin, Justus-Liebig-Universität, Giessen, Germany; and the Finsen Laboratory, Rigshospitalet, Copenhagen, Denmark. The urokinase receptor (urokinase plasminogen activator receptor; uPAR) regulates monocyte adhesion by direct binding to vitronectin and by forming complexes with integrins. Therefore, possible up-regulation of uPAR in acute myocardial infarction (AMI) may affect monocyte adhesion. In 20 patients with AMI, uPAR surface expression (measured by flow cytometry) was increased compared with that in patients with chronic stable angina (mean ± SD fluorescence, 179 ± 96 vs 80 ± 53; P = .002). Expression of uPAR correlated with activation of 2-integrins lymphocyte function-associated antigen 1 (LFA-1) and macrophage antigen 1 (Mac-1), measured by using monoclonal antibodies (mAbs) 24 and CBRM1/5. Isolated mononuclear cells (MNCs) from patients with AMI showed enhanced adhesiveness to human umbilical vein endothelial cells (HUVECs), to fibrinogen (Mac-1 ligand), and to vitronectin (uPAR ligand). Excessive adhesion of MNCs to HUVECs was inhibited by mAbs anti-CD18 (84%), anti-CD11a (51%), and anti-CD11b (57%), indicating a major contribution of LFA-1 and Mac-1. The mAb anti-uPAR R3 blocked adhesion of cells from patients with AMI to vitronectin (95%) but also 2-integrin-mediated adhesion to fibrinogen (79%) and HUVECs (66%). Incubation of monocytic MonoMac6 cells with plasma from patients with AMI enhanced uPAR messenger RNA expression and cell adhesion to HUVECs. Thus, released soluble factors may contribute to enhanced monocyte adhesion in AMI. Mouse pre-B lymphocytes (BAF3 cells) transfected with various amounts of uPAR complementary DNA showed a strong correlation of uPAR expression with 2-integrin-dependent adhesion to intercellular adhesion molecule 1, thus providing evidence for the functional relevance of uPAR up-regulation in an isolated in vitro system. In conclusion, we found that uPAR expression is elevated on monocytes in AMI and contributes to enhanced cell adhesion. Thus, uPAR may be a novel target for prevention of unwanted monocyte recruitment as part of inflammatory cardiovascular processes. © 2002 by The American Society of Hematology.   CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: R. Schmidt, A. Bultmann, S. Fischel, A. Gillitzer, P. Cullen, A. Walch, P. Jost, M. Ungerer, N. D. Tolley, S. Lindemann, et al. Extracellular Matrix Metalloproteinase Inducer (CD147) Is a Novel Receptor on Platelets, Activates Platelets, and Augments Nuclear Factor {kappa}B-Dependent Inflammation in Monocytes Circ. Res., February 15, 2008; 102(3): 302 - 309. [Abstract] [Full Text] [PDF] Y. Orr, J. M. Taylor, S. Cartland, P. G. Bannon, C. Geczy, and L. Kritharides Conformational activation of CD11b without shedding of L-selectin on circulating human neutrophils J. Leukoc. Biol., November 1, 2007; 82(5): 1115 - 1125. [Abstract] [Full Text] [PDF] K. Ohwaki, H. Bujo, M. Jiang, H. Yamazaki, W. J. Schneider, and Y. Saito A Secreted Soluble Form of LR11, Specifically Expressed in Intimal Smooth Muscle Cells, Accelerates Formation of Lipid-Laden Macrophages Arterioscler. Thromb. Vasc. Biol., May 1, 2007; 27(5): 1050 - 1056. [Abstract] [Full Text] [PDF] S. Herold, W. von Wulffen, M. Steinmueller, S. Pleschka, W. A. Kuziel, M. Mack, M. Srivastava, W. Seeger, U. A. Maus, and J. Lohmeyer Alveolar Epithelial Cells Direct Monocyte Transepithelial Migration upon Influenza Virus Infection: Impact of Chemokines and Adhesion Molecules J. Immunol., August 1, 2006; 177(3): 1817 - 1824. [Abstract] [Full Text] [PDF] S. M. Kanse, R. L. Matz, K. T. Preissner, and K. Peter Promotion of Leukocyte Adhesion by a Novel Interaction Between Vitronectin and the {beta}2 Integrin Mac-1 ({alpha}M{beta}2, CD11b/CD18) Arterioscler. Thromb. Vasc. Biol., December 1, 2004; 24(12): 2251 - 2256. [Abstract] [Full Text] [PDF] A. E. May, V. Redecke, S. Gruner, R. Schmidt, S. Massberg, T. Miethke, B. Ryba, C. Prazeres da Costa, A. Schomig, and F.-J. Neumann Recruitment of Chlamydia pneumoniae-Infected Macrophages to the Carotid Artery Wall in Noninfected, Nonatherosclerotic Mice Arterioscler. Thromb. Vasc. Biol., May 1, 2003; 23(5): 789 - 794. [Abstract] [Full Text] [PDF]

	Blood Online is supported in part by Genentech BioOncology and Biogen Idec
	Copyright © 2002 by American Society of Hematology         Online ISSN: 1528-0020