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Prepublished online as a Blood First Edition Paper on July 12, 2002; DOI 10.1182/blood-2002-03-0778. This Article 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 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. Social Bookmarking                   What's this? Submitted March 13, 2002 Accepted July 2, 2002 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 Schomig, Klaus T Preissner, and Franz-Josef Neumann 1. Medizinische Klinik und Deutsches Herzzentrum, Technische Universitat Munchen, Munich, Germany Institut fuer Biochemie, Fachbereich Humanmedizin, Justus-Liebig-Universitat, Giessen, Germany The Finsen Laboratory, Rigshospitalet, Copenhagen, Denmark * Corresponding author; email: may{at}dhm.mhn.de. The urokinase receptor (uPAR) regulates monocyte adhesion by direct binding to vitronectin and by forming complexes with integrins. Potential upregulation of uPAR in acute myocardial infarction (AMI) may, therefore, affect monocyte adhesion. In 20 patients with AMI uPAR surface expression (measured by flow cytometry) was increased as compared to patients with chronic stable angina (CSA) (179±96 vs. 80±53, mean fluorescence±SD, p=0.002). uPAR expression correlated with activation of ß2-integrins LFA-1 and Mac-1, measured by mAbs 24 and CBRM1/5. Isolated mononuclear cells (MNC) from patients with AMI showed enhanced adhesivity to endothelial cells (HUVEC), to fibrinogen (Mac-1-ligand) and to vitronectin (uPAR-ligand). Excessive adhesion of MNC to HUVEC was inhibited by mAbs anti-CD18 (84%), anti-CD11a (51%) or anti-CD11b (57%), indicating a major contribution of LFA-1 and Mac-1. MAb anti-uPAR R3 blocked adhesion of cells from AMI-patients to vitronectin (95%) but also ß2-integrin-mediated adhesion to fibrinogen (79%) or HUVEC (66%). Incubation of monocytic MonoMac6 cells with AMI-plasma enhanced uPAR mRNA expression and cell adhesion to HUVEC. Thus, released soluble factors may contribute to enhanced monocyte adhesion in AMI. Mouse pre-B-lymphocytes (BAF3-cells), transfected with various amounts of uPAR-cDNA, showed strong correlation of uPAR expression with [beta]2-integrin-dependent adhesion to ICAM-1, thus providing evidence for the functional relevance of uPAR upregulation in an isolated in vitro system. In conclusion, uPAR expression is elevated on monocytes in AMI and contributes to enhanced cell adhesion. Thus, uPAR may present a novel target for prevention of unwanted monocyte recruitment as part of inflammatory cardiovascular processes. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: K. Viswanathan, J. Richardson, B. Togonu-Bickersteth, E. Dai, L. Liu, P. Vatsya, Y.-m. Sun, J. Yu, G. Munuswamy-Ramanujam, H. Baker, et al. 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