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Prepublished online as a Blood First Edition Paper on August 14, 2003; DOI 10.1182/blood-2002-12-3872. This Article Full Text (PDF) All Versions of this Article: 2002-12-3872v1 102/13/4377    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 Kunigal, S. Articles by Dumler, I. Search for Related Content PubMed PubMed Citation Articles by Kunigal, S. Articles by Dumler, I. Social Bookmarking                   What's this? Submitted December 20, 2002 Accepted July 26, 2003 Monocyte-expressed urokinase inhibits vascular smooth muscle cell growth by activating Stat1 Sateesh Kunigal, Angelika Kusch, Natalia Tkachuk, Sergey Tkachuk, Uwe Jerke, Hermann Haller, and Inna Dumler* Nephrology Department, Hannover Medical School, Hannover, Germany; Charite - Franz Volhard Clinic and Max Delbrueck Center for Molecular Medicine, Humboldt University Berlin, Berlin, Germany * Corresponding author; email: dumler{at}fvk-berlin.de. After vascular injury, a remodeling process occurs that features leukocyte migration and infiltration. Loss of endothelial integrity allows the leukocytes to interact with vascular smooth muscle cells (VSMC) and to elicit 'marching orders'; however, the signaling processes are poorly understood. We found that human monocytes inhibit VSMC proliferation and induce a migratory potential. The monocytes signal the VSMC via the urokinase-type plasminogen activator (uPA). The VSMC uPA receptor (uPAR) receives the signal and activates the transcription factor Stat1 that in turn mediates the antiproliferative effects. These results provide the first evidence that monocytes signal VSMC via mechanisms involving the fibrinolytic system and imply an important link between the uPA/uPAR-related signaling machinery and human vascular disease. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: A. Kusch, S. Tkachuk, N. Tkachuk, M. Patecki, J.-K. Park, R. Dietz, H. Haller, and I. Dumler The tight junction protein ZO-2 mediates proliferation of vascular smooth muscle cells via regulation of Stat1 Cardiovasc Res, July 1, 2009; 83(1): 115 - 122. [Abstract] [Full Text] [PDF] H. Loppnow, K. Werdan, and M. Buerke Invited review: Vascular cells contribute to atherosclerosis by cytokine- and innate-immunity-related inflammatory mechanisms Innate Immunity, April 1, 2008; 14(2): 63 - 87. [Abstract] [PDF] N. Shushakova, G. Eden, M. Dangers, J. Zwirner, J. Menne, F. Gueler, F. C. Luft, H. Haller, and I. Dumler The Urokinase/Urokinase Receptor System Mediates the IgG Immune Complex-Induced Inflammation in Lung J. Immunol., September 15, 2005; 175(6): 4060 - 4068. [Abstract] [Full Text] [PDF] N. Shushakova, N. Tkachuk, M. Dangers, S. Tkachuk, J.-K. Park, K. Hashimoto, H. Haller, and I. Dumler Urokinase-induced activation of the gp130/Tyk2/Stat3 pathway mediates a pro-inflammatory effect in human mesangial cells via expression of the anaphylatoxin C5a receptor J. Cell Sci., June 15, 2005; 118(12): 2743 - 2753. [Abstract] [Full Text] [PDF]

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