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Prepublished online as a Blood First Edition Paper on January 23, 2003; DOI 10.1182/blood-2002-07-2303. This Article Full Text (PDF) All Versions of this Article: 2002-07-2303v1 101/10/3940    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 Pawlinski, R. Articles by Mackman, N. Search for Related Content PubMed PubMed Citation Articles by Pawlinski, R. Articles by Mackman, N. Social Bookmarking                   What's this? Submitted July 31, 2002 Accepted December 30, 2002 Regulation of tissue factor and inflammatory mediators by Egr-1 in a mouse endotoxemia model Rafal Pawlinski, Brian Pedersen, Bettina Kehrle, William C Aird, Rolf D Frank, Mausumee Guha, and Nigel Mackman* Department of Immunology, The Scripps Research Institute, La Jolla, CA, USA Molecular Medicine Unit, Beth Israel Deaconess Medical Center, Boston, MA, USA * Corresponding author; email: nmackman{at}scripps.edu. In septic shock, tissue factor (TF) activates blood coagulation and cytokines and chemokines orchestrate an inflammatory response. In this study, the role of Egr-1 in LPS induction of TF and inflammatory mediators in vivo was evaluated using Egr-1+/+ and Egr-1-/- mice. Administration of LPS transiently increased the steady-state levels of Egr-1 mRNA in the kidneys and lungs of Egr-1+/+ mice with maximal induction at 1 hour. Egr-1 was expressed in epithelial cells in the kidneys and lungs in untreated and LPS-treated mice. LPS induction of MCP-1 mRNA in the kidneys and lungs of Egr-1-/- mice was not affected at 3 hours but its expression was significantly reduced at 8 hours compared with the expression observed in Egr-1+/+ mice. Similarly, LPS induction of TF mRNA expression in the kidneys and lungs at 8 hours was reduced in Egr-1-/- mice. However, Egr-1 deficiency did not affect plasma levels of TNF in endotoxemic mice. Moreover, Egr-1+/+ and Egr-1-/- mice exhibited similar survival times in a model of acute endotoxemia. These data indicate that Egr-1 does not contribute to the early inflammatory response in the kidneys and lungs or the early systemic inflammatory response in endotoxemic mice. However, Egr-1 does contribute to the sustained expression of inflammatory mediators and to the maximal expression of TF at 8 hours in the kidneys and lungs. CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this? This article has been cited by other articles: Y. J. Yang, W. Chen, A. 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