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Prepublished online as a Blood First Edition Paper on January 23, 2003; DOI 10.1182/blood-2002-07-2303.
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Blood, 15 May 2003, Vol. 101, No. 10, pp. 3940-3947
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY
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
From the Department of Immunology, The Scripps Research
Institute, La Jolla, CA; and the Molecular Medicine Unit, Beth Israel
Deaconess Medical Center, Boston, MA.
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 lipopolysaccharide (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 one hour. Egr-1 was expressed in epithelial cells
in the kidneys and lungs in untreated and LPS-treated mice. LPS
induction of monocyte chemoattractant protein 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 tumor necrosis factor  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.
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