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J. Biol. Chem., Vol. 276, Issue 5, 3302-3309, February 2, 2001

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ESE-1 Is a Novel Transcriptional Mediator of Inflammation That Interacts with NF-B to Regulate the Inducible Nitric-oxide Synthase Gene^*

Susan Rudders^§, John Gaspar^§, Rebecca Madore^§, Carole Voland^§, Franck Grall^§, Anand Patel^¶, Andrea Pellacani^¶, Mark A. Perrella^¶, Towia A. Libermann^§, and Peter Oettgen^§

From the  Cardiology Division, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, the ^§ New England Baptist Bone and Joint Institute, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, and the ^¶ Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115

Inflammation is a hallmark of several vascular diseases. The nuclear factor B (NF-B) transcription factors are dimeric proteins involved in the activation of a large number of genes in response to inflammatory stimuli. We report the involvement of a novel member of the ETS transcription factor, ESE-1, in mediating vascular inflammation. ESE-1 is induced in response to inflammatory cytokines and lipopolysaccharide in vascular smooth muscle cells, endothelial cells, and cells of the monocyte-macrophage lineage. This induction occurs within hours of stimulation and is mediated by NF-B transactivation of the ESE-1 promoter. We have identified the inducible form of nitric-oxide synthase (NOS2) as a putative target for ESE-1. ESE-1 can bind to the p50 subunit of NF-B, and cotransfection of ESE-1 with the p50 and p65 subunits of NF-B synergistically enhances transactivation of the NOS2 promoter by ESE-1. An ESE-1-binding site within the NOS2 promoter has been identified, the site-directed mutagenesis of which completely abolishes the ability of ESE-1 to transactivate the NOS2 promoter. Finally, in a mouse model of endotoxemia, associated with acute vascular inflammation, ESE-1 is strongly expressed in vascular endothelium and smooth muscle cells. In summary, ESE-1 represents a novel mediator of vascular inflammation.

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