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Papers In Press, published online ahead of print October 17, 2000
J. Biol. Chem, 10.1074/jbc.M006507200
Submitted on July 21, 2000
Revised on October 17, 2000
Accepted on October 17, 2000
Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02115
Corresponding Author: joettgen{at}caregroup.harvard.edu
Inflammation is a hallmark of several vascular diseases. The nuclear factor kappa B (NF-kB) 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 LPS 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-kB 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-kB, and cotransfection of ESE-1 with the p50 and p65 subunits of NF-kB 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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