Author Correction: Elevated complement mediator levels in endothelial-derived plasma exosomes implicate endothelial innate inflammation in diminished brain function of aging humans
Fanny M. ElahiDanielle HarveyMarie AltendahlNivetha BrathabanNicole FernandesKaitlin B. CasalettoAdam M. StaffaroniPauline MaillardJason D. HinmanBruce L. MillerCharles DeCarliJoel H. KramerEdward J. Goetzl
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Inflammation is a hallmark of several vascular diseases. The nuclear factor κB (NF-κB) 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-κB 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-κB, and cotransfection of ESE-1 with the p50 and p65 subunits of NF-κB synergistically enhances transactivation of theNOS2 promoter by ESE-1. An ESE-1-binding site within theNOS2 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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