Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-5-23
pubmed:abstractText
Inflammation is a hallmark of several vascular diseases. The nuclear factor kappaB (NF-kappaB) 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-kappaB 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-kappaB, and cotransfection of ESE-1 with the p50 and p65 subunits of NF-kappaB 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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/Calcium-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/DNA-Binding Proteins, http://linkedlifedata.com/resource/pubmed/chemical/ELF3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Inflammation Mediators, http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins, http://linkedlifedata.com/resource/pubmed/chemical/NF-kappa B, http://linkedlifedata.com/resource/pubmed/chemical/NOS2 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Nerve Tissue Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase, http://linkedlifedata.com/resource/pubmed/chemical/Nitric Oxide Synthase Type II, http://linkedlifedata.com/resource/pubmed/chemical/Proto-Oncogene Proteins, http://linkedlifedata.com/resource/pubmed/chemical/Synaptotagmin I, http://linkedlifedata.com/resource/pubmed/chemical/Synaptotagmins, http://linkedlifedata.com/resource/pubmed/chemical/Trans-Activators, http://linkedlifedata.com/resource/pubmed/chemical/Transcription Factors
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
2
pubmed:volume
276
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3302-9
pubmed:dateRevised
2011-10-27
pubmed:meshHeading
pubmed-meshheading:11036073-Binding Sites, pubmed-meshheading:11036073-Calcium-Binding Proteins, pubmed-meshheading:11036073-Cells, Cultured, pubmed-meshheading:11036073-Cytokines, pubmed-meshheading:11036073-DNA-Binding Proteins, pubmed-meshheading:11036073-Humans, pubmed-meshheading:11036073-Inflammation, pubmed-meshheading:11036073-Inflammation Mediators, pubmed-meshheading:11036073-Membrane Glycoproteins, pubmed-meshheading:11036073-Mutation, pubmed-meshheading:11036073-NF-kappa B, pubmed-meshheading:11036073-Nerve Tissue Proteins, pubmed-meshheading:11036073-Nitric Oxide Synthase, pubmed-meshheading:11036073-Nitric Oxide Synthase Type II, pubmed-meshheading:11036073-Promoter Regions, Genetic, pubmed-meshheading:11036073-Protein Structure, Tertiary, pubmed-meshheading:11036073-Proto-Oncogene Proteins, pubmed-meshheading:11036073-Synaptotagmin I, pubmed-meshheading:11036073-Synaptotagmins, pubmed-meshheading:11036073-Trans-Activators, pubmed-meshheading:11036073-Transcription Factors, pubmed-meshheading:11036073-Transcriptional Activation, pubmed-meshheading:11036073-Vascular Diseases
pubmed:year
2001
pubmed:articleTitle
ESE-1 is a novel transcriptional mediator of inflammation that interacts with NF-kappa B to regulate the inducible nitric-oxide synthase gene.
pubmed:affiliation
Cardiology Division, Beth Israel Deaconess Medical Center, and Harvard Medical School, Boston, Massachusetts 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.