Linked Life Data

18292602

Source:http://linkedlifedata.com/resource/pubmed/id/18292602

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2008-4-11
pubmed:abstractText
Activation of complement stimulates inflammation and provides an initial vigorous defense against infection. Insertion of the membrane attack complex in cell membranes of vascular endothelial cells induces changes in cell differentiation that promote coagulation, thrombosis, inflammation, and immunity. These changes are mediated by production of interleukin (IL)-1alpha by endothelial cells, which acts locally on endothelial cells to contain infection and promote healing of the affected site. In healthy tissues, however, promoting coagulation and inflammation would be dysphysiologic. Accordingly, endothelial cell activation by the membrane attack complex depends on both transcriptional regulation of IL-1alpha and availability of that cytokine to broadly modify endothelial cell physiology. Here, we report that the IL-1alpha gene contains a suppressor sequence that cooperates with histone modification to regulate production of IL-1alpha by endothelial cells. The suppressor sequence binds C/EBP (CCAAT enhancer-binding protein) family DNA-binding proteins isolated from the nucleus of quiescent endothelial cells. These results suggest constitutive suppression of IL-1alpha maintains quiescence of endothelium and that terminal complement complexes remove that suppression, allowing IL-1alpha transcription and, ultimately, activation of endothelium to proceed.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
1524-4571
pubmed:author
pubmed:issnType
Electronic
pubmed:day
11
pubmed:volume
102
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
823-30
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed:year
2008
pubmed:articleTitle
Constitutive repression of interleukin-1alpha in endothelial cells.
pubmed:affiliation
Department of Surgery, Mayo Clinic College of Medicine, Rochester, Minn, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural