Linked Life Data

2182712

Source:http://linkedlifedata.com/resource/pubmed/id/2182712

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
1990-5-17
pubmed:abstractText
Inflammation, thrombosis, and immunity involve close interactions between leukocytes and vascular endothelium. Endothelial cells represent both targets and producers of lymphokines. Our study was designed to define the capacity of human endothelial cells (HEC) to produce a novel, recently purified, and molecularly cloned monocyte chemotactic and activating factor. This factor has been identified in the culture supernatants of tumor cell lines (tumor-derived chemotactic factor (TDCF)) as well as activated monocytes and fibroblasts (monocyte chemotactic and activating protein, MCAF, or monocyte chemoattractant protein-1, MCP-1). IL-1 induced high levels of production of chemotactic activity for monocytes in culture supernatants of HEC. IL-1-treated HEC expressed high levels of MCAF/MCP-1/TDCF mRNA transcripts, as assessed by Northern blot analysis. TNF and LPS, unlike IL-6, also induced MCAF/MCP-1/TDCF gene expression. Nuclear run off experiments revealed that IL-1-activated transcription of the MCAF/MCP-1/TDCF gene. The production of MCAF/MCP-1/TDCF may represent one of the mechanisms whereby endothelial cells, exposed to inflammatory signals, participate in the regulation of leukocyte extravasation. Production of this cytokine by vascular cells may in particular be relevant under conditions of selective extravasation and activation of mononuclear phagocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
144
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3034-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1990
pubmed:articleTitle
Monocyte chemotactic and activating factor gene expression induced in endothelial cells by IL-1 and tumor necrosis factor.
pubmed:affiliation
Istituto di Richerche Farmacologiche Mario Negri, Milan, Italy.
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't