Linked Life Data

7949102

Source:http://linkedlifedata.com/resource/pubmed/id/7949102

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
1994-12-20
pubmed:abstractText
The pentraxins C-reactive protein (CRP) and serum amyloid P component (SAP) are acute-phase proteins produced by liver epithelial cells. PTX3 was recently cloned as an interleukin-1 (IL-1)-inducible gene in endothelial cells, with structural similarities to pentraxins in the C-terminal half of the molecule. The present study was designed to investigate the expression of PTX3 in the human leukocyte populations. Human peripheral blood mononuclear cells exposed to lipopolysaccharide (LPS) or IL-1 beta expressed significant levels of PTX3 mRNA. Tumor necrosis factor-alpha (TNF-alpha) was a less-effective inducer of PTX3, whereas IL-6, monocyte chemotactic protein-1, macrophage colony-stimulating factor, granulocyte-macrophage colony-stimulating factor, and interferon-gamma were inactive. Among leukocytes, only monocytes exposed to inflammatory cytokines or LPS expressed the PTX3 transcript, which was undetectable in resting or stimulated polymorphonuclear cells, T or B lymphocytes, and natural killer cells. PTX3 mRNA was also inducible in in vitro monocyte-derived macrophages, in tumor-associated macrophages, and in the myelomonocytic cell lines HL60, U937, and THP1, but not in GFD8, with the latter possibly representative of earlier stages of myelomonocytic differentiation. T- and B-cell lines had no detectable PTX3. Inhibition of transcription by actinomycin D blocked induction of PTX3 in monocytes and nuclear run-on analysis showed that LPS induces the expression of the PTX3 gene at the transcriptional level in isolated monocytes. Cycloheximide had no effect on PTX3 induction in U937 cells, but was inhibitory on monocytes exposed to LPS or IL-1 beta. Monoclonal antibody against TNF and the IL-1 receptor antagonists did not inhibit induction of PTX3 in monocytes by LPS, thus excluding these cytokines as secondary stimulators of PTX3. IL-4, but not dexamethasone or transforming growth factor-beta, inhibited PTX3 expression in monocytes. Using a PTX3-specific antiserum, release of PTX3 protein was demonstrated for the first time in stimulated monocytes as well as in endothelial and fibroblastic cells. Thus, PTX3, unlike the classical pentraxins CRP and SAP, is expressed and released by cells of the monocyte-macrophage lineage exposed to inflammatory signals.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
84
pubmed:geneSymbol
PTX3
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3483-93
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:7949102-Blotting, Northern, pubmed-meshheading:7949102-Blotting, Western, pubmed-meshheading:7949102-C-Reactive Protein, pubmed-meshheading:7949102-Cell Line, pubmed-meshheading:7949102-Cells, Cultured, pubmed-meshheading:7949102-Cycloheximide, pubmed-meshheading:7949102-Cytokines, pubmed-meshheading:7949102-Dactinomycin, pubmed-meshheading:7949102-Fibroblasts, pubmed-meshheading:7949102-Gene Expression, pubmed-meshheading:7949102-Humans, pubmed-meshheading:7949102-Interleukin-1, pubmed-meshheading:7949102-Leukocytes, pubmed-meshheading:7949102-Lipopolysaccharides, pubmed-meshheading:7949102-Macrophages, pubmed-meshheading:7949102-Monocytes, pubmed-meshheading:7949102-Neutrophils, pubmed-meshheading:7949102-RNA, Messenger, pubmed-meshheading:7949102-Serum Amyloid P-Component, pubmed-meshheading:7949102-T-Lymphocytes, pubmed-meshheading:7949102-Transcription, Genetic, pubmed-meshheading:7949102-Tumor Cells, Cultured, pubmed-meshheading:7949102-Tumor Necrosis Factor-alpha
pubmed:year
1994
pubmed:articleTitle
Inducible expression of PTX3, a new member of the pentraxin family, in human mononuclear phagocytes.
pubmed:affiliation
Laboratory of Immunology, Istituto di Ricerche Farmacologiche, Mario Negri, Milano, Italy.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't