Linked Life Data

12695514

Source:http://linkedlifedata.com/resource/pubmed/id/12695514

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
26
pubmed:dateCreated
2003-6-23
pubmed:abstractText
Whether deletion of tumor necrosis factor (TNF) receptor 1 or 2 affects lipopolysaccharide (LPS)-mediated signaling is not understood. In this report, we used macrophages derived from wild type (wt) mice and from mice null for the type 1 receptor (p60-/-), the type 2 receptor (p80-/-), or both (p60-/- p80-/-) to investigate the effect of these receptors on LPS-mediated activation of NF-kappaB, mitogen-activated protein kinases, and apoptosis. LPS activated NF-kappaB by 3-4-fold in wt cells but by 9-10-fold in p60-/-, p80-/-, and p60-/- p80-/- macrophages. These results correlated with the IkappaBalpha kinase activation, which is needed for NF-kappaB activation. LPS-induced cyclooxygenase-2 and inducible NO synthase proteins and NO production were maximum in p60-/- p80-/- macrophages and minimum in wt cells. LPS activated C-Jun N-terminal kinase, p38MAPK, and extracellular signal-regulated kinase in wt cells, but the levels were much higher in p60-/-, p80-/-, and p60-/- p80-/- cells. LPS-induced cytotoxicity, poly(ADP-ribose) polymerase cleavage, and annexin V staining were also highest in p60-/- p80-/- cells and lowest in wt cells. The difference in LPS signaling was unrelated to the expression of LPS receptors, CD14, or toll-like receptor 4. Overall, our studies indicate that deletion of either of the TNF receptors sensitizes the macrophages to LPS and provide evidence for cross-talk between TNF and LPS signaling.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
27
pubmed:volume
278
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
23390-7
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:12695514-Animals, pubmed-meshheading:12695514-Antigens, CD, pubmed-meshheading:12695514-Apoptosis, pubmed-meshheading:12695514-Cell Line, Transformed, pubmed-meshheading:12695514-Dose-Response Relationship, Drug, pubmed-meshheading:12695514-Lipopolysaccharides, pubmed-meshheading:12695514-Macrophages, pubmed-meshheading:12695514-Mice, pubmed-meshheading:12695514-Mice, Knockout, pubmed-meshheading:12695514-Mitogen-Activated Protein Kinases, pubmed-meshheading:12695514-NF-kappa B, pubmed-meshheading:12695514-Nitric Oxide, pubmed-meshheading:12695514-Receptor Cross-Talk, pubmed-meshheading:12695514-Receptors, Tumor Necrosis Factor, pubmed-meshheading:12695514-Receptors, Tumor Necrosis Factor, Type I, pubmed-meshheading:12695514-Receptors, Tumor Necrosis Factor, Type II, pubmed-meshheading:12695514-Signal Transduction
pubmed:year
2003
pubmed:articleTitle
Genetic deletion of the tumor necrosis factor receptor p60 or p80 sensitizes macrophages to lipopolysaccharide-induced nuclear factor-kappa B, mitogen-activated protein kinases, and apoptosis.
pubmed:affiliation
Department of Bioimmunotherapy, The University of Texas MD Anderson Cancer Center, Houston, Texas 77030, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't