Linked Life Data

10066673

Source:http://linkedlifedata.com/resource/pubmed/id/10066673

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1999-4-13
pubmed:abstractText
-During myocardial reperfusion, polymorphonuclear neutrophil (PMN) adhesion involving the intercellular adhesion molecule-1 (ICAM-1) may lead to aggravation and prolongation of reperfusion injury. We studied the role of early tumor necrosis factor-alpha (TNF-alpha) cleavage and nuclear factor-kappaB (NF-kappaB) activation on ICAM-1 expression and venular adhesion of PMN in isolated hearts after ischemia (15 minutes) and reperfusion (30 to 480 minutes). NF-kappaB activation (electromobility shift assay) was found after 30 minutes of reperfusion and up to 240 minutes. ICAM-1 mRNA, assessed by Northern blot, increased during the same interval. Functional effect of newly synthesized adhesion molecules was found by quantification (in situ fluorescence microscopy) of PMN, given as bolus after ischemia, which became adherent to small coronary venules (10 to 50 microm in diameter). After 480 minutes of reperfusion, ICAM-1-dependent PMN adhesion increased 2.5-fold compared with PMN adhesion obtained during acute reperfusion. To study the influence of NF-kappaB on PMN adhesion, we inhibited NF-kappaB activation by transfection of NF-kappaB decoy oligonucleotides into isolated hearts using HJV-liposomes. Decoy NF-kappaB but not control oligonucleotides blocked ICAM-1 upregulation and inhibited the subacute increase in PMN adhesion. Similar effects were obtained using BB 1101 (10 microg), an inhibitor of TNF-alpha cleavage enzyme. These data suggest that ischemia and reperfusion in isolated hearts cause liberation of TNF-alpha, activation of NF-kappaB, and upregulation of ICAM-1, an adhesion molecule involved in inflammatory response after ischemia and reperfusion.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0009-7330
pubmed:author
pubmed:issnType
Print
pubmed:day
5
pubmed:volume
84
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
392-400
pubmed:dateRevised
2007-11-15
pubmed:meshHeading
pubmed-meshheading:10066673-Animals, pubmed-meshheading:10066673-Cell Adhesion, pubmed-meshheading:10066673-Coronary Circulation, pubmed-meshheading:10066673-Endothelium, Vascular, pubmed-meshheading:10066673-Gene Expression Regulation, pubmed-meshheading:10066673-Hemodynamics, pubmed-meshheading:10066673-Intercellular Adhesion Molecule-1, pubmed-meshheading:10066673-Male, pubmed-meshheading:10066673-Myocardial Contraction, pubmed-meshheading:10066673-Myocardial Ischemia, pubmed-meshheading:10066673-Myocardial Reperfusion Injury, pubmed-meshheading:10066673-NF-kappa B, pubmed-meshheading:10066673-Neutrophils, pubmed-meshheading:10066673-RNA, Messenger, pubmed-meshheading:10066673-Rats, pubmed-meshheading:10066673-Transcription Factors, pubmed-meshheading:10066673-Tumor Necrosis Factor-alpha
pubmed:year
1999
pubmed:articleTitle
Tumor necrosis factor-alpha contributes to ischemia- and reperfusion-induced endothelial activation in isolated hearts.
pubmed:affiliation
Institute of Physiology Surgical Research, Ludwig-Maximilians-University, Munich, Germany. Pathology. c.kupatt@lrz-muenchen.de
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't