Source:http://linkedlifedata.com/resource/pubmed/id/12218072
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
9
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pubmed:dateCreated |
2002-9-9
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pubmed:abstractText |
Fas ligand (FasL) induces apoptotic cell death when bound to Fas antigen. The engagement of FasL has anti-inflammatory effects through the prevention of cell proliferation and cytokine secretion. However, the role of FasL in myocardial ischemia/reperfusion (MI/R) injury is unclear. We examined the expression of FasL mRNA in the myocardium of MI/R rats by ligating the left coronary artery for 30 minutes and allowing reperfusion to occur for 0, 1, 3, and 24 hours. The expression of FasL mRNA was enhanced 1 hour after reperfusion, and enhanced levels were consistently seen after 24 hours of reperfusion. FasL immunostaining was observed on neutrophils, macrophages, T cells, and vascular endothelial cells. We then assessed the potential role of FasL in the cell proliferation and cytokine production seen in MI/R injury after 24 hours of reperfusion. Rats were divided into three groups; Group A, without treatment; Group B, treated with nonspecific rabbit IgG; and Group C, treated with anti-FasL antibody. Anti-FasL antibody or rabbit IgG were administered intravenously before coronary artery occlusion. In Group C, interleukin-1beta and interleukin-2 mRNA levels were decreased, and neutrophil and T cell accumulation was attenuated. The infarct area determined by triphenyltetrazolium chloride staining was significantly smaller in Group C (18 +/- 4%) than in Group A (34 +/- 2%) or Group B (33 +/- 4%) (p< 0.0001). However, there was no significant difference in the prevalence of terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling-positive cardiomyocytes among the three groups. These findings suggest that the cardioprotective effect of anti-FasL antibody is due to its anti-inflammatory action, rather than antiapoptotic action. The Fas/FasL system may be involved in the development of MI/R injury.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antibodies,
http://linkedlifedata.com/resource/pubmed/chemical/Chemokine CCL2,
http://linkedlifedata.com/resource/pubmed/chemical/Cytokines,
http://linkedlifedata.com/resource/pubmed/chemical/Fas Ligand Protein,
http://linkedlifedata.com/resource/pubmed/chemical/Membrane Glycoproteins,
http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger,
http://linkedlifedata.com/resource/pubmed/chemical/Tnfsf6 protein, rat
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0023-6837
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
82
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1121-9
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pubmed:dateRevised |
2006-11-15
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pubmed:meshHeading |
pubmed-meshheading:12218072-Animals,
pubmed-meshheading:12218072-Antibodies,
pubmed-meshheading:12218072-Apoptosis,
pubmed-meshheading:12218072-Chemokine CCL2,
pubmed-meshheading:12218072-Cytokines,
pubmed-meshheading:12218072-Fas Ligand Protein,
pubmed-meshheading:12218072-Male,
pubmed-meshheading:12218072-Membrane Glycoproteins,
pubmed-meshheading:12218072-Myocardial Infarction,
pubmed-meshheading:12218072-Myocardial Reperfusion Injury,
pubmed-meshheading:12218072-Neutrophils,
pubmed-meshheading:12218072-RNA, Messenger,
pubmed-meshheading:12218072-Rats,
pubmed-meshheading:12218072-Rats, Sprague-Dawley
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pubmed:year |
2002
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pubmed:articleTitle |
Antibody binding to fas ligand attenuates inflammatory cell infiltration and cytokine secretion, leading to reduction of myocardial infarct areas and reperfusion injury.
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pubmed:affiliation |
Department of Cardiovascular Science and Medicine, Graduate School of Medicine, Chiba University, Chiba, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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