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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
12
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pubmed:dateCreated |
2007-11-5
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pubmed:abstractText |
Ischemia/reperfusion injury (IRI) has a major impact on short- and long-term renal allograft survival by increasing graft immunogenicity. Donor preconditioning by inducing heme oxygenase 1 (HO-1) has been proven to exert cytoprotective and antiinflammatory effects on the graft, thus resulting in reduced graft immunogenicity. The study analyzed the effects and mechanisms of HO-1-mediated cytoprotection in rat kidney transplants exposed to cold preservation. We studied the differential gene-expression patterns of allografts after either short or long cold ischemia using a customized cDNA microarray. Prolonged cold ischemia led, 12 h after engraftment, to enhanced levels of adhesion molecules, heat-shock proteins, chemokines (CXCL10), and a remarkable upregulation of immunoproteasomes. Next we addressed the question whether induction of HO-1 or its byproduct carbon monoxide (CO) in organ donors targets these candidate markers related to enhanced immunogenicity. Induction of HO-1 or CO in organ donors 24 h before organ harvesting resulted in reduced mRNA levels of immunoproteasomes, MHC class II expression, and co-stimulatory molecules in the recipient's spleen, suggesting diminished migration and activation of donor dendritic cells. This observation suggests that HO-1/CO induction protects marginal allografts by inhibiting the immunogenicity of donor-derived dendritic cells.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
1523-0864
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
2049-63
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:17854277-Animals,
pubmed-meshheading:17854277-Biological Markers,
pubmed-meshheading:17854277-Carbon Monoxide,
pubmed-meshheading:17854277-Cell Movement,
pubmed-meshheading:17854277-Cells, Cultured,
pubmed-meshheading:17854277-Cold Temperature,
pubmed-meshheading:17854277-DNA, Complementary,
pubmed-meshheading:17854277-Dendritic Cells,
pubmed-meshheading:17854277-Heme Oxygenase-1,
pubmed-meshheading:17854277-Kidney Transplantation,
pubmed-meshheading:17854277-Male,
pubmed-meshheading:17854277-Oligonucleotide Array Sequence Analysis,
pubmed-meshheading:17854277-Organ Preservation,
pubmed-meshheading:17854277-Organ Transplantation,
pubmed-meshheading:17854277-RNA, Messenger,
pubmed-meshheading:17854277-Rats,
pubmed-meshheading:17854277-Rats, Inbred F344,
pubmed-meshheading:17854277-Rats, Inbred Lew,
pubmed-meshheading:17854277-Reperfusion Injury,
pubmed-meshheading:17854277-Time Factors,
pubmed-meshheading:17854277-Transplantation, Homologous
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pubmed:year |
2007
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pubmed:articleTitle |
Heme oxygenase-1 ameliorates ischemia/reperfusion injury by targeting dendritic cell maturation and migration.
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pubmed:affiliation |
Institute of Medical Immunology, Universitätsmedizin Charité Campus Mitte, Berlin, Germany. katja.kotsch@charite.de
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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