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rdf:type |
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lifeskim:mentions |
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pubmed:dateCreated |
2003-9-12
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pubmed:abstractText |
Monocyte chemoattractant protein-1 (MCP-1), a potent chemotactic factor for monocytes, is induced during ischemia-reperfusion. As monocytes might play an important causative role in reperfusion injury, we investigated if inhibition of monocyte activation could attenuate ischemia-reperfusion injury and thereby improve cardiac preservation. To inhibit monocyte activation, we transfected a dominant-negative inhibitor of MCP-1 (7ND) gene in an animal model.
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1524-4539
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
9
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pubmed:volume |
108 Suppl 1
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
II213-8
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:12970235-Animals,
pubmed-meshheading:12970235-Cell Movement,
pubmed-meshheading:12970235-Chemokine CCL2,
pubmed-meshheading:12970235-Cold Temperature,
pubmed-meshheading:12970235-Creatine Kinase,
pubmed-meshheading:12970235-Creatine Kinase, MB Form,
pubmed-meshheading:12970235-Heart,
pubmed-meshheading:12970235-Interleukin-1,
pubmed-meshheading:12970235-Isoenzymes,
pubmed-meshheading:12970235-Monocytes,
pubmed-meshheading:12970235-Mutation,
pubmed-meshheading:12970235-Myocardial Reperfusion Injury,
pubmed-meshheading:12970235-Myocardium,
pubmed-meshheading:12970235-Organ Preservation,
pubmed-meshheading:12970235-Rabbits,
pubmed-meshheading:12970235-Time Factors,
pubmed-meshheading:12970235-Transfection,
pubmed-meshheading:12970235-Tumor Necrosis Factor-alpha,
pubmed-meshheading:12970235-Ventricular Function, Left
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pubmed:year |
2003
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pubmed:articleTitle |
Transfection with a dominant-negative inhibitor of monocyte chemoattractant protein-1 gene improves cardiac function after 6 hours of cold preservation.
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pubmed:affiliation |
Department of Cardiovascular Surgery, Graduate School of Medical Sciences, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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