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http://purl.uniprot.org/citations/11164850http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/11164850http://www.w3.org/2000/01/rdf-schema#comment"

Objective

We studied the effects of temporary myocardial ischemia and reperfusion on myocyte injury and ventricular remodelling in wildtype and intercellular adhesion molecule-1-(ICAM-1) deficient mice.

Methods

ICAM-1-/- and ICAM-1+/+ mice were subjected to 30 min of myocardial ischemia and subsequent reperfusion for 2 h, 1 week and 3 weeks, respectively. The evaluation of tissue damage and scar size was performed with histological sections stained with hematoxilin and eosin. Serum levels of troponin T, creatine kinase and lactate dehydrogenase isoenzyme 1 were evaluated as an index of cardiac cellular damage. Immunohistological analysis was employed to determine cell compositions in ischemic regions.

Results

After myocardial ischemia (30 min) and 2 h reperfusion, elevation in serum troponin T, creatine kinase and lactate dehydrogenase isoenzyme 1 were found in both groups, but significantly reduced in ICAM-1-/-mice compared with wildtype mice (P<0.05). Absence of a functional ICAM-1 gene in ICAM-1-/-mice resulted in a marked reduction of ischemia-reperfusion injury at the early stage. The damage score and size of the infarct area were lower in ICAM-1 -/-mice by 30 min of ischemia and 2 h of reperfusion (1.4+/-0.54 vs. 2.4+/-0.47, P<0.05). The percentage of MAC-1-positive cells in the ischemic region and the border zone was also significantly diminished in groups of ICAM-1-/-mice. Surprisingly, the scar size in ventricles in animals 1 or 3 weeks after ischemia was similar between ICAM-1-/- and ICAM-1+/+ mice, although the number of infiltrated MAC-1 positive cells in the scar in wildtype mice was higher.

Conclusion

Our results demonstrate that the absence of ICAM-1 expression results in less myocardial damage induced by ischemia-reperfusion at the early stage, but does not influence the size of myocardial infarction and scar formation."xsd:string
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http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/author"Xu Q."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/author"Metzler B."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/author"Mair J."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/author"Hintringer F."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/author"Lercher A."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/author"Pachinger O."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/author"Schaber C."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/date"2001"xsd:gYear
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/name"Cardiovasc Res"xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/pages"399-407"xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/title"Mouse model of myocardial remodelling after ischemia: role of intercellular adhesion molecule-1."xsd:string
http://purl.uniprot.org/citations/11164850http://purl.uniprot.org/core/volume"49"xsd:string
http://purl.uniprot.org/citations/11164850http://www.w3.org/2004/02/skos/core#exactMatchhttp://purl.uniprot.org/pubmed/11164850
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