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http://purl.uniprot.org/citations/10318667http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/10318667http://www.w3.org/2000/01/rdf-schema#comment"

Background

The role of plasminogen system components in focal cerebral ischemic infarction (FCI) was studied in mice deficient in plasminogen (Plg-/-), in tissue or urokinase plasminogen activator (tPA-/- or uPA-/-), or in plasminogen activator inhibitor-1 or alpha2-antiplasmin (PAI-1(-/-) or alpha2-AP-/-).

Methods and results

FCI was produced by ligation of the left middle cerebral artery and measured after 24 hours by planimetry of stained brain slices. In control (wild-type) mice, infarct size was 7.6+/-1.1 mm3 (mean+/-SEM), uPA-/- mice had similar infarcts (7.8+/-1.0 mm3, P=NS), tPA-/-mice smaller (2.6+/-0.80 mm3, P<0.0001), PAI-1(-/-) mice larger (16+/-0.52 mm3, P<0.0001), and Plg-/- mice larger (12+/-1.2 mm3, P=0.037) infarcts. alpha2-AP-/-mice had smaller infarcts (2. 2+/-1.1 mm3, P<0.0001 versus wild-type), which increased to 13+/-2.5 mm3 (P<0.005 versus alpha2-AP-/-) after intravenous injection of human alpha2-AP. Injection into alpha2-AP-/-mice of Fab fragments of affinospecific rabbit IgG against human alpha2-AP, after injection of 200 microg human alpha2-AP, reduced FCI from 11+/-1.5 to 5.1+/-1.1 mm3 (P=0.004).

Conclusions

Plg system components affect FCI at 2 different levels: (1) reduction of tPA activity (tPA gene inactivation) reduces whereas its augmentation (PAI-1 gene inactivation) increases infarct size, and (2) reduction of Plg activity (Plg gene inactivation or alpha2-AP injection) increases whereas its augmentation (alpha2-AP gene inactivation or alpha2-AP neutralization) reduces infarct size. Inhibition of alpha2-AP may constitute a potential avenue to treatment of FCI."xsd:string
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http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/author"Collen D."xsd:string
http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/author"Lijnen H.R."xsd:string
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http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/author"Nagai N."xsd:string
http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/author"De Mol M."xsd:string
http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/date"1999"xsd:gYear
http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/name"Circulation"xsd:string
http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/pages"2440-2444"xsd:string
http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/title"Role of plasminogen system components in focal cerebral ischemic infarction: a gene targeting and gene transfer study in mice."xsd:string
http://purl.uniprot.org/citations/10318667http://purl.uniprot.org/core/volume"99"xsd:string
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