| http://purl.uniprot.org/citations/10845862 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/10845862 | http://www.w3.org/2000/01/rdf-schema#comment | "The hypothesis that alpha(2)-antiplasmin (alpha(2)-AP), the main physiological plasmin inhibitor, plays a role in neointima formation was tested with use of a vascular injury model in wild-type (alpha(2)-AP(+/+)) and alpha(2)-AP-deficient (alpha(2)-AP(-/-)) mice. The neointimal and medial areas were similar 1 to 3 weeks after electric injury of the femoral artery in alpha(2)-AP(+/+) and alpha(2)-AP(-/-) mice, resulting in comparable intima/media ratios (eg, 0.43+/-0.12 and 0.42+/-0.11 2 weeks after injury). Nuclear cell counts in cross-sectional areas of the intima of the injured region were also comparable in arteries from alpha(2)-AP(+/+) and alpha(2)-AP(-/-) mice (78+/-19 and 69+/-8). Fibrin deposition was not significantly different in arteries of both genotypes 1 day after injury, and no mural thrombosis was detected 1 week after injury. Fibrinolytic activity in femoral arterial sections, as monitored by fibrin zymography, was higher in alpha(2)-AP(-/-) mice 1 week after injury (P<0.001) but was comparable in both genotypes 2 and 3 weeks after injury. Staining for elastin did not reveal significant degradation of the internal elastica lamina in either genotype. Immunocytochemical analysis revealed a comparable distribution pattern of alpha-actin-positive smooth muscle cells in both genotypes. These findings indicate that the endogenous fibrinolytic system of alpha(2)-AP(+/+) mice is capable of preventing fibrin deposition after vascular injury and suggest that alpha(2)-AP does not play a major role in smooth muscle cell migration and neointima formation in vivo."xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.org/dc/terms/identifier | "doi:10.1161/01.atv.20.6.1488"xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/author | "Collen D."xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/author | "Lijnen H.R."xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/author | "Dewerchin M."xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/author | "Van Hoef B."xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/date | "2000"xsd:gYear |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/name | "Arterioscler Thromb Vasc Biol"xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/pages | "1488-1492"xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/title | "Alpha(2)-antiplasmin gene deficiency in mice does not affect neointima formation after vascular injury."xsd:string |
| http://purl.uniprot.org/citations/10845862 | http://purl.uniprot.org/core/volume | "20"xsd:string |
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