Urokinase, @entity3479 and @entity2289 expression in severely stenosed and occluded vein grafts with XXXX .

@entity1 @entity2289 @entity61945 @entity1373 @entity2279 @entity1427 @entity715 @entity3479 @entity2290
Intimal @entity1373 and subsequent @entity715 limit the success of vascular reconstructive procedures. Plasminogen activation in situ may be an important factor affecting re-stenosis of the graft. Tissue specimens from eight @entity1 with failing or failed infra-inguinal vein bypasses and three specimens from normal veins were harvested to study @entity2290 ( @entity2290 ), @entity3479 ( @entity3479 ) and @entity2289 ( @entity2289 ) by in situ hybridization and immunohistochemistry. The possible presence of thrombi was monitored by platelet and fibrin-specific stainings. In occluded grafts, platelet @entity61945 ( @entity2279 ) antibody stained the thrombi but not the endothelial area, indicating the absence of endothelium. Platelet glycoprotein (GP) IIb/IIIa co-localized with @entity2279 and, furthermore, @entity1427 /IIIa staining was positive on the vein walls with thrombi and to some extent in the grafts without thrombi. @entity2289 and @entity2290 were uniformly upregulated in intimal thickening in grafts without @entity715 . In organized thrombi, enhanced @entity2290 , @entity3479 and @entity2289 reactivity was detected in the ingrowing subendothelium. In non-occluded grafts with small thrombi, @entity2290 expression was enriched beneath microthrombi co-localizing with the graft wall injury, while @entity2289 was scattered in the (sub)endothelium. We conclude that fibrinolytic system is upregulated at sites of graft stenosis, and local proteolytic degradation of the graft wall associates with @entity715 formation.
