Background
We recently assigned a new fibrinolytic function to cell-derived microparticles in vitro. In this study we explored the relevance of this novel property of microparticles to the in vivo situation.Design and Methods
Circulating microparticles were isolated from the plasma of patients with thrombotic thrombocytopenic purpura or cardiovascular disease and from healthy subjects. Microparticles were also obtained from purified human blood cell subpopulations. The plasminogen activators on microparticles were identified by flow cytometry and enzyme-linked immunosorbent assays; their capacity to generate plasmin was quantified with a chromogenic assay and their fibrinolytic activity was determined by zymography.Results
Circulating microparticles isolated from patients generate a range of plasmin activity at their surface. This property was related to a variable content of urokinase-type plasminogen activator and/or tissue plasminogen activator. Using distinct microparticle subpopulations, we demonstrated that plasmin is generated on endothelial and leukocyte microparticles, but not on microparticles of platelet or erythrocyte origin. Leukocyte-derived microparticles bear urokinase-type plasminogen activator and its receptor whereas endothelial microparticles carry tissue plasminogen activator and tissue plasminogen activator/inhibitor complexes.Conclusions
Endothelial and leukocyte microparticles, bearing respectively tissue plasminogen activator or urokinase-type plasminogen activator, support a part of the fibrinolytic activity in the circulation which is modulated in pathological settings. Awareness of this blood-borne fibrinolytic activity conveyed by microparticles provides a more comprehensive view of the role of microparticles in the hemostatic equilibrium.Key words: fibrinolytic microparticles, plasmin, plasminogen, uPA, tPA 相似文献Materials and methods: A total of 290 patients underwent elective EVAR. All patients regularly underwent scheduled surveillance with contrast-enhanced computed tomography (CT). Two hundred thirty-five patients were followed for ≥24?months after EVAR. Aneurysmal sac expansion of ≥10?mm was observed in 20 patients. The patients with sac expansion of ≥10?mm with no evidence of endoleak were treated with graft reinforcement. Graft reinforcement consisted of graft extension and graft relining. The patients with sac expansion at 6?months after graft reinforcement received PDSE using metallic coils and n-butyl cyanoacrylate–Lipiodol mixture. The aneurysm diameter was measured by CT performed 6?months and every year after the final intervention.
Results: Seven patients (7 men, 0 women; mean age, 69.1?±?4.2?years, Zenith®:5/Excluder®:1/Powerlink®:1) underwent graft reinforcement. Two patients underwent graft reinforcement alone, and five patients underwent PDSE after graft reinforcement. Mean follow-up time after the final intervention was 21.1?months. The sac diameter stabilized after the final intervention in all patients.
Conclusion: Graft reinforcement followed by complementary PDSE could be a useful treatment strategy for endotension. 相似文献