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A Journal on Angiology
Official Journal of the , the International Union of Phlebology and the
Indexed/Abstracted in: BIOSIS Previews, Current Contents/Clinical Medicine, EMBASE, PubMed/MEDLINE, Science Citation Index Expanded (SciSearch), Scopus
Impact Factor 0,899
International Angiology 2009 February;28(1):44-9
Quantification of plasminogen activator inhibitor type 1 in the aortic wall
Kríková V. 1, Korabecná M. 2, Kocová J. 1, Treska V. 3, Molácek J. 3, Tonar Z. 1, Tolinger P. 1, Nedorost L.1
1 Department of Histology and Embryology, Faculty of Medicine, Charles University, Pilsen, Czech Republic
2 Department of Biology, Faculty of Medicine, Charles University, Pilsen, Czech Republic
3 Department of Surgery, Faculty of Medicine and Teaching Hospital, Charles University, Pilsen, Czech Republic
Aim. Plasminogen activator inhibitor type 1 (PAI-1) plays a key role in regulation of fibrinolytic system, cell-associated proteolysis and migration of smooth muscle cells (SMC). This study is focused on the types of PAI-1 expressing cells, quantification of PAI-1 expression in the walls of aneurysmatic abdominal aortas (AAA) and correlation between histological and clinical findings.
Methods. A group of nine patients who underwent surgery for AAA: asymptomatic (aAAA), symptomatic (sAAA) and ruptured (rAAA) and one control specimen (CA) were included in the study. Samples underwent histological processing and immunohistochemistry in comparison with in situ hybridisation. In order to assess the PAI-1 area fraction in histological sections through the aortic wall the Line System module of Ellipse software was used. PAI-1 expressing cells were measured in CA and AAA: endothelium, SMC, and foam cells. Photomicrographs with a total area of 0.7 mm2 for each specimen were analysed by two independent observers. Mean values of PAI-1 positive components per section area were calculated as average values.
Results. The results of both observers are as follows: 28.6% in CA; 18.1% in aAAA; 10.9% in sAAA; 11.0% in rAAA. During the progression of AAA, the SMC (PAI-1 expression was found mainly in them) became less abundant – in agreement with the values of PAI-1 area fraction. In rAAA immunohistochemistry detected PAI-1 in necrotic centres of atheromathous plaques.
Conclusion. AAA may be evaluated as the result of gradual changes in regulation of fibrinolysis that is observed as redistribution of cells expressing PAI-1. The area fraction of PAI-1 positive components correlates with clinical classification of AAA.