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Fibrinolysis inhibi...
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Rylander, A. C. J.
(author)
Fibrinolysis inhibitors in plaque stability: a morphological association of PAI-1 and TAFI in advanced carotid plaque
- Article/chapterEnglish2017
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LIBRIS-ID:oai:gup.ub.gu.se/254251
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https://gup.ub.gu.se/publication/254251URI
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https://doi.org/10.1111/jth.13641DOI
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
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Background: Fibrinolysis plays an important role in destabilization of atherosclerotic plaques and is tightly regulated by specific inhibitors. Objective: The fibrinolysis inhibitors plasminogen activator inhibitor type-1 (PAI-1) and thrombin-activatable fibrinolysis inhibitor (TAFI) were quantified and described in the morphological context of advanced carotid plaques American Heart Association VI-VIII to elucidate their role in plaque stability. Methods: Immunohistochemistry in serial sections along the longitudinal axis of endarterectomies from patients with symptomatic carotid stenosis (n = 19) were studied using an antibody specific for free PAI-1 (I205), an antibody with high affinity for TAFI/TAFIa (CP17) and established antibodies for smooth muscle cells (alpha-actin), endothelial cells (von Willebrand factor [VWF]), macrophages (CD68) and platelets (CD42). Results: PAI-1 and TAFI show a specific distribution in these advanced plaques with a maximum corresponding to the internal carotid artery (ICA). Free PAI-1 was mainly detected in macrophages and in intravascular thrombi, and TAFI in endothelial cells (ECs) but also macrophages. The one-way ANOVA analysis with Bonferroni's correction showed a significant increase of macrophages and ECs, TAFI and PAI-1 in areas with high neovascularization in endarterectomy sections corresponding to ICA. High Spearman factors for TAFI, PAI-1 and VWF indicate neovascularization as the main source of plasma proteins, transported by platelets into the atheroma (PAI-1) or expressed by ECs (TAFI). CD68 was highly associated with VWF, PAI-1 and especially TAFI, underlining the role of macrophages in fibrinolytic activity and inflammation. Conclusion: The abundance of free PAI-1 and TAFI in the plaque may inhibit plasmin generation and thereby counteract plaque destabilization by fibrinolysis, cell migration and inflammation.
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Lindgren, A.
(author)
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Deinum, J.
(author)
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Bergström, Göran,1964Gothenburg University,Göteborgs universitet,Institutionen för medicin,Institute of Medicine(Swepub:gu)xbgort
(author)
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Bottcher, G.
(author)
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Kalies, I.
(author)
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Wahlander, K.
(author)
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Göteborgs universitetInstitutionen för medicin
(creator_code:org_t)
Related titles
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In:Journal of Thrombosis and Haemostasis: Elsevier BV15:4, s. 758-7691538-79331538-7836
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