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Urokinase-type plasminogen activator receptor is associated with macrophages and plaque rupture in symptomatic carotid atherosclerosis.

Journal article
Authors Per-Arne Svensson
Fredrik J. Olson
Daniel Hägg
Mikael Ryndel
Olov Wiklund
Lars Karlström
Johannes Hulthe
Lena M S Carlsson
Björn Fagerberg
Published in International journal of molecular medicine
Volume 22
Issue 4
Pages 459-64
ISSN 1107-3756
Publication year 2008
Published at Wallenberg Laboratory
Institute of Medicine, Department of Molecular and Clinical Medicine
Institute of Clinical Sciences
Pages 459-64
Language en
Keywords Aged, Aged, 80 and over, Antigens, CD, metabolism, Antigens, Differentiation, Myelomonocytic, metabolism, Carotid Artery Diseases, complications, genetics, pathology, Carotid Stenosis, complications, genetics, pathology, Cells, Cultured, Endarterectomy, Carotid, Female, Gene Expression Regulation, Humans, Macrophages, metabolism, pathology, Male, Middle Aged, Protein Transport, Receptors, Cell Surface, genetics, metabolism
Subject categories Medical and Health Sciences


There is a strong correlation between macrophage infiltration and plaque instability in recently symptomatic carotid atherosclerotic plaques, and it is hypothesised that mechanisms related to macrophages may be involved in plaque vulnerability and rupture. We previously found high expression of urokinase-type plasminogen activator receptor (UPAR) in human macrophages. The aim of this study was to investigate whether UPAR co-localises with macrophages in symptomatic carotid plaques, and whether UPAR expression is associated with plaque rupture. Real-time RT-PCR assays showed that UPAR expression levels were high in monocyte-derived macrophages and in carotid endarterectomies compared with a tissue panel. Serial transverse sections were prepared from carotid endarterectomies from 12 symptomatic patients, and analyzed with immunohistochemical staining for UPAR and for CD68-positive macrophages, and with histopathological assessment. UPAR co-localised with CD68-positive macrophages, with a high correlation (r=0.90, p<0.001) between immunostained areas in 12 carotid endarterectomies from symptomatic patients. High degrees of UPAR and CD68 staining were found in sections around the bifurcation level where rupture was most common, while low degrees of staining were found in sections of the common carotid artery end of the endarterectomy (p<0.05). Higher degrees of UPAR staining were observed in ruptured plaque sections compared with non-ruptured sections. In conclusion, UPAR was highly expressed in monocyte-derived macrophages and in symptomatic carotid plaques, UPAR co-localised with macrophages in carotid symptomatic plaques and UPAR was predominantly found in ruptured plaque segments. These findings support the hypothesis that UPAR is related to plaque rupture in symptomatic atherosclerotic lesions.

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