Urokinase-type plasminogen activator receptor is associated with macrophages and plaque rupture in symptomatic carotid atherosclerosis.
Artikel i vetenskaplig tidskrift, 2008

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.

complications

metabolism

Antigens

Middle Aged

genetics

metabolism

CD

Differentiation

Cells

Humans

pathology

Carotid Stenosis

Carotid

Cultured

complications

Male

pathology

Endarterectomy

Receptors

Cell Surface

Myelomonocytic

Protein Transport

Female

Aged

Gene Expression Regulation

Carotid Artery Diseases

Aged

Macrophages

metabolism

genetics

Antigens

pathology

80 and over

metabolism

genetics

Författare

Per-Arne Svensson

Göteborgs universitet

Fredrik J. Olson

Göteborgs universitet

Daniel Hägg

Göteborgs universitet

Mikael Ryndel

Göteborgs universitet

Olov Wiklund

Göteborgs universitet

Lars Karlström

Göteborgs universitet

Johannes Hulthe

Göteborgs universitet

Lena M S Carlsson

Göteborgs universitet

Björn Fagerberg

Göteborgs universitet

International Journal of Molecular Medicine

1107-3756 (ISSN)

Vol. 22 4 459-64

Ämneskategorier

MEDICIN OCH HÄLSOVETENSKAP

DOI

10.3892/ijmm_00000043

PubMed

18813852