In vivo detection of urokinase-type plasminogen activator receptor (uPAR) expression in arterial atherogenesis using [


Journal

Atherosclerosis
ISSN: 1879-1484
Titre abrégé: Atherosclerosis
Pays: Ireland
ID NLM: 0242543

Informations de publication

Date de publication:
07 2022
Historique:
received: 19 10 2021
revised: 23 02 2022
accepted: 25 03 2022
pubmed: 10 4 2022
medline: 29 6 2022
entrez: 9 4 2022
Statut: ppublish

Résumé

Urokinase-type plasminogen activator receptor (uPAR) is associated with extracellular matrix (ECM) degradation and cancer aggressiveness. Its role in arterial atherogenesis as a molecular imaging target is not well-established. The aim of this study was to non-invasively visualize uPAR expression in atherosclerosis by a novel uPAR-targeting positron emission tomography (PET) tracer [ We used molecular biology to investigate uPAR expression by analyzing human atherosclerotic plaques and cultured cells. A retrospective analysis was performed on patients, who underwent combined PET/CT (n = 10) to measure [ The in vitro assay for THP-1 monocytes displayed a significantly upregulated uPAR expression upon stimulation (5.2-fold upregulation, p < 0.0001 by a one-way ANOVA followed by Tukey's test) by single-cell flowcytometric analysis. Freshly excised human atherosclerotic plaques underwent flow cytometric and microarray analyses manifesting 73.9 ± 2.9% of mononuclear phagocyte system (MPS) cells expressing uPAR and had a greater than 7-fold higher gene expression of plasminogen activator urokinase receptor (PLAUR, p = 0.002), integrin subunit alpha X (ITGAX, p = 0.0008), and cluster of differentiation 163 (CD163, p < 0.0001). The tissue-to-background ratios (TBR uPAR is abundantly expressed by MPS cells in atherosclerotic plaques and can be visualized by the novel PET tracer [

Sections du résumé

BACKGROUND AND AIMS
Urokinase-type plasminogen activator receptor (uPAR) is associated with extracellular matrix (ECM) degradation and cancer aggressiveness. Its role in arterial atherogenesis as a molecular imaging target is not well-established. The aim of this study was to non-invasively visualize uPAR expression in atherosclerosis by a novel uPAR-targeting positron emission tomography (PET) tracer [
METHODS
We used molecular biology to investigate uPAR expression by analyzing human atherosclerotic plaques and cultured cells. A retrospective analysis was performed on patients, who underwent combined PET/CT (n = 10) to measure [
RESULTS
The in vitro assay for THP-1 monocytes displayed a significantly upregulated uPAR expression upon stimulation (5.2-fold upregulation, p < 0.0001 by a one-way ANOVA followed by Tukey's test) by single-cell flowcytometric analysis. Freshly excised human atherosclerotic plaques underwent flow cytometric and microarray analyses manifesting 73.9 ± 2.9% of mononuclear phagocyte system (MPS) cells expressing uPAR and had a greater than 7-fold higher gene expression of plasminogen activator urokinase receptor (PLAUR, p = 0.002), integrin subunit alpha X (ITGAX, p = 0.0008), and cluster of differentiation 163 (CD163, p < 0.0001). The tissue-to-background ratios (TBR
CONCLUSIONS
uPAR is abundantly expressed by MPS cells in atherosclerotic plaques and can be visualized by the novel PET tracer [

Identifiants

pubmed: 35396143
pii: S0021-9150(22)00159-9
doi: 10.1016/j.atherosclerosis.2022.03.026
pii:
doi:

Substances chimiques

Copper Radioisotopes 0
Heterocyclic Compounds, 1-Ring 0
Oligopeptides 0
Receptors, Urokinase Plasminogen Activator 0
beta-cyclohexylalanyl-phenylalanyl-seryl-arginyl-tyrosyl-leucyl-tryptophyl-serine 0
1,4,7,10-tetraazacyclododecane- 1,4,7,10-tetraacetic acid 1HTE449DGZ
Urokinase-Type Plasminogen Activator EC 3.4.21.73

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

103-111

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2022 The Authors. Published by Elsevier B.V. All rights reserved.

Auteurs

Harshvardhan A Khare (HA)

Department of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Department of Biomedical Sciences, Rigshospitalet and University of Copenhagen, 2100, Copenhagen, Denmark. Electronic address: h.khare@sund.ku.dk.

Kristina B V Døssing (KBV)

Department of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Department of Biomedical Sciences, Rigshospitalet and University of Copenhagen, 2100, Copenhagen, Denmark.

Lars Ringgaard (L)

Department of Health Technology, Technical University of Denmark, 2800, Lyngby, Denmark.

Esben Christensen (E)

Department of Health Technology, Technical University of Denmark, 2800, Lyngby, Denmark.

Laerke Urbak (L)

Department of Vascular Surgery, Rigshospitalet, Blegdamsvej 9, Copenhagen, DK, 2100, Denmark.

Henrik Sillesen (H)

Department of Vascular Surgery, Rigshospitalet, Blegdamsvej 9, Copenhagen, DK, 2100, Denmark.

Rasmus S Ripa (RS)

Department of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Department of Biomedical Sciences, Rigshospitalet and University of Copenhagen, 2100, Copenhagen, Denmark.

Tina Binderup (T)

Department of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Department of Biomedical Sciences, Rigshospitalet and University of Copenhagen, 2100, Copenhagen, Denmark.

Sune F Pedersen (SF)

Department of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Department of Biomedical Sciences, Rigshospitalet and University of Copenhagen, 2100, Copenhagen, Denmark.

Andreas Kjaer (A)

Department of Clinical Physiology, Nuclear Medicine & PET and Cluster for Molecular Imaging, Department of Biomedical Sciences, Rigshospitalet and University of Copenhagen, 2100, Copenhagen, Denmark. Electronic address: akjaer@sund.ku.dk.

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Classifications MeSH