Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2019 Apr;197(2):189-197.
doi: 10.1007/s00408-019-00211-w. Epub 2019 Feb 28.

Soluble Urokinase-Type Plasminogen Activator Receptor and Arterial Stiffness in Patients with COPD

Renáta M Böcskei  1 , Béla Benczúr  2 , György Losonczy  3 , Miklós Illyés  4 , Attila Cziráki  4 , Veronika Müller  3 , Anikó Bohács  3 , András Bikov  3
Affiliations

Soluble Urokinase-Type Plasminogen Activator Receptor and Arterial Stiffness in Patients with COPD

Renáta M Böcskei et al. Lung. 2019 Apr.

Abstract

Introduction: Soluble urokinase-type plasminogen activator receptor (suPAR) is upregulated by inflammation and plays a role in the pathogenesis of atherosclerosis. Chronic obstructive pulmonary disease (COPD) is associated with enhanced systemic inflammation and increased risk for atherosclerosis, however, studies analysing the circulating suPAR levels in COPD are contradictory. The aim of the study was to investigate plasma suPAR concentrations together with markers of arterial stiffness in COPD.

Materials and methods: Twenty-four patients with COPD and 18 non-COPD, control subjects participated in the study. Plasma suPAR was measured, together with lung volumes, symptom burden, exacerbation history, markers of arterial stiffness and soluble inflammatory biomarkers, such as endothelin-1, high-sensitivity C-reactive protein (hsCRP), interleukin-6 (IL-6).

Results: Plasma suPAR levels were higher in COPD (2.84 ± 0.67 ng/ml vs. 2.41 ± 0.57 ng/ml, p = 0.03) and were related to lung function measured with FEV1 (r = - 0.65, p < 0.01) and symptom burden determined with the modified Medical Research Council questionnaire (r = 0.55, p < 0.05). Plasma suPAR concentrations correlated with various measures of arterial stiffness in all subjects, but only with ejection duration in COPD (r = - 0.44, p = 0.03).

Conclusions: Plasma suPAR levels are elevated in COPD and relate to arterial stiffness. Our results suggest that suPAR may be a potential link between COPD and atherosclerosis.

Keywords: Arterial stiffness; COPD; Cardiovascular risk; IL-6; SuPAR.

PubMed Disclaimer

Conflict of interest statement

Conflict of interest

Miklós Illyés is a patent owner of the Arteriograph method and has shares in TensioMed Ltd., a company that manufactures the Arteriograph device for measuring arterial stiffness. The other authors declare no conflict of interest.

Ethical Approval

All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki Declaration and its later amendments or comparable ethical standards.

Informed Consent

Informed consent was obtained from all individual participants included in the study.

Figures

Fig. 1
Fig. 1
Flow chart of the number and selection of individuals in the study population
Fig. 2
Fig. 2
Plasma suPAR levels in COPD and controls. Significantly higher plasma suPAR levels were detected in COPD (*p = 0.03). Individual data are presented with mean ± standard deviation
Fig. 3
Fig. 3
Relationship between plasma suPAR levels and lung function. A significant relationship was detected between plasma suPAR levels and FEV1 (r = − 0.65, p < 0.01)
Fig. 4
Fig. 4
Relationship between plasma suPAR levels and symptoms burden. A significant relationship was detected between plasma suPAR levels and mMRC score (r = 0.55, p < 0.01)
See this image and copyright information in PMC

References

    1. Vogelmeier CF, Criner GJ, Martinez FJ, et al. Global strategy for the diagnosis, management, and prevention of chronic obstructive lung disease 2017 Report: GOLD executive summary. Eur Respir J. 2017 - PubMed
    1. Barnes PJ, Burney PG, Silverman EK, Celli BR, Vestbo J, Wedzicha JA, Wouters EF. Chronic obstructive pulmonary disease. Nat Rev Dis Primers. 2015;1:15076. doi: 10.1038/nrdp.2015.76. - DOI - PubMed
    1. Bourdin A, Burgel PR, Chanez P, Garcia G, Perez T, Roche N. Recent advances in COPD: pathophysiology, respiratory physiology and clinical aspects, including comorbidities. Eur Respir Rev. 2009;18(114):198–212. doi: 10.1183/09059180.00005509. - DOI - PubMed
    1. Coxson HO, Dirksen A, Edwards LD, Evaluation of. CLtIPSEI et al. The presence and progression of emphysema in COPD as determined by CT scanning and biomarker expression: a prospective analysis from the ECLIPSE study. Lancet Respir Med. 2013;1(2):129–136. doi: 10.1016/S2213-2600(13)70006-7. - DOI - PubMed
    1. Packard RR, Libby P. Inflammation in atherosclerosis: from vascular biology to biomarker discovery and risk prediction. Clin Chem. 2008;54(1):24–38. doi: 10.1373/clinchem.2007.097360. - DOI - PubMed

Publication types

MeSH terms