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Circulating endothelial cells and their progenitors in systemic lupus erythematosus and early rheumatoid arthritis patients
Authors:Rodríguez-Carrio Javier  Prado Catuxa  de Paz Banesa  López Patricia  Gómez Jesús  Alperi-López Mercedes  Ballina-García Francisco J  Suárez Ana
Affiliation:Department of Functional Biology, Immunology Area, Faculty of Medicine, University of Oviedo, C/ Julián Clavería s/n, 33006 Oviedo, Spain. anasua@uniovi.es.
Abstract:Objective. The aim of this study was to investigate the endothelial progenitor cell population in SLE and early RA patients and its potential relationships with disease features and cytokine serum levels. Methods. Endothelial progenitor cells (EPCs), mature EPCs (mEPCs) and endothelial cells (ECs) were measured in peripheral blood samples from 83 SLE and 85 early RA patients and 39 healthy controls by flow cytometry on the basis of CD34, VEGF receptor 2 and CD133 expression. Serum levels of IL-1β, IL-6, IL-8, IL-17, VEGF-A, IFN-α, TGF-β and GM-CSF were quantified by immunoassays. Clinical and immunological data were obtained by reviewing clinical histories. Results. Circulating EPCs were increased in SLE but not in early RA patients associated with an enhanced CD34(+) bone marrow-progenitor cell release but unrelated to disease features. The amount of mEPCs, however, was significantly higher in SLE patients presenting anti-SSA/SSB antibodies and/or malar rash, whereas the presence of specific autoantibodies was associated with EC counts in early RA and SLE patients. As expected, most cytokines tested were altered in both diseases but, interestingly, IFN-α levels, and to a lesser extent IL-6 and IL-1β, were associated with CD133 loss and increased mEPC number, whereas VEGF and TGF-β seem to exert an opposite effect. Conclusion. Our results show that high IFN-α levels and/or the presence of disease-specific antibodies may identify a group of SLE patients with increased mEPC and EC counts, and consequently probably defective endothelial repair, thus supporting their use as surrogate biomarkers of endothelial damage and high cardiovascular risk.
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