期刊
RHEUMATOLOGY
卷 51, 期 10, 页码 1775-1784出版社
OXFORD UNIV PRESS
DOI: 10.1093/rheumatology/kes152
关键词
systemic lupus erythematosus; rheumatoid arthritis; endothelial progenitor cells; vascular damage; autoantibodies; interferon-alpha
类别
资金
- European Union FEDER funds
- Fondo de Investigacion Sanitaria (FIS) [PI080570]
- Fundacion para el Fomento en Asturias de la Investigacion Cientifica Aplicada y la Tecnologia (FICYT) [IB08-091]
- FPU grant from the Ministerio de Educacion
- FIS
- FICYT
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-1 beta, IL-6, IL-8, IL-17, VEGF-A, IFN-alpha, TGF-beta 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-alpha levels, and to a lesser extent IL-6 and IL-1 beta, were associated with CD133 loss and increased mEPC number, whereas VEGF and TGF-beta seem to exert an opposite effect. Conclusion. Our results show that high IFN-alpha 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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