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Endothelial progenitor cells in active rheumatoid arthritis: effects of tumour necrosis factor and glucocorticoid therapy
  1. Johannes Grisar1,
  2. Daniel Aletaha1,
  3. Carl W Steiner1,
  4. Theresa Kapral1,
  5. Sabine Steiner2,
  6. Marcus Säemann3,
  7. Ilse Schwarzinger4,
  8. Barbara Buranyi5,
  9. Günter Steiner1,6,
  10. Josef S Smolen1,6
  1. 1
    Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
  2. 2
    Division of Angiology, Department of Internal Medicine II, Medical University of Vienna, Vienna, Austria
  3. 3
    Division of Nephrology, Department of Internal Medicine III, Medical University of Vienna, Vienna, Austria
  4. 4
    Department of Medical and Chemical Laboratory, Medical University of Vienna, Vienna, Austria
  5. 5
    Ludwig Boltzmann Institute of Experimental Endocrinology, Medical University of Vienna, Vienna, Austria
  6. 6
    Center of Molecular Medicine of the Austrian Academy of Sciences
  1. Johannes Grisar, MD, Division of Rheumatology, Department of Internal Medicine III, Medical University of Vienna, Waehringer Guertel 18–20, A-1090 Vienna, Austria; johannes.grisar{at}meduniwien.ac.at

Abstract

Objectives: To study the effects of short-term intermediate dose glucocorticoid (GC) therapy in patients with active rheumatoid arthritis (RA) on circulating endothelial progenitor cells (EPC), which are known to influence cardiovascular risk, and to elucidate mechanisms potentially responsible for the reduction of EPCs in patients with active RA.

Methods: EPCs were quantified in 29 patients with active RA by flow cytometry, colony forming unit (CFU) and circulating angiogenic cell (CAC) assays before and after 7 days of intermediate dose GC therapy. CFU from patients with RA and from healthy referents (HR) were cultured in vitro in the absence or presence of dexamethasone (Dex) and/or TNF.

Results: After 1 week of GC therapy, EPC increased from 0.026 (SD 0.003)% to 0.053 (SD 0.010)% (p<0.01), and from 12 (SD 4) to 27 (SD 7) CFU/well (p<0.02); CAC also increased from 7 (SD 2) to 29 (SD 8) cells/high power field (p<0.05). In parallel, disease activity decreased significantly after GC treatment. TNF serum levels also decreased from 36 (SD 10) to 14 (SD 6) pg/ml (p<0.0001). Addition of Dex to the RA CFU led to a significant increase of mean CFU counts, whereas addition of TNF induced a decrease of CFU.

Conclusions: Our data indicate that TNF may be at least partly responsible for the reduction of EPC seen in patients with RA. Intermediate doses of GCs for a short period of time, apart from reducing disease activity, significantly increase circulating EPC.

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Footnotes

  • Competing interests: None.

  • Funding: This work was supported by “Medizinisch-Wissenschaftlicher Fonds des Bürgermeisters der Bundeshauptstadt Wien” and the Center of Molecular Medicine of the Austrian Academy of Sciences.

  • Abbreviations:
    bFGF
    basic fibroblast growth factor
    CAC
    circulating angiogenic cell
    CFU
    colony forming unit
    Dex
    dexamethasone
    DMARD
    disease-modifying antirheumatic drugs
    EPC
    endothelial progenitor cell
    EPO
    erythropoietin
    GC
    glucocorticoids
    HR
    healthy referents
    IL
    interleukin
    VEGF
    vascular endothelial growth factor

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