Background Patients affected by Rheumathoid arthtritis (RA) present accelerated atherosclerosis and increased cardiovascular morbidity and mortality, with respect to the general population. In RA an impairment of the number and the activity of circulating progenitor cells, including CD34+ cells and endothelial progenitor cells (EPC), is involved in development of endothelial damage and cardiovascular diseases (CVD).
Objectives This study explores the effects of oxidative stress and flogosis on endothelial progenitor cell property and activity.
Methods Circulating progenitor cells (CPCs) were isolated from 33 pz affected by RA and from 33 controls matched for age and gender. In these cells mRNA expression, protein levels and enzymatic activity of antioxidants: manganese superoxide dismutase (MnSOD), catalase (CAT), and glutathione peroxidase-type 1 (GPx-1) were evaluated. C-reactive protein (CRP) levels were measured. We also investigated the accumulation of intracellular reactive oxygen species (ROS) in CPCs and the relationships among some inflammatory markers and cell number and enzymes.
Results In RA CPCs number (0.39±0.10 vs 0.62±0.08, p<0.001) was significantly reduced. Intracellular ROS levels (107.35±73.36 vs 49.19±10.70, p<0.001) were higher, as well as MnSOD (mRNA, protein and activity), while CAT and GPx-1 (mRNA, proteins and activity) were reduced. CPCs number was correlated with CRP, ROS and enzyme levels and activity. In patients with RA the levels of CRP correlates linearly with the expression of MnSOD (rs=0.63, p<0.001), with levels of ROS (rs=0.51, p<0.001), with biomarkers of arterial stiffness (PWV, rs=0.44, p<0.005; AI%, rs=0.36, p<0.01) while appears not correlate with CAT or GPx-1 (rs=0.08, and rs=0.04, respectively, both p=ns). CPCs number correlate inversely with arterial stiffness indices (PWV, rs 0.48 p<0.001, AI, rs 0.73, p<0.001).
Conclusions Our data show that in RA inflammation and oxidative stress impair CPCs antioxidant system, reduce their number in peripheral blood, induce the develop of endothelial damage leading to accelerated atherosclerosis.
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Disclosure of Interest None Declared
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