Angiogenesis plays a critical role in the pathogenesis of several connective tissue diseases. There is, however, relatively little information available on the role of angiogenesis in systemic lupus erythematosus (SLE). The aim of this study was to investigate the angiogenic activity in sera of patients with SLE and to determine the association between angiogenic activity and clinical complications. Sera from 66 Tunisian females with SLE and from 32 healthy blood donors were studied for their angiogenic activity using the in-vitro tube formation test on Matrigel. Samples were divided into five groups according to their angiogenic activity, which was scored from 0 (no angiogenesis) to 4 (high angiogenic activity). Samples from each group were then tested randomly to assess serum concentration of vascular endothelial growth factor (VEGF). No correlation was found between angiogenic activity scores and serum VEGF levels. Considering angiogenesis assessment in-vitro, sera of patients with SLE showed a much higher angiogenic activity than healthy controls since a high angiogenic score (score 4) is present in 43.9% of patients and in 6.3% of controls (P < 0.0002). This high angiogenic activity is not correlated with disease activity; however, SLE patients with anti-dsDNA antibodies and those with nephritis showed higher angiogenic activity compared with patients without these complications since score 4 is found in 50.9% and 67.9% versus 9.1% (P = 0.017) and 26.3% (P < 0.001), respectively. In conclusion, our study showed that high serum angiogenic activity in SLE was not correlated with the VEGF levels. We suggest the use of the 'in-vitro' tube formation test as a better tool to study the angiogenic potential of sera. We found that in patients with SLE, serum angiogenic activity is increased compared with healthy controls. This high angiogenic activity is associated with renal complications and with the presence of anti-dsDNA antibodies. These findings suggest an involvement of angiogenesis disturbance in the pathogenesis of SLE.
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