OBJECTIVE: Inflammation and atherosclerosis are the major causes of cardiovascular disease (CVD) in SLE. Both traditional and disease-specific risk factors contribute to the formation of endothelial dysfunction. Endothelial progenitor cells (EPCs) have the ability to restore endothelial integrity. The aim of this study was to determine whether the number and function of EPCs are altered in SLE. METHODS: Nineteen patients with SLE and 19 controls were analysed. VEGF receptor-2 (VEGFR-2)(+)/CD133(+) and CD34(+)/VEGFR-2(+) cells were quantified by flow cytometry. EPC differentiation was measured by DiI-acLDL/Lectin I staining. Furthermore, apoptosis, proliferation capacity, migration capacity and clonogenic ability of EPCs were determined. RESULTS: VEGFR-2(+)/CD133(+) cells were enhanced in SLE [215 (37) vs 122 (11) cells/1 x 10(6) lymphocytes; P = 0.029], whereas the number [106 (13) vs 215 (27) cells/1 x 10(6) lymphocytes; P = 0.002] and the proliferation rate [96% (6%) vs 143% (19%); P = 0.008] of CD34(+)/VEGFR-2(+) cells were decreased compared with controls. Additionally, EPCs in SLE showed an increased apoptosis [7% (1.4%) vs 3% (0.4%); P = 0.004], an impaired differentiation [36 (5) vs 121 (20) cells/mm(2); P < 0.001] and a reduced migratory capacity [116% (4%) vs 139% (4%); P = 0.001]. CONCLUSIONS: Our results suggest that the mobilization of progenitor cells is unaffected in SLE, but the diminished number and the altered functionality of circulating CD34(+)/VEGFR-2(+) cells reduce the ability to repair vascular damage and thus may trigger the development of atherosclerosis in SLE.
OBJECTIVE: Inflammation and atherosclerosis are the major causes of cardiovascular disease (CVD) in SLE. Both traditional and disease-specific risk factors contribute to the formation of endothelial dysfunction. Endothelial progenitor cells (EPCs) have the ability to restore endothelial integrity. The aim of this study was to determine whether the number and function of EPCs are altered in SLE. METHODS: Nineteen patients with SLE and 19 controls were analysed. VEGF receptor-2 (VEGFR-2)(+)/CD133(+) and CD34(+)/VEGFR-2(+) cells were quantified by flow cytometry. EPC differentiation was measured by DiI-acLDL/Lectin I staining. Furthermore, apoptosis, proliferation capacity, migration capacity and clonogenic ability of EPCs were determined. RESULTS:VEGFR-2(+)/CD133(+) cells were enhanced in SLE [215 (37) vs 122 (11) cells/1 x 10(6) lymphocytes; P = 0.029], whereas the number [106 (13) vs 215 (27) cells/1 x 10(6) lymphocytes; P = 0.002] and the proliferation rate [96% (6%) vs 143% (19%); P = 0.008] of CD34(+)/VEGFR-2(+) cells were decreased compared with controls. Additionally, EPCs in SLE showed an increased apoptosis [7% (1.4%) vs 3% (0.4%); P = 0.004], an impaired differentiation [36 (5) vs 121 (20) cells/mm(2); P < 0.001] and a reduced migratory capacity [116% (4%) vs 139% (4%); P = 0.001]. CONCLUSIONS: Our results suggest that the mobilization of progenitor cells is unaffected in SLE, but the diminished number and the altered functionality of circulating CD34(+)/VEGFR-2(+) cells reduce the ability to repair vascular damage and thus may trigger the development of atherosclerosis in SLE.
Authors: John A Reynolds; Sahena Haque; Kate Williamson; David W Ray; M Yvonne Alexander; Ian N Bruce Journal: Sci Rep Date: 2016-03-01 Impact factor: 4.379