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However, the underlying mechanisms are not fully understood. Endothelial dysfunction has been identified as having involvement in pathogenesis of cardiovascular diseases and SLE. This study aims to evaluate endothelial cell injury in mice with the combination of lupus and atherosclerosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The mouse model of accelerated atherosclerosis in lupus (\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mouse) was generated from apolipoprotein E\u2010deficient (apoE\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      ) and Fasl\n                      <jats:sup>gld<\/jats:sup>\n                      C57BL\/6 mice. The lupus\u2010like autoimmunity and atherosclerotic lesions were evaluated. The endothelial cell injury was determined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      The results showed that the double\u2010mutant\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice were generated. Spleens from 5\u2010month\u2010old\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice were significantly enlarged compared with wild\u2010type mice (WT mice). The\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice produced high levels of total immunoglobulin G (IgG) and IgM and showed marked increase of IgG and C3 deposits in the glomeruli. The\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice displayed a pattern of glomerulonephritis typically found in SLE. The\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice have high levels of serum creatinine. The total cholesterol, low\u2010density lipoprotein cholesterol and triglycerides were significantly increased, while high\u2010density lipoprotein cholesterol decreased in the double\u2010mutant mice. The circulating endothelial progenitor cells were significantly decreased. The serum levels of thrombomodulin and vascular cell adhesion molecule\u20101 were significantly elevated in\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice. The\n                      <jats:italic>gld.apoE<\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      <jats:italic>\n                        <jats:sup>\/<\/jats:sup>\n                      <\/jats:italic>\n                      <jats:sup>\u2212<\/jats:sup>\n                      mice simultaneously exhibited SLE and atherosclerosis characteristics.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>Our findings indicated that endothelial cell injury might be a biomarker for evaluating risks of cardiovascular disease in SLE and targeting endothelial cell dysfunction might prevent and treat atherosclerosis in SLE.<\/jats:p>\n                  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