BACKGROUND: Circulating beta(2)-glycoprotein-I-oxidized low-density lipoprotein (beta(2)-GPI-ox-LDL) complexes have been found in patients with systemic lupus erythematosus (SLE) and other autoimmune diseases as a contributor to the development of autoimmune-mediated atherosclerosis. In vitro study showed that beta(2)-GPI also bound with high affinity to atherogenic lipoprotein (a) [Lp(a)] which shares structural similarity to LDL. We examined the existence and clinical significance of serum complexes of beta(2)-GPI with Lp(a) in SLE patients. METHODS: A "sandwich" ELISA was developed for measuring serum concentrations of beta(2)-GPI-Lp(a) complexes, using rabbit anti-human beta(2)-GPI antibody as capturing antibody, and quantitating with antibody against apo(a). Forty-seven SLE patients and 42 healthy controls were studied. RESULTS: Both Lp(a) (400+/-213 mg/l vs. 181+/-70 mg/l) and ox-Lp(a) (27.07+/-22.30 mg/l vs. 8.20+/-4.55 mg/l) concentrations were higher in SLE patients than in controls (P<0.0001). beta(2)-GPI-Lp(a) complexes were detectable in both controls and SLE. The complexes levels in SLE were higher than in controls (0.96+/-0.41 U/ml vs. 0.59+/-0.20 U/ml, P<0.0001) and was positively correlated with ox-Lp(a) (P<0.001). CONCLUSIONS: We report the existence of beta(2)-GPI-Lp(a) complexes in both controls and SLE patients. The complexes levels increase in SLE. Copyright 2009 Elsevier B.V. All rights reserved.
BACKGROUND: Circulating beta(2)-glycoprotein-I-oxidized low-density lipoprotein (beta(2)-GPI-ox-LDL) complexes have been found in patients with systemic lupus erythematosus (SLE) and other autoimmune diseases as a contributor to the development of autoimmune-mediated atherosclerosis. In vitro study showed that beta(2)-GPI also bound with high affinity to atherogenic lipoprotein (a) [Lp(a)] which shares structural similarity to LDL. We examined the existence and clinical significance of serum complexes of beta(2)-GPI with Lp(a) in SLEpatients. METHODS: A "sandwich" ELISA was developed for measuring serum concentrations of beta(2)-GPI-Lp(a) complexes, using rabbit anti-humanbeta(2)-GPI antibody as capturing antibody, and quantitating with antibody against apo(a). Forty-seven SLEpatients and 42 healthy controls were studied. RESULTS: Both Lp(a) (400+/-213 mg/l vs. 181+/-70 mg/l) and ox-Lp(a) (27.07+/-22.30 mg/l vs. 8.20+/-4.55 mg/l) concentrations were higher in SLEpatients than in controls (P<0.0001). beta(2)-GPI-Lp(a) complexes were detectable in both controls and SLE. The complexes levels in SLE were higher than in controls (0.96+/-0.41 U/ml vs. 0.59+/-0.20 U/ml, P<0.0001) and was positively correlated with ox-Lp(a) (P<0.001). CONCLUSIONS: We report the existence of beta(2)-GPI-Lp(a) complexes in both controls and SLEpatients. The complexes levels increase in SLE. Copyright 2009 Elsevier B.V. All rights reserved.
Authors: Cláudia Sá E Cunha; Britta Nyboer; Kirsten Heiss; Margarida Sanches-Vaz; Diana Fontinha; Ellen Wiedtke; Dirk Grimm; Jude Marek Przyborski; Maria M Mota; Miguel Prudêncio; Ann-Kristin Mueller Journal: Proc Natl Acad Sci U S A Date: 2017-01-30 Impact factor: 11.205