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. Author manuscript; available in PMC: 2015 Sep 1.
Published in final edited form as: Arthritis Rheumatol. 2014 Sep;66(9):2532–2544. doi: 10.1002/art.38703

Figure 1. HDL isolated from SLE patients is significantly oxidized and dysfunctional.

Figure 1

Plasma and HDL were purified from healthy controls (N=20), and SLE patients (N=40). (A) ABCA1-mediated cholesterol efflux capacity (determined in J774 cells loaded with radiolabeled [3H]-cholesterol and then incubated with SLE or control apoB depleted plasma). (B) MPO-specific 3-chlorotyrosine (Cl-Tyr) levels and RNS- and MPO-mediated 3-nitrotyrosine (N-Tyr) levels in lupus and control HDL (in log base 10). The length of the box defines the interquartile range (IQR). Medians (IQR) are on raw scale. (C) Box blots display distributions of isotopically labeled chlorinated or nitrated tyrosines. Native apoA-1 peptides were spiked into HDL samples from control (N=20, white) and SLE patients (N=40, shaded). Extracted ion chromatograms from specific fragment ions were used for quantitative analysis. Values are expressed in log base 10 and significant differences between controls and SLE are denoted by an asterisk (*p<0.05). The length of the box defines the IQR. (D) For all subjects, correlations between levels of N-Tyr and Cl-Tyr HDL oxidation, MPO and Cl-Tyr HDL oxidation, MPO and N-Tyr HDL oxidation, and MPO and chlorination levels at tyrosine 192 within apoA1 from patients. Figure D displays the scatter plot and least square regression line.