Protective effects of HDL on endothelial cells are impaired in diabetes, correlate with S1P and negatively associate with <i>in vivo</i> measure of endothelial dysfunction.

<p><b>(A)</b> The ability of HDL to suppress NFκB activation was measured as phosphorylation of p65 in HMEC after 16 h incubation with HDL (50 μg/mL) followed by 4 h stimulation with TNFα (n = 41 per group). <b>(B)</b> The ability of HDL to stimulate eNOS Ser1179 phosphorylation was measured in BAEC after 30 min incubation with HDL (50 μg/mL) (n = 38 non-diabetic, n = 41 diabetic subjects). (Data is expressed relative to cells not treated with HDL). <b>(C)</b> Sphigosine-1-phosphate concentration measured by LC-MS is reduced in patients with diabetes and <b>(D)</b> correlates positively with HDL ability to stimulate eNOS phosphorylation (n = 40 non-diabetic, n = 39 diabetic subjects; *excluded outlier and <i>P</i>-value after exclusion). <b>(E)</b> The ability of HDL to stimulate eNOS is inversely correlated negatively with level of P-selectin in plasma, an <i>in vivo</i> measure of endothelial dysfunction (Pearson correlation coefficient; n = 81 after an outlier exclusion).