Fig. 1.
The characteristics and functions of HDL from healthy subjects and patients with coronary artery disease (nHDL and dHDL, respectively) and their effects on angiogenesis.(A) The levels of lipid hydroperoxide in nHDL and dHDL. *p < 0.05 (n = 95). (B and C) The correlation between levels of lipid hydroperoxide in dHDL and C reactive protein (CRP) and serum amyloid A (SAA). *p < 0.05 (n = 78). (D) The cholesterol efflux capacities of nHDL and dHDL(100 μg/ml). *p < 0.05 (n = 31). (E) Immunofluorescence assays showing the effects of nHDL and dHDL with or without pretreatment with TNF-α on VCAM-1 expression (n = 6). (F–G) Images and dot plot show that nHDL stimulated endothelial cell (ECs) tube formation. The dHDL had less effect on EC tube formation. Both the ERK1/2 and AKT inhibitors impaired nHDL and dHDL-induced EC tube formation. * vs. control; # vs. nHDL; & vs. dHDL, p < 0.05 (n = 10). (H–I) The image and dot plot show that nHDL promoted angiogenesis in zebrafish. The dHDL had a lower effect on angiogenesis. Both ERK1/2 and AKT inhibitors decreased nHDL and dHDL-induced angiogenesis. * vs. control; # vs. nHDL; & vs. dHDL, p < 0.05 (n = 30). (J–K) Image and dot plot show that nHDL increased EC nitric oxide (NO) production. The dHDL had a lower effect on EC NO production. AU, arbitrary units. * vs. control; # vs. nHDL, p < 0.05 (n = 10). (L) The dot plot shows that dHDL, but not nHDL, was enhanced endothelial O2− generation. l-NAME inhibited dHDL-induced O2− generation. AU, arbitrary units. * vs. control; # vs. nHDL; & vs. dHDL; ∧ vs. TNF-α, p < 0.05 (n = 10).