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. 2011 Jun 23;121(7):2693–2708. doi: 10.1172/JCI42946

Figure 6. Differential effects of HDL from healthy subjects and patients with sCAD or ACS on endothelial LOX-1 and PKCβII activation — role of PKCβII activation in the altered effects of HDL on endothelial Akt and eNOS-activating/inhibiting phosphorylation in patients with CAD.

Figure 6

(A) Effect of HDL from healthy subjects and patients with sCAD and ACS on PKCβII-activating phosphorylation at Ser660 and (B) membrane translocation of PKCβII in endothelial cells (n = 8–12 per group). (C) Incubation of endothelial cells with the nonselective inhibitor of PKCβI and PKCβII isoforms LY379196 and CGP53353, a highly selective inhibitor of PKCβII, restored the ability of HDL from patients with CAD to stimulate endothelial NO production and (D) the activating eNOS phosphorylation at Ser1177 (n = 8–10 per group). (E) Pretreatment of endothelial cells with an anti–LOX-1 blocking antibody prevented the increase in PKCβII phosphorylation at Ser660 (n = 6–8 per group). (F) Moreover, incubation of endothelial cells with an anti–LOX-1 blocking antibody improved the capacity of HDL from patients with CAD, but not from healthy subjects, to stimulate endothelial NO production (n = 8–10 per group).