Diabetic HDL Is Dysfunctional in Stimulating Endothelial Cell Migration and Proliferation Due to Down Regulation of SR-BI Expression
Figure 6
Akt phosphorylation induced by HDL. A)
HUVECs were treated without (control) or with the addition of N-HDL or D-HDL for 5, 10, 20, 30, 60 minutes, 3, 6, 12, or 24 hours. Expression levels of phospho-Akt (Ser473) and Akt1/2 were analyzed by western blotting. B) HUVECs were treated with N-HDL or D-HDL (n = 3 each) for 20 minutes or 24 hours. Expression levels of phospho-Akt (Ser473), Akt1/2, and β-actin were analyzed by western blotting. C) The density of the phospho-Akt bands at 20 minutes was normalized to the β-actin band (ns, p>0.05). D) The density of the phospho-Akt bands at 24 hours was normalized to the β-actin band (**, p<0.01 by a student’s t test). E) The density of the phospho-Akt bands at 20 minutes was normalized to the Akt1/2 band (ns, p>0.05). F) The density of the phospho-Akt bands at 24 hours was normalized to the Akt1/2 band (*, p<0.05 by a student’s t test). G) MAECs from SR-BI (+/+) or SR-BI (−/−) mice were treated without (control) or with N-HDL or D-HDL for 24 hours, and expression levels of phospho-Akt (Ser473), Akt1/2, and β-actin were analyzed by western blotting. H) The density of the phospho-Akt bands of MAECs from SR-BI (+/+) or SR-BI (−/−) mice was normalized to the Akt1/2 band (*, p<0.05 and **, p<0.01 by a student’s t test).