Impaired Autophagy Induced by oxLDL/β2GPI/anti-β2GPI Complex through PI3K/AKT/mTOR and eNOS Signaling Pathways Contributes to Endothelial Cell Dysfunction

Figure 4

The phosphorylation of PI3K/AKT/mTOR and eNOS induced by the oxLDL/β2GPI/anti-β2GPI complex in endothelial cells. HUVECs and bEnd.3 cells were treated with oxLDL/β2GPI/anti-β2GPI complex for 5, 15, 30, 45, and 60 min. Western blotting analysis of p-PI3K, PI3K, p-AKT, AKT, p-mTOR, and mTOR in HUVECs (a) and bEnd.3 cells (e). Quantification of the ratio of p-AMPK/PI3K (b), p-AKT/AKT (c), and p-mTOR/mTOR (d) in HUVECs. Quantification of the ratio of p-AMPK/PI3K (f), p-AKT/AKT (g), and p-mTOR/mTOR (h) in bEnd.3 cells. Western blotting analysis and quantification for p-eNOS/eNOS expression in HUVECs (i) and bEnd.3 cells (j). , , and indicate statistically significant differences. ns: nonsignificant differences. All values are denoted as from three independent experiments (), and a representative blot was shown.

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