Activated Protein C Induces Endoplasmic Reticulum Stress and Attenuates Lipopolysaccharide-Induced Apoptosis Mediated by Glycogen Synthase Kinase-3β
Figure 4
Upregulation of GSK-3β expression following APC treatment and decreased antiapoptotic activity following GSK-3β-siRNA transfection of HUVECs. HUVECs exposed to 10 ng/mL LPS for 24 h, were treated with 150 nM APC for 0, 6, 12, and 24 h. Upregulated GSK-3β expression was detected, peaking at 6 h after APC treatment (a). Transfection of HUVECs with GSK-3β-siRNA decreased the abundance of GSK-3β protein significantly (b). Compared with normal HUVECs treated with 150 nM APC, a significant increase of the percentage of apoptosis cells was found in HUVECs pretreated with GSK-3β-siRNA (GSK-3β versus GSK-3β-siRNA, ), indicating that the antiapoptotic activity of APC was inhibited by GSK-3β-siRNA (c).
