Department of Respiratory Medicine, Jinling Hospital, Nanjing University School of Medicine, Nanjing 210002, China.
Mediators Inflamm. 2012;2012:485279. doi: 10.1155/2012/485279. Epub 2012 May 28.
This study investigated the relationship between antiapoptotic activities induced by activated protein C and endoplasmic reticulum stress. In this study, it was observed that activated protein C elicited a rise in glucose-regulated protein 78 and glycogen synthase kinase-3β and inhibited apoptosis in human umbilical vein endothelial cells induced by lipopolysaccharide. Calcium inhibition did not alter the antiapoptotic effect of activated protein C. The antiapoptotic efficiency of activated protein C was reduced in human umbilical vein endothelial cells following treatment with glycogen synthase kinase-3β-siRNA. In summary, activated protein C induced endoplasmic reticulum stress and attenuated lipopolysaccharide-induced human umbilical vein endothelial cell apoptosis mediated by glycogen synthase kinase-3β.
本研究探讨了激活蛋白 C 诱导的抗凋亡活性与内质网应激之间的关系。在这项研究中,观察到激活蛋白 C 引起葡萄糖调节蛋白 78 和糖原合酶激酶-3β 的增加,并抑制脂多糖诱导的人脐静脉内皮细胞凋亡。钙抑制不改变激活蛋白 C 的抗凋亡作用。糖原合酶激酶-3β-siRNA 处理后人脐静脉内皮细胞中激活蛋白 C 的抗凋亡效率降低。总之,激活蛋白 C 诱导内质网应激,并减弱糖原合酶激酶-3β 介导的脂多糖诱导的人脐静脉内皮细胞凋亡。