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Activated Protein C Induces Endoplasmic Reticulum Stress and Attenuates Lipopolysaccharide-Induced Apoptosis Mediated by Glycogen Synthase Kinase-3β

机译:活化的蛋白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凋亡

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摘要

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-3βand 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.
机译:本研究探讨了活化蛋白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,观察到活化蛋白C引起葡萄糖调节蛋白78和糖原合酶激酶3β升高,并抑制脂多糖诱导的人脐静脉内皮细胞凋亡。钙抑制不会改变活化蛋白C的抗凋亡作用。用糖原合酶激酶3β-siRNA处理后,活化蛋白C在人脐静脉内皮细胞中的抗凋亡效率降低。总之,活化蛋白C诱导糖原合酶激酶3β介导的内质网应激和脂多糖诱导的人脐静脉内皮细胞凋亡。

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