Members of the CCAAT/enhancer binding protein (C/EBP) family of transcription factors have been reported to be up-regulated in Alzheimer's disease. In the present study, we have investigated the effects of amyloid-beta (Abeta) peptides on C/EBPbeta and C/EBPdelta, previously shown to be induced by inflammatory stimuli in glial cells. Surprisingly, electrophoretic mobility shift assay showed that both Abeta(1-42) and Abeta(25-35) blocked C/EBP activation induced by the inflammatory cytokine interleukin-1beta (IL-1beta) or lipopolysaccharide (LPS) in mixed primary glial cell cultures from rat. Abeta also blocked IL-1beta- or LPS-induced C/EBP protein levels. The most prominent effects were observed on DNA binding activity and protein levels of C/EBPdelta. Our results demonstrate a dysregulation of C/EBP when glial cells are activated in the presence of Alzheimer Abeta peptides.

译文

据报道,转录因子CCAAT/增强子结合蛋白 (C/EBP) 家族的成员在阿尔茨海默氏病中被上调。在本研究中,我们研究了淀粉样 β (Abeta) 肽对C/eppbeta和C/eppdelta的影响,这些蛋白先前被证明是由神经胶质细胞中的炎症刺激诱导的。令人惊讶的是,电泳迁移率变化测定表明,在来自大鼠的混合原代神经胶质细胞培养物中,Abeta(1-42) 和Abeta(25-35) 都阻断了由炎性细胞因子interleukin-1beta (IL-1beta) 或脂多糖 (LPS) 诱导的C/EBP激活。Abeta还阻断IL-1beta或LPS诱导的C/EBP蛋白水平。观察到对C/eppdelta的DNA结合活性和蛋白质水平最显着的影响。我们的结果表明,当存在阿尔茨海默氏病 β 肽时,神经胶质细胞被激活时,C/EBP失调。

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