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首页> 外文期刊>Life sciences >EFFECT OF A CARBOXY-TERMINAL FRAGMENT OF THE ALZHEIMERS AMYLOID PRECURSOR PROTEIN ON EXPRESSION OF PROINFLAMMATORY CYTOKINES IN RAT GLIAL CELLS
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EFFECT OF A CARBOXY-TERMINAL FRAGMENT OF THE ALZHEIMERS AMYLOID PRECURSOR PROTEIN ON EXPRESSION OF PROINFLAMMATORY CYTOKINES IN RAT GLIAL CELLS

机译：拟南芥淀粉前体蛋白的羧基末端片段对大鼠胶质细胞促炎细胞因子表达的影响

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To explore factors involved in the induction of cytokines that may contribute to the pathogenesis of Alzheimer's disease (AD), the effect of a carboxy terminal 105 amino acid fragment (CT105) of the amyloid precursor protein (APP) on the gene expression of proinflammatory cytokines, IL-1 beta and IL-6 was determined in cultured rat cortical glial cells in comparision to amyloid beta protein (A beta). Cells were incubated with 1 mu M of insoluble CT105 aggregates or aged A beta 1-40 peptide deposits which were mainly composed of stable monomeric and dimeric forms as assessed on Western blots. The levels of mRNAs were analyzed by reverse transcription polymerase chain reaction (RT-PCR). Highest levels of both IL-1 beta and IL-6 transcripts were detected in the culture exposed to CT105 aggregates for 4 days. CT105 aggregates markedly increased IL-1 beta mRNA level by 3.5 fold of the control level and this effect was more potent than that produced by aged A beta 1-40 peptides. Furthermore, CT105 strongly induced accumulation of IL-6 mRNA level by 2 fold of the value potentiated by A beta 1-40. Such induction was not observed with A beta 12-28 treatment. On the other hand, CT105 did not significantly alter either APP or glial fibrillary acidic protein (GFAP) mRNA levels. These results together imply that CT peptide besides its cytotoxic potency may act as a potent immunological component, strongly inducing both IL-1 beta and IL-6 mRNA levels in the cultured glial cells. This CT peptide associated exacerbation of cytokine expression may be in part responsible for chronic inflammation linked to slowly progressive neurodegeneration characteristic to AD. [References: 48]
机译：为了探索可能诱导阿尔茨海默氏病（AD）发病机理的细胞因子诱导相关因素，淀粉样蛋白前体蛋白（APP）的羧基末端105个氨基酸片段（CT105）对促炎性细胞因子基因表达的影响，在培养的大鼠皮质神经胶质细胞中与淀粉样β蛋白（A beta）相比，测定了IL-1β和IL-6。将细胞与1μM不溶性CT105聚集体或老化的A beta 1-40肽沉积物温育，这些沉积物主要由稳定的单体和二聚体形式组成，如Western blot所评估。通过逆转录聚合酶链反应（RT-PCR）分析mRNA的水平。在暴露于CT105聚集体4天的培养物中检测到最高水平的IL-1β和IL-6转录物。 CT105聚集体使IL-1βmRNA水平显着增加，为对照水平的3.5倍，并且这种作用比老化的A beta 1-40肽产生的作用更强。此外，CT105强烈诱导IL-6 mRNA水平的积累，是A beta 1-40增强值的2倍。用A beta 12-28处理未观察到这种诱导。另一方面，CT105并未显着改变APP或神经胶质纤维酸性蛋白（GFAP）mRNA的水平。这些结果共同暗示，CT肽除了具有细胞毒性作用外，还可以作为有效的免疫学成分，在培养的神经胶质细胞中强烈诱导IL-1β和IL-6 mRNA的水平。这种与细胞因子表达相关的CT肽加重可能部分归因于慢性炎症，而慢性炎症与AD的缓慢进行性神经变性有关。 [参考：48]

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