Taipei Medical University Institutional Repository:Item 987654321/3794
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    题名: The epigenetic effects of amyloid-beta(1-40) on global DNA and neprilysin genes in murine cerebral endothelial cells
    作者: 楊沂淵
    Chen KL;Wang SS;Yang YY;Yuan RY;Chen RM;Hu CJ
    贡献者: 醫學檢驗暨生物技術學系
    日期: 2008
    上传时间: 2009-08-25 10:39:05 (UTC+8)
    摘要: Amyloid-b (Ab) is the core component of senile plaques, which are the pathological markers for Alzheimer’s
    disease and cerebral amyloid angiopathy. DNA methylation/demethylation plays a crucial role in
    gene regulation and could also be responsible for presentation of senescence. Oxidative stress, which
    may be induced by Ab, is thought to be an important contributor of DNA hyper-methylation; however,
    contradicting this is the fact that global DNA hypo-methylation has been found in aging brains. It therefore
    remains largely unknown as to whether Ab does in fact cause DNA methylation/demethylation.
    Neprilysin (NEP) is one of the enzymes responsible for Ab degradation, with its expression decreasing
    in both Alzheimer and aging brains. Using high-performance liquid chromatography (HPLC), we explore
    whether Ab is responsible for alteration of the global DNA methylation status on a murine cerebral endothelial
    cells model, and also use methylation-specific PCR (MSPCR) to examine whether DNA methylation
    status is altered on the NEP promoter region. We find that Ab reduces global DNA methylation whilst
    increasing NEP DNA methylation and further suppressing the NEP expression in mRNA and protein levels.
    Our results support that Ab induces epigenetic effects, implying that DNA methylation may be part of a
    vicious cycle involving the reduction in NEP expression along with a resultant increase in Ab accumulation,
    and that Ab may induce global DNA hypo-methylation.
    關聯: Biochem Biophys Res Commun.
    数据类型: article
    显示于类别:[醫學檢驗暨生物技術學系所] 期刊論文

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