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首页> 外文期刊>Disease Prevention Daily. >The Alzheimer's disease risk factor AP0E4 drives pro-inflammation in human astrocytes via HDAC-dependent repression of TAGLN3
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The Alzheimer's disease risk factor AP0E4 drives pro-inflammation in human astrocytes via HDAC-dependent repression of TAGLN3

机译：阿尔茨海默病的危险因素AP0E4驱动器在人类星形胶质细胞通过下HDAC-dependent镇压TAGLN3

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2021 MAY 03 (NewsRx) - By a News Reporter-Staff News Editor at Disease Prevention Daily - According to news reporting based on a preprint abstract, our journalists obtained the following quote sourced from biorxiv.org: "The Apolipoprotein E4 (AP0E4) is the major allelic risk factor for late-onset Alzheimer's disease (AD). AP0E4 associates with a pro-inflammatory phenotype increasingly considered as critical in AD initiation and progression. Yet, the mechanisms driving an APOE4-dependent neuroinflammation remain unelucidated. Leveraging patient specific human induced Pluripotent Stem Cells (iPSCs) we demonstrate inflammatory chronicity and hyperactivated responses upon cytokines in human AP0E4 astrocytes via a novel mechanism. "We uncovered that AP0E4 represses Transgelin 3 (TAGLN3), a new interacting partner of l{kappa}B, thus increasing the NF-{kappa}B activity. The transcriptional repression of TAGLN3 was shown to result from an APOE4-dependent histone deacetylase (HDAC) activity. The functional relevance of TAGLN3 was demonstrated by the attenuation of AP0E4-driven neuroinflammation after TAGLN3 supplementation. Importantly, TAGLN3 downregulation was confirmed in the brain of AD patients.
机译：2021年5月03 (NewsRx)——由一个新闻记者新闻编辑在日常——疾病预防根据新闻报道基于预印本抽象,我们记者获得以下引用来自biorxiv.org:“载脂蛋白E4 (AP0E4)是主要的等位基因晚发性阿尔茨海默病的危险因素(广告)。在表型越来越认为是至关重要的广告起始和进展。驾驶一个APOE4-dependent机制神经炎症仍然unelucidated。病人具体的人类诱导多能干细胞(万能)我们将演示炎性细胞慢性和hyperactivated响应细胞因子在人类AP0E4星形胶质细胞通过一个小说机制。Transgelin 3 (TAGLN3),一个新的互动伙伴l B {kappa},因此增加了NF - B {kappa}活动。TAGLN3被证明的结果APOE4-dependent组蛋白脱乙酰酶(HDAC)活动。证明了AP0E4-driven的衰减神经炎症后TAGLN3补充。重要的是,确认差别TAGLN3对这些在AD患者的大脑。

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