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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Research Article

L1CAM可有效抑制阿尔茨海默病条件下组蛋白去乙酰化酶2的表达

卷 17, 期 4, 2020

页: [382 - 392] 页: 11

弟呕挨: 10.2174/1567205017666200422155323

价格: $65

摘要

背景:组蛋白去乙酰化酶2 (HDAC2)介导的表观遗传阻滞会损害阿尔茨海默病(AD)患者的认知能力，该阻滞会阻止对突触可塑性至关重要的基因的转录。目的:探讨细胞粘附分子L1与HDAC2在AD中的功能关系。 方法:文化分离皮层和海马神经元从野生型或L1-deficient老鼠对待Aβ1-42 24 h。Aβ1-42细胞治疗后的重组L1细胞外域(rL1) 24小时其次是免疫组织化学、免疫印迹和逆转录PCR评估L1和HDAC2之间的交互。 结果:与APPSWE突变脑相比，APPSWE/L1+/-突变脑中A蛋白和HDAC2蛋白水平升高。将L1重组细胞外结构域应用于培养的皮质和海马神经元可降低HDAC2 mRNA和蛋白水平。同时，糖皮质激素受体1 (GR1)磷酸化水平降低，参与调节HDAC2水平，观察到L1的响应。糖皮质激素受体抑制剂的应用减少了酪氨酸诱导的GR1磷酸化，并阻止了HDAC2水平的升高。在l1缺失小鼠培养的皮质神经元中，HDAC2蛋白水平升高。这种变化可以通过L1的重组细胞外结构域来逆转。 结论:我们的研究结果表明，L1和HDAC2在功能上相互依赖，GR1去磷酸化导致HDAC2表达降低，从而改善AD的表型。这些联合发现鼓励进一步研究L1在治疗AD中的有益作用。

关键词: 阿尔兹海默症

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