首页> 美国卫生研究院文献>Journal of Cerebral Blood Flow Metabolism >O-linked β-N-acetylglucosamine modification of proteins is activated in post-ischemic brains of young but not aged mice: Implications for impaired functional recovery from ischemic stress
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O-linked β-N-acetylglucosamine modification of proteins is activated in post-ischemic brains of young but not aged mice: Implications for impaired functional recovery from ischemic stress

机译:O联结的β-N-乙酰氨基葡糖对蛋白质的修饰在年轻但未衰老的小鼠的缺血后脑中被激活:从缺血性应激中恢复功能受损的意义

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摘要

To evaluate the effect of age on the response of brains to an ischemic challenge, we subjected young and aged mice to transient forebrain ischemia, and analyzed the heat shock response and unfolded protein response, ubiquitin conjugation and SUMO conjugation, and O-linked β-N-acetylglucosamine modification of proteins (O-GlcNAcylation). The most prominent age-related difference was an inability of aged mice to activate O-GlcNAcylation. Considering many reports on the protective role of O-GlcNAcylation in various stress conditions including myocardial ischemia, this pathway could be a promising target for therapeutic intervention to improve functional recovery of aged patients following brain ischemia.
机译:为了评估年龄对大脑对缺血性挑战的反应的影响,我们对年轻和成年小鼠进行了短暂性前脑缺血,并分析了热休克反应和未折叠蛋白反应,泛素结合和SUMO结合以及O-联β-蛋白质的N-乙酰氨基葡萄糖修饰(O-GlcNAcylation)。与年龄有关的最显着差异是衰老小鼠无法激活O-GlcNAcylation。考虑到许多关于O-GlcNAcylation在包括心肌缺血在内的各种应激条件下的保护作用的报道,该途径可能成为治疗干预以改善老年患者脑缺血后功能恢复的有希望的靶标。

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