Full-length apolipoprotein E protects against the neurotoxicity of an apoE-related peptide.
Full-length apolipoprotein E protects against the neurotoxicity of an apoE-related peptide.
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全长载脂蛋白 E 可防止 apoE 相关肽的神经毒性。
DOI：
10.1016/j.brainres.2009.10.021
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发表时间：
2010
期刊：
影响因子：
2.9
通讯作者：
Narayanaswami,V
中科院分区：
文献类型：
--
作者：
Crutcher,KA;Lilley,HN;Anthony,SR;Zhou,W;Narayanaswami,V
载脂蛋白E被发现保护免受来自该蛋白的受体结合区（残基141-149）的二聚体肽的神经毒性作用。apoE 3和apoE 4都具有保护作用，但每个亚型的主要N-末端片段没有。牛血清白蛋白或apoA-I也没有提供显著的保护作用。全长apoE 3和apoE 4也抑制了肽的荧光标记衍生物的摄取，这表明抑制机制可能涉及对介导内吞作用和/或信号传导途径的细胞表面受体/蛋白聚糖的竞争。这些结果可能与apoE在神经元变性中的作用有关，例如发生在阿尔茨海默病中，其中apoE 4赋予显著更大的病理风险。
Apolipoprotein E was found to protect against the neurotoxic effects of a dimeric peptide derived from the receptor-binding region of this protein (residues 141–149). Both apoE3 and apoE4 conferred protection but the major N-terminal fragment of each isoform did not. Nor was significant protection provided by bovine serum albumin or apoA-I. Full-length apoE3 and apoE4 also inhibited the uptake of a fluorescent-labeled derivative of the peptide, suggesting that the mechanism of inhibition might involve competition for cell surface receptors/proteoglycans that mediate endocytosis and/or signaling pathways. These results might bear on the question of the role of apoE in neuronal degeneration, such as occurs in Alzheimer's disease where apoE4 confers a significantly greater risk of pathology.