Small Liposomes Accelerate the Fibrillation of Amyloid β (1-40)
Small Liposomes Accelerate the Fibrillation of Amyloid β (1-40)
复制标题
DOI：
10.1074/jbc.m114.592527
复制
发表时间：
2015-01-09
影响因子：
4.8
通讯作者：
Goto, Yuji
中科院分区：
文献类型：
--
作者：
Terakawa, Mayu S.;Yagi, Hisashi;Goto, Yuji
淀粉样蛋白β（A β）肽的沉积是阿尔茨海默病的病理标志。以前认为β肽与含有神经节苷脂的膜特异性相互作用。几项研究表明，A β肽也与磷脂酰胆碱膜结合，导致膜变形和A β纤维化。此外，膜曲率（蛋白质与膜结合产生的一种变形）在A β结合和纤维化中的作用仍不清楚。为了清楚地理解A β的结合、随之发生的膜变形和原纤化之间的关系，我们检查了在各种大小的脂质体存在下A β-（1-40）的淀粉样蛋白原纤化。膜曲率随着脂质体尺寸的减小而增加。我们使用由1，2-二油酰-sn-甘油-3-磷酸胆碱制成的脂质体来消除静电效应。结果表明，较小粒径的脂质体（
The deposition of amyloid beta (A beta) peptides is a pathological hallmark of Alzheimer disease. A beta peptides were previously considered to interact specifically with ganglioside-containing membranes. Several studies have suggested that A beta peptides also bind to phosphatidylcholine membranes, which lead to deformation of membranes and fibrillation of A beta. Moreover, the role of membrane curvature, one type of deformation produced by binding of proteins to a membrane, in the binding and fibrillation of A beta remains unclear. To clearly understand the relationship between the binding, consequent membrane deformation, and fibrillation of A beta, we examined the amyloid fibrillation of A beta-(1-40) in the presence of liposomes of various sizes. Membrane curvature increased with a decrease in the size of the liposomes. We used liposomes made of 1,2-dioleoyl-sn-glycero-3-phosphocholine to eliminate electrostatic effects. The results obtained showed that liposomes of smaller sizes (