Departments of Biophysics and Chemistry, University of Michigan, Ann Arbor, Michigan 48109-1055, United States.
Biochemistry. 2012 Oct 2;51(39):7676-84. doi: 10.1021/bi3009888. Epub 2012 Sep 21.
The toxicity of amyloid-forming peptides has been hypothesized to reside in the ability of protein oligomers to interact with and disrupt the cell membrane. Much of the evidence for this hypothesis comes from in vitro experiments using model membranes. However, the accuracy of this approach depends on the ability of the model membrane to accurately mimic the cell membrane. The effect of membrane composition has been overlooked in many studies of amyloid toxicity in model systems. By combining measurements of membrane binding, membrane permeabilization, and fiber formation, we show that lipids with the phosphatidylethanolamine (PE) headgroup strongly modulate the membrane disruption induced by IAPP (islet amyloid polypeptide protein), an amyloidogenic protein involved in type II diabetes. Our results suggest that PE lipids hamper the interaction of prefibrillar IAPP with membranes but enhance the membrane disruption correlated with the growth of fibers on the membrane surface via a detergent-like mechanism. These findings provide insights into the mechanism of membrane disruption induced by IAPP, suggesting a possible role of PE and other amyloids involved in other pathologies.
淀粉样肽的毒性作用被认为在于其寡聚体与细胞膜相互作用并破坏细胞膜的能力。这一假说的大部分证据来自于使用模型膜的体外实验。然而,这种方法的准确性取决于模型膜准确模拟细胞膜的能力。在模型系统中研究淀粉样毒性时,许多研究都忽略了膜组成的影响。通过结合膜结合、膜通透性和纤维形成的测量,我们表明带磷酸乙醇胺(PE)头基的脂质强烈调节淀粉样多肽(IAPP)诱导的膜破坏,IAPP 是一种与 II 型糖尿病有关的淀粉样蛋白。我们的结果表明,PE 脂质阻碍了前纤维状 IAPP 与膜的相互作用,但通过去污剂样机制增强了与纤维在膜表面生长相关的膜破坏。这些发现为 IAPP 诱导的膜破坏机制提供了新的见解,提示了 PE 和其他与其他病理学相关的淀粉样蛋白可能的作用。