Department of Chemistry, Ben-Gurion University of the Negev, Beersheba, Israel.
Department of Chemistry, Ben-Gurion University of the Negev, Beersheba, Israel; Ilse Katz Institute for Nanoscale Science and Technology, Ben-Gurion University of the Negev, Beersheba, Israel.
Biophys J. 2020 Mar 24;118(6):1270-1278. doi: 10.1016/j.bpj.2020.01.018. Epub 2020 Jan 28.
Membrane interactions of amyloidogenic proteins constitute central determinants both in protein aggregation as well as in amyloid cytotoxicity. Most reported studies of amyloid peptide-membrane interactions have employed model membrane systems combined with application of spectroscopy methods or microscopy analysis of individual binding events. Here, we applied for the first time, to our knowledge, imaging flow cytometry for investigating interactions of representative amyloidogenic peptides, namely, the 106-126 fragment of prion protein (PrP(106-126)) and the human islet amyloid polypeptide (hIAPP), with giant lipid vesicles. Imaging flow cytometry was also applied to examine the inhibition of PrP(106-126)-membrane interactions by epigallocatechin gallate, a known modulator of amyloid peptide aggregation. We show that imaging flow cytometry provided comprehensive population-based statistical information upon morphology changes of the vesicles induced by PrP(106-126) and hIAPP. Specifically, the experiments reveal that both PrP(106-126) and hIAPP induced dramatic transformations of the vesicles, specifically disruption of the spherical shapes, reduction of vesicle circularity, lobe formation, and modulation of vesicle compactness. Interesting differences, however, were apparent between the impact of the two peptides upon the model membranes. The morphology analysis also showed that epigallocatechin gallate ameliorated vesicle disruption by PrP(106-126). Overall, this study demonstrates that imaging flow cytometry provides powerful means for disclosing population-based morphological membrane transformations induced by amyloidogenic peptides and their inhibition by aggregation modulators.
淀粉样蛋白原纤维形成蛋白的膜相互作用是蛋白质聚集以及淀粉样细胞毒性的核心决定因素。大多数报道的淀粉样肽-膜相互作用的研究都采用了模型膜系统,并结合光谱方法或单个结合事件的显微镜分析。在此,我们首次应用成像流式细胞术研究了代表性的淀粉样蛋白原纤维形成肽,即朊病毒蛋白(PrP(106-126))和人胰岛淀粉样多肽(hIAPP)与巨脂质体的相互作用。成像流式细胞术还用于研究表没食子儿茶素没食子酸酯(一种已知的淀粉样肽聚集调节剂)对 PrP(106-126)-膜相互作用的抑制作用。我们表明,成像流式细胞术提供了有关 PrP(106-126)和 hIAPP 诱导的囊泡形态变化的全面基于群体的统计信息。具体而言,实验表明,PrP(106-126)和 hIAPP 都引起了囊泡的剧烈转化,特别是破坏了球形,降低了囊泡的圆度,形成了叶状结构,并调节了囊泡的紧密度。然而,两种肽对模型膜的影响存在明显的差异。形态分析还表明,表没食子儿茶素没食子酸酯可改善 PrP(106-126)引起的囊泡破坏。总体而言,这项研究表明,成像流式细胞术为揭示淀粉样蛋白原纤维形成肽引起的基于群体的形态膜转化及其对聚集调节剂的抑制作用提供了强大的手段。