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脂质过氧化驱动液-液相分离并破坏生物膜中筏蛋白的分配。

Lipid peroxidation drives liquid-liquid phase separation and disrupts raft protein partitioning in biological membranes.

作者信息

Balakrishnan Muthuraj, Kenworthy Anne K

机构信息

Center for Membrane and Cell Physiology, University of Virginia, Charlottesville, VA USA.

Department of Molecular Physiology and Biological Physics, University of Virginia School of Medicine, Charlottesville, VA, USA.

出版信息

bioRxiv. 2023 Sep 14:2023.09.12.557355. doi: 10.1101/2023.09.12.557355.

Abstract

The peroxidation of membrane lipids by free radicals contributes to aging, numerous diseases, and ferroptosis, an iron-dependent form of cell death. Peroxidation changes the structure, conformation and physicochemical properties of lipids, leading to major membrane alterations including bilayer thinning, altered fluidity, and increased permeability. Whether and how lipid peroxidation impacts the lateral organization of proteins and lipids in biological membranes, however, remains poorly understood. Here, we employ cell-derived giant plasma membrane vesicles (GPMVs) as a model to investigate the impact of lipid peroxidation on ordered membrane domains, often termed membrane rafts. We show that lipid peroxidation induced by the Fenton reaction dramatically enhances phase separation propensity of GPMVs into co-existing liquid ordered (raft) and liquid disordered (non-raft) domains and increases the relative abundance of the disordered, non-raft phase. Peroxidation also leads to preferential accumulation of peroxidized lipids and 4-hydroxynonenal (4-HNE) adducts in the disordered phase, decreased lipid packing in both raft and non-raft domains, and translocation of multiple classes of proteins out of rafts. These findings indicate that peroxidation of plasma membrane lipids disturbs many aspects of membrane rafts, including their stability, abundance, packing, and protein and lipid composition. We propose that these disruptions contribute to the pathological consequences of lipid peroxidation during aging and disease, and thus serve as potential targets for therapeutic intervention.

摘要

自由基引发的膜脂过氧化作用与衰老、多种疾病以及铁死亡(一种铁依赖性细胞死亡形式)相关。过氧化作用改变了脂质的结构、构象和物理化学性质,导致细胞膜出现重大改变,包括双层变薄、流动性改变以及通透性增加。然而,脂质过氧化作用是否以及如何影响生物膜中蛋白质和脂质的侧向组织,目前仍知之甚少。在此,我们采用细胞衍生的巨型质膜囊泡(GPMVs)作为模型,研究脂质过氧化对有序膜结构域(通常称为膜筏)的影响。我们发现,芬顿反应诱导的脂质过氧化作用显著增强了GPMVs相分离为共存的液相有序(筏状)和液相无序(非筏状)结构域的倾向,并增加了无序非筏状相的相对丰度。过氧化作用还导致过氧化脂质和4-羟基壬烯醛(4-HNE)加合物在无序相中优先积累,筏状和非筏状结构域中的脂质堆积减少,以及多类蛋白质从筏状结构域中移位。这些发现表明,质膜脂质的过氧化作用扰乱了膜筏的许多方面,包括其稳定性、丰度、堆积以及蛋白质和脂质组成。我们认为,这些破坏作用导致了衰老和疾病过程中脂质过氧化的病理后果,因此可作为治疗干预的潜在靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5296/10515805/b6f059571bc6/nihpp-2023.09.12.557355v1-f0001.jpg

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