Nesterenko Alexey M, Korzhenevskii Dmitry A, Tereshchuk Vasilisa M, Kudryashova Olga M, Belousov Vsevolod V, Shokhina Arina G
Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, Moscow 117997, Russia.
Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Science, Moscow 117997, Russia.
Data Brief. 2023 Apr 20;48:109170. doi: 10.1016/j.dib.2023.109170. eCollection 2023 Jun.
Ferroptosis is a type of programmed cell death distinct from apoptosis and necroptosis that plays an essential role in pathophysiological conditions such as neurodegenerative diseases and tumorigenesis. Massive lipid oxidation in an iron-dependent manner is a hallmark of ferroptosis.This modality of cell death is also characterized by perturbation of several metabolic pathways, predominantly fatty acid metabolism, thiol metabolism, iron homeostasis and the mevalonate pathway. We aimed to acquire data from different timepoints of ferroptotic death in order to get information about the primary and delayed phases of the ferroptotic response. For this purpose, we used model Pfa1 cells, which are 4-OH-TAM-inducible mouse immortalized fibroblasts [1]. GPX4 is one of the main intracellular ferroptosis regulators and inhibiting it is a classic approach to induce ferroptosis. Measuring protein fold changes at different ferroptotic stages and in nontreated Pfa1 cells could give useful information on the activation of genes involved in ferroptosis and non-genomic protein regulation during ferroptotic progression. Bottom-up proteomic data were acquired from samples obtained 24 and 48 hours after genetic induction of ferroptosis. Chromato-mass spectra were registered in DDA mode and are suitable for further label-free quantification. These data might be a valuable proteome basis for further investigation of ferroptosis and complement other available omics.
铁死亡是一种不同于凋亡和坏死性凋亡的程序性细胞死亡类型，在神经退行性疾病和肿瘤发生等病理生理状况中起重要作用。以铁依赖方式进行的大量脂质氧化是铁死亡的一个标志。这种细胞死亡方式还具有若干代谢途径紊乱的特征，主要是脂肪酸代谢、硫醇代谢、铁稳态和甲羟戊酸途径。我们旨在从铁死亡的不同时间点获取数据，以便了解铁死亡反应的早期和延迟阶段的信息。为此，我们使用了Pfa1细胞模型，它是4-羟基他莫昔芬诱导的小鼠永生化成纤维细胞[1]。谷胱甘肽过氧化物酶4（GPX4）是主要的细胞内铁死亡调节因子之一，抑制它是诱导铁死亡的经典方法。测量不同铁死亡阶段以及未处理的Pfa1细胞中的蛋白质折叠变化，可以提供有关铁死亡过程中涉及的基因激活以及非基因组蛋白质调节的有用信息。自下而上的蛋白质组学数据是从铁死亡基因诱导后24小时和48小时获得的样本中获取的。色谱质谱以数据依赖采集（DDA）模式记录，适用于进一步的无标记定量分析。这些数据可能是进一步研究铁死亡的有价值的蛋白质组基础，并可补充其他可用的组学数据。
