Proteomic Shift in Mouse Embryonic Fibroblasts Pfa1 during Erastin, ML210, and BSO-Induced Ferroptosis

Olga M. Kudryashova, Alexey M. Nesterenko, Dmitry A. Korzhenevskii, Valeriy K. Sulyagin, Vasilisa M. Tereshchuk, Vsevolod V. Belousov and Arina G. Shokhina ()
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Olga M. Kudryashova: Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia
Alexey M. Nesterenko: Shemyakin-Ovchinnikov Institute of Bioorganic Chemistry, Russian Academy of Science, 117997 Moscow, Russia
Dmitry A. Korzhenevskii: Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia
Valeriy K. Sulyagin: Faculty of Biology, Lomonosov Moscow State University, 119234 Moscow, Russia
Vasilisa M. Tereshchuk: Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia
Vsevolod V. Belousov: Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia
Arina G. Shokhina: Neurotechnology Laboratory, Federal Center of Brain Research and Neurotechnologies, Federal Medical Biological Agency, 117997 Moscow, Russia

Data, 2023, vol. 8, issue 7, 1-7

Abstract: Ferroptosis is a unique variety of non-apoptotic cell death, driven by massive lipid oxidation in an iron-dependent manner. Since ferroptosis was introduced as a concept in 2012, it has demonstrated its essential role in the pathogenesis in neurodegenerative diseases and an important role in therapy-resistant cancer cells. Thus, detailed molecular understanding of both canonical and alternative ferroptosis pathways is required. There is a set of widely used chemical agents to modulate ferroptosis using different pathway targets: erastin blocks cystine–glutamate antiporter, system xc - ; ML210 directly inactivates GPX4; and L-buthionine sulfoximine (BSO) inhibits γ-glutamylcysteine synthetase, an essential enzyme for glutathione synthesis de novo. Most studies have focused on the lipidomic profiling of model systems undergoing death in a ferroptotic modality. In this study, we developed high-quality shotgun proteome sequencing during ferroptosis induction by three widely used chemical agents (erastin, ML210, and BSO) before and after 24 and 48 h of treatment. Chromato-mass spectra were registered in DDA mode and are suitable for further label-free quantification. Both processed and raw files are publicly available and could be a valuable dynamic proteome map for further ferroptosis investigation.

Keywords: ferroptosis; proteomics; LC-MS/MS; mouse embryonic fibroblasts; Pfa1; cell death; glutathione peroxidase 4; erastin; ML210; L-Buthionine-sulfoximine; BSO (search for similar items in EconPapers)
JEL-codes: C8 C80 C81 C82 C83 (search for similar items in EconPapers)
Date: 2023
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