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Topics {✒️}

radiation-induced lung fibrosis subsequent lc–ms/ms analysis system xc−/gpx4 axis light-chain subunit xct heavy-chain subunit cd98 xc−/gpx4 axis resulting negative-sense rna virus retinoic acid-inducible gene article  google scholar quantitative real-time pcr lc–ms/ms analysis higher-energy collision dissociation sds–polyacrylamide gel electrophoresis reactive oxygen species iron-dependent cell death siv-induced cell death virus-induced autophagy contributes gssg/gsh quantification kit lc–ms/ms proteomic iron-dependent lipid peroxidation avian influenza virus iav-induced cell death article download pdf siv-induced cytokine expression nadp+/nadph assay kit transferrin-mediated iron transport enhance virus replication siv-induced ros generation system xc− pathways siv infection triggers siv-induced ferroptosis depends excellent research team alveolar epithelial cells itraq-labeled peptide mixtures cell death induced ncoa4-mediated autophagy pathway lipid peroxidation products lc–ms/ms privacy choices/manage cookies intercellular iron disorder regulated cell death proteomics data normalization ms/ms analysis iron assay kit western blot analysis huili liu veterinary research institute excessive iron uptake pathway enrichment analysis intracellular iron uptake

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         headline:Swine influenza virus triggers ferroptosis in A549 cells to enhance virus replication
         description:Recently, Influenza A virus (IAV) has been shown to activate several programmed cell death pathways that play essential roles in host defense. Indeed, cell death caused by viral infection may be mediated by a mixed pattern of cell death instead of a certain single mode. Ferroptosis is a novel form of regulated cell death (RCD) that is mainly mediated by iron-dependent lipid peroxidation. Based on the proteomic data, we wondered whether IAV causes ferroptosis in host cells. In this study, a quantitative proteomics approach based on an iTRAQ combined with LC–MS/MS was used to profile proteins expressed in A549 cells infected with H1N1 swine influenza virus (SIV). Meanwhile, we measured the intracellular iron content, reactive oxygen species (ROS) release and lipid peroxidation in response to SIV infection. Finally, a drug experiment was conducted to investigate the effects of ferroptosis on modulating SIV survival. The bioinformatics analysis revealed several proteins closely relevant to iron homeostasis and transport, and the ferroptosis signaling pathway are highly enriched in response to SIV infection. In our experiment, aberrant expression of iron-binding proteins disrupted labile iron uptake and storage after SIV infection. Meanwhile, SIV infection inhibited system the Xc−/GPX4 axis resulting in GSH depletion and the accumulation of lipid peroxidation products. Notably, cell death caused by SIV as a result of iron-dependent lipid peroxidation can be partially rescued by ferroptosis inhibitor. Additionally, blockade of the ferroptotic pathway by ferrostatin-1 (Fer-1) treatment decreased viral titers and inflammatory response. This study revealed a new mode of cell death induced by IAV infection, and our findings might improve the understanding of the underlying mechanism involved in the interaction of virus and host cells.
         datePublished:2022-06-17T00:00:00Z
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            Ferroptosis
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      headline:Swine influenza virus triggers ferroptosis in A549 cells to enhance virus replication
      description:Recently, Influenza A virus (IAV) has been shown to activate several programmed cell death pathways that play essential roles in host defense. Indeed, cell death caused by viral infection may be mediated by a mixed pattern of cell death instead of a certain single mode. Ferroptosis is a novel form of regulated cell death (RCD) that is mainly mediated by iron-dependent lipid peroxidation. Based on the proteomic data, we wondered whether IAV causes ferroptosis in host cells. In this study, a quantitative proteomics approach based on an iTRAQ combined with LC–MS/MS was used to profile proteins expressed in A549 cells infected with H1N1 swine influenza virus (SIV). Meanwhile, we measured the intracellular iron content, reactive oxygen species (ROS) release and lipid peroxidation in response to SIV infection. Finally, a drug experiment was conducted to investigate the effects of ferroptosis on modulating SIV survival. The bioinformatics analysis revealed several proteins closely relevant to iron homeostasis and transport, and the ferroptosis signaling pathway are highly enriched in response to SIV infection. In our experiment, aberrant expression of iron-binding proteins disrupted labile iron uptake and storage after SIV infection. Meanwhile, SIV infection inhibited system the Xc−/GPX4 axis resulting in GSH depletion and the accumulation of lipid peroxidation products. Notably, cell death caused by SIV as a result of iron-dependent lipid peroxidation can be partially rescued by ferroptosis inhibitor. Additionally, blockade of the ferroptotic pathway by ferrostatin-1 (Fer-1) treatment decreased viral titers and inflammatory response. This study revealed a new mode of cell death induced by IAV infection, and our findings might improve the understanding of the underlying mechanism involved in the interaction of virus and host cells.
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         Proteomics analysis
         Ferroptosis
         Iron disorder
         Virology
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      name:Shanghai Key Laboratory of Agricultural Genetic Breeding, Shanghai, People’s Republic of China
      name:Shanghai Engineering Research Center of Pig Breeding, Shanghai, People’s Republic of China

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