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mice, cells, gpx, ferroptosis, cell, hspcs, vitamin, article, fig, lipid, hematopoietic, gpxfloxflox, cas, google, scholar, system, lthscs, ros, death, peroxidation, vavcre, data, deficiency, lsk, levels, results, vivo, nature, function, vitro, stem, supplementary, hscs, transplantation, hsc, significant, flow, homeostasis, biol, depletion, αtoc, mxcre, chimerism, cancer, diet, blood, gmps, china, essential, number,

Topics {✒️}

nature portfolio privacy policy gpx4flox/flox mx-cre mice gpx4flox/flox vav-cre mice advertising single-cell colony-forming assay nature 2019 nature 2017 nature gpx4flox/flox vav-cre social media reprints vivo haematopoietic-stem-cell expansion received gpx4-depleted hscs open project aif-mediated cell death produce single-cell colonies friedmann angeli jp n-acetyl-l-cysteine supplementary table 1 bd cytofix/cytoperm buffer bd perm/wash buffer lineage−sca1+c-kit+ 4 mx-cre mice mx-cre mice figure legend hematopoietic stem-cell transplantation generate single-cell colonies long-term rebuilding capacity original author gpx4flox/flox mice = 2 vav-cre mice vav-cre mice cd34−flt3−lsk cells permissions stem cell biology donor-derived hscs home acute renal injury vitamin e-depleted diet gpx4-deleted mice compared rsl3-treated lt-hscs fluorophore-conjugated antibodies purchased lt-hsc single cells rsl3-treated lsk cells cell stem cell full size image individual long-term hscs professor fudi wang programmed cell death gpx4−/− lt-hscs lost

Questions {❓}

• Does vitamin E prevent or promote cancer?
• What leads to the entirely different destiny of the Gpx4-deficient HSPCs in vivo and ex vivo?

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         description:Ferroptosis, a newly defined mode of regulated cell death caused by unbalanced lipid redox metabolism, is implicated in various tissue injuries and tumorigenesis. However, the role of ferroptosis in stem cells has not yet been investigated. Glutathione peroxidase 4 (GPX4) is a critical suppressor of lipid peroxidation and ferroptosis. Here, we study the function of GPX4 and ferroptosis in hematopoietic stem and progenitor cells (HSPCs) in mice with Gpx4 deficiency in the hematopoietic system. We find that Gpx4 deletion solely in the hematopoietic system has no significant effect on the number and function of HSPCs in mice. Notably, hematopoietic stem cells (HSCs) and hematopoietic progenitor cells lacking Gpx4 accumulated lipid peroxidation and underwent ferroptosis in vitro. α-Tocopherol, the main component of vitamin E, was shown to rescue the Gpx4-deficient HSPCs from ferroptosis in vitro. When Gpx4 knockout mice were fed a vitamin E-depleted diet, a reduced number of HSPCs and impaired function of HSCs were found. Furthermore, increased levels of lipid peroxidation and cell death indicated that HSPCs undergo ferroptosis. Collectively, we demonstrate that GPX4 and vitamin E cooperatively maintain lipid redox balance and prevent ferroptosis in HSPCs.
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      headline:GPX4 and vitamin E cooperatively protect hematopoietic stem and progenitor cells from lipid peroxidation and ferroptosis
      description:Ferroptosis, a newly defined mode of regulated cell death caused by unbalanced lipid redox metabolism, is implicated in various tissue injuries and tumorigenesis. However, the role of ferroptosis in stem cells has not yet been investigated. Glutathione peroxidase 4 (GPX4) is a critical suppressor of lipid peroxidation and ferroptosis. Here, we study the function of GPX4 and ferroptosis in hematopoietic stem and progenitor cells (HSPCs) in mice with Gpx4 deficiency in the hematopoietic system. We find that Gpx4 deletion solely in the hematopoietic system has no significant effect on the number and function of HSPCs in mice. Notably, hematopoietic stem cells (HSCs) and hematopoietic progenitor cells lacking Gpx4 accumulated lipid peroxidation and underwent ferroptosis in vitro. α-Tocopherol, the main component of vitamin E, was shown to rescue the Gpx4-deficient HSPCs from ferroptosis in vitro. When Gpx4 knockout mice were fed a vitamin E-depleted diet, a reduced number of HSPCs and impaired function of HSCs were found. Furthermore, increased levels of lipid peroxidation and cell death indicated that HSPCs undergo ferroptosis. Collectively, we demonstrate that GPX4 and vitamin E cooperatively maintain lipid redox balance and prevent ferroptosis in HSPCs.
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