We are analyzing https://link.springer.com/article/10.1186/s12964-019-0437-0.

Title:
Flipping the dogma – phosphatidylserine in non-apoptotic cell death | Cell Communication and Signaling
Description:
Abstract The exposure of phosphatidylserine (PS) on the outer plasma membrane has long been considered a unique feature of apoptotic cells. Together with other “eat me” signals, it enables the recognition and phagocytosis of dying cells (efferocytosis), helping to explain the immunologically-silent nature of apoptosis. Recently, however, PS exposure has also been reported in non-apoptotic forms of regulated inflammatory cell death, such as necroptosis, challenging previous dogma. In this review, we outline the evidence for PS exposure in non-apoptotic cells and extracellular vesicles (EVs), and discuss possible mechanisms based on our knowledge of apoptotic-PS exposure. In addition, we examine the outcomes of non-apoptotic PS exposure, including the reversibility of cell death, efferocytosis, and consequent inflammation. By examining PS biology, we challenge the established approach of distinguishing apoptosis from other cell death pathways by AnnexinV staining of PS externalization. Finally, we re-evaluate how PS exposure is thought to define apoptosis as an immunologically silent process distinct from other non-apoptotic and inflammatory cell death pathways. Ultimately, we suggest that a complete understanding of how regulated cell death processes affect the immune system is far from being fully elucidated. Graphical abstract
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Keywords {🔍}

cell, pubmed, cells, google, scholar, article, cas, death, necroptosis, apoptosis, exposure, apoptotic, necroptotic, ripk, membrane, central, mlkl, necrosis, inflammation, phosphatidylserine, phagocytosis, activation, nonapoptotic, protein, plasma, biol, nat, caspase, tmemf, signaling, kinase, molecular, psexposing, sci, macrophages, addition, immune, mechanism, activity, role, necrotic, immunol, induce, intracellular, reported, disease, cellular, release, bodies, complex,

Topics {✒️}

ripk1/caspase-8/fadd/c-flip cytosolic complex receptor-interacting kinase-3-mediated pathway anti-apoptotic b-cell lymphoma-2 antigen-specific ifn-γ production rip1-rip3-drp1 signaling pathway tnf-related apoptosis-inducing ligand bone marrow-derived macrophages mort1/fadd-interacting protease article download pdf anti-fas-treated jurkat cells inflammasome−/gasdermin-d-dependent rcd fadd-homologous ice/ced-3 retinoic acid-inducible gene escrt-iii acts downstream endotoxin-induced serum factor significantly elevated tnf-α epstein-barr virus apaf-1/caspase-9 complex initiates cycloheximide-treated u937 cells atp-dependent aminophospholipid translocases escrt membrane-scission machinery cancer search search releasing pro-apoptotic bax damaged ps-exposing membrane xk-related protein 8 ps-exposing necroptotic cells death receptor-induced apoptotic fluorescence-activated cell sorting ca2+-triggered escrt assembly ps-exposing necroptotic bodies tim4-deficient macrophages failed death-inducing signaling complex anti-cancer therapy rip3-mediated macrophage necrosis adaptor-inducing interferon- β mlkl-mediated ca2+ influx calcium-dependent phospholipid scrambling prevents necroptotic-ps exposure regulates endosomal trafficking mycobacterium tuberculosis-infected macrophages il-1β-converting enzyme facilitates phagosome maturation mlkl-dependent ca2+ influx kaiser wj ps-exposing bodies released ripk1-independent necroptotic pathway caspase-dependent phospholipid scramblase intracellular ca2+-dependent manner ps-exposing vesicles pore-forming executer

Questions {❓}

Commitment issues – are PS-exposing necroptotic cells committed to die?
Protease activation during apoptosis: death by a thousand cuts?
What is ‘inflammation’?

Schema {🗺️}

WebPage:
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         headline:Flipping the dogma – phosphatidylserine in non-apoptotic cell death
         description:The exposure of phosphatidylserine (PS) on the outer plasma membrane has long been considered a unique feature of apoptotic cells. Together with other “eat me” signals, it enables the recognition and phagocytosis of dying cells (efferocytosis), helping to explain the immunologically-silent nature of apoptosis. Recently, however, PS exposure has also been reported in non-apoptotic forms of regulated inflammatory cell death, such as necroptosis, challenging previous dogma. In this review, we outline the evidence for PS exposure in non-apoptotic cells and extracellular vesicles (EVs), and discuss possible mechanisms based on our knowledge of apoptotic-PS exposure. In addition, we examine the outcomes of non-apoptotic PS exposure, including the reversibility of cell death, efferocytosis, and consequent inflammation. By examining PS biology, we challenge the established approach of distinguishing apoptosis from other cell death pathways by AnnexinV staining of PS externalization. Finally, we re-evaluate how PS exposure is thought to define apoptosis as an immunologically silent process distinct from other non-apoptotic and inflammatory cell death pathways. Ultimately, we suggest that a complete understanding of how regulated cell death processes affect the immune system is far from being fully elucidated.
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      headline:Flipping the dogma – phosphatidylserine in non-apoptotic cell death
      description:The exposure of phosphatidylserine (PS) on the outer plasma membrane has long been considered a unique feature of apoptotic cells. Together with other “eat me” signals, it enables the recognition and phagocytosis of dying cells (efferocytosis), helping to explain the immunologically-silent nature of apoptosis. Recently, however, PS exposure has also been reported in non-apoptotic forms of regulated inflammatory cell death, such as necroptosis, challenging previous dogma. In this review, we outline the evidence for PS exposure in non-apoptotic cells and extracellular vesicles (EVs), and discuss possible mechanisms based on our knowledge of apoptotic-PS exposure. In addition, we examine the outcomes of non-apoptotic PS exposure, including the reversibility of cell death, efferocytosis, and consequent inflammation. By examining PS biology, we challenge the established approach of distinguishing apoptosis from other cell death pathways by AnnexinV staining of PS externalization. Finally, we re-evaluate how PS exposure is thought to define apoptosis as an immunologically silent process distinct from other non-apoptotic and inflammatory cell death pathways. Ultimately, we suggest that a complete understanding of how regulated cell death processes affect the immune system is far from being fully elucidated.
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         Protein-Ligand Interactions
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               name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
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      name:Department of Molecular and Translational Science, Monash University, Clayton, Australia
      name:Department of Clinical Microbiology and Immunology, Sackler Faculty of Medicine, Tel Aviv University, Tel Aviv, Israel

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