Programmed cell death in mature erythrocytes: a model for investigating death effector pathways operating in the absence of mitochondria
| Autor: | Alonso C, Jean-Claude Ameisen, Daniela Bratosin, Jean-Pierre Tissier, Jérôme Estaquier, Quatannens B, Frédéric Petit, Slomianny C, Sartiaux C, Damien Arnoult, Jean Montreuil, J.-J. Huart |
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| Přispěvatelé: | Laboratoire de Génie des Procédés et Technologie Alimentaires (LGPTA), Institut National de la Recherche Agronomique (INRA), ProdInra, Migration |
| Jazyk: | angličtina |
| Rok vydání: | 2001 |
| Předmět: |
Programmed cell death
Death Domain Receptor Signaling Adaptor Proteins Erythrocytes [SPI.GPROC] Engineering Sciences [physics]/Chemical and Process Engineering Leupeptins [SDV]Life Sciences [q-bio] Cell Caspase 3 Apoptosis Models Biological Mice Phospholipid scrambling [SDV.IDA]Life Sciences [q-bio]/Food engineering medicine Macrophage Animals Humans [SPI.GPROC]Engineering Sciences [physics]/Chemical and Process Engineering Molecular Biology Caspase biology Intracellular Signaling Peptides and Proteins Cell Biology [SDV.IDA] Life Sciences [q-bio]/Food engineering Macrophage Activation Cell biology Mitochondria [SDV] Life Sciences [q-bio] DNA-Binding Proteins Cysteine Endopeptidases medicine.anatomical_structure Caspases biology.protein Calcium Apoptosome Oligopeptides |
| Zdroj: | Cell Death and Differentiation Cell Death and Differentiation, Nature Publishing Group, 2001, 8, pp.1143-1156 HAL |
| ISSN: | 1350-9047 1476-5403 |
| Popis: | Human mature erythrocytes have been considered as unable to undergo programmed cell death (PCD), due to their lack of mitochondria, nucleus and other organelles, and to the finding that they survive two conditions that induce PCD in vitro in all human nucleated cells, treatment with staurosporine and serum deprivation. Here we report that mature erythrocytes can undergo a rapid self-destruction process sharing several features with apoptosis, including cell shrinkage, plasma membrane microvesiculation, phosphatidylserine externalization, and leading to erythrocyte disintegration, or, in the presence of macrophages, to macrophage ingestion of dying erythrocytes. This regulated form of PCD was induced by Ca2+ influx, and prevented by cysteine protease inhibitors that allowed erythrocyte survival in vitro and in vivo. The cysteine proteinases involved seem not to be caspases, since (i) proforms of caspase 3, while present in erythrocytes, were not activated during erythrocyte death; (ii) cytochrome c, a critical component of the apoptosome, was lacking; and (iii) cell-free assays did not detect activated effectors of nuclear apoptosis in dying erythrocytes. Our findings provide the first identification that a death program can operate in the absence of mitochondria. They indicate that mature erythrocytes share with all other mammalian cell types the capacity to self-destruct in response to environmental signals, and imply that erythrocyte survival may be modulated by therapeutic intervention. Cell Death and Differentiation (2001) 8, 1143–1156 |
| Databáze: | OpenAIRE |
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