A receptor for phosphatidylserine-specific clearance of apoptotic cells

Fadok, Valerie A.; Bratton, Donna L.; Rose, David M.; Pearson, Adam J.; Ezekewitz, R. Alan B.; Henson, Peter M.

doi:10.1038/35011084

Cited by 1,364 publications

(1,116 citation statements)

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“…Eryptotic cells bind to phosphatidylserine receptors on macrophages [22], which engulf and degrade phosphatidylserine-exposing cells [8]. Accordingly, eryptotic cells are rapidly cleared from circulating blood [36], and stimulation of eryptosis leads to anemia, if the accelerated loss of circulating erythrocytes is not matched by a similarly increased formation of new erythrocytes.…”

Section: Discussionmentioning

confidence: 99%

Hemin-induced suicidal erythrocyte death

2009

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Several diseases, such as malaria, sickle cell disease, and ischemia/reperfusion may cause excessive formation of hemin, which may in turn trigger hemolysis. A variety of drugs and diseases leading to hemolysis triggers suicidal erythrocyte death or eryptosis, i.e., cell membrane scrambling and cell shrinkage. Eryptosis is elicited by increased cytosolic Ca 2+ activity and by ceramide. The present study explored whether hemin stimulates eryptosis. Cell membrane scrambling was estimated from annexin Vbinding to phosphatidylserine exposed at the cell surface, cell shrinkage from forward scatter in fluorescence-activated cell sorter analysis, cytosolic Ca 2+ activity from Fluo3 fluorescence and ceramide formation from fluorescencelabeled antibody binding. Exposure to hemin (1-10 μM) within 48 h significantly increased annexin V-binding, decreased forward scatter, increased cytosolic Ca 2+ activity, and stimulated ceramide formation. In conclusion, hemin stimulates suicidal cell death, which may in turn contribute to the clearance of circulating erythrocytes and thus to anemia.

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Section: Discussionmentioning

confidence: 99%

Hemin-induced suicidal erythrocyte death

2009

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“…Molecular mechanisms participating in the clearance of apoptotic cells by macrophages have been described in detail and, to a lesser extent, this can be said about non-professional phagocytes. 14,18,19,26,27 It has been suggested that autophagy as a mechanism of cell death may have been developed because in some forms of PCD the availability of engulfing cells is insufficient for the clearance of dead cells and autophagy has been evoked for elimination of excess cells by their own lysosomes. 13 In the present study we clearly demonstrate this is not the case: autophagic MCF-7 cells of different origin are recognized and eaten by both differentiated macrophages and non-dying MCF-7 cells.…”

Section: Discussionmentioning

confidence: 99%

Clearance of dying autophagic cells of different origin by professional and non-professional phagocytes

et al. 2007

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MCF-7 cells undergo autophagic death upon tamoxifen treatment. Plated on non-adhesive substratum these cells died by anoikis while inducing autophagy as revealed by monodansylcadaverine staining, elevated light-chain-3 expression and electron microscopy. Both de novo and anoikis-derived autophagic dying cells were engulfed by human macrophages and MCF-7 cells. Inhibition of autophagy by 3-methyladenine abolished engulfment of cells dying through de novo autophagy, but not those dying through anoikis. Blocking exposure of phosphatidylserine (PS) on both dying cell types inhibited phagocytosis by MCF-7 but not by macrophages. Gene expression profiling showed that though both types of phagocytes expressed full repertoire of the PS recognition and signaling pathway, macrophages could evolve during engulfment of de novo autophagic cells the potential of calreticulin-mediated processes as well. Our data suggest that cells dying through autophagy and those committing anoikis with autophagy may engage in overlapping but distinct sets of clearance mechanisms in professional and non-professional phagocytes.

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“…1). The protein was initially identified as the receptor of phosphatidylserine, a specific marker present at the surface of apoptotic cells, and is involved in apoptotic cell phagocytosis (Fadok et al, 2000). However, PTDSR is localized in the nucleus (Cikala et al, 2004;Cui et al, 2004).…”

Section: Ptdsrmentioning

confidence: 99%

Roles of jumonji and jumonji family genes in chromatin regulation and development

Takeuchi

Watanabe

Takano-Shimizu

et al. 2006

Developmental Dynamics

176

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The jumonji (jmj) gene was identified by a mouse gene trap approach and has essential roles in the development of multiple tissues. The Jmj protein has a DNA binding domain, ARID, and two conserved jmj domains (jmjN and jmjC). In many diverse species including bacteria, fungi, plants, and animals, there are many jumonji family proteins that have only the jmjC domain or both jmj domains. Recently, Jmj protein was found to be a transcriptional repressor. Several proteins in the jumonji family are involved in transcriptional repression and/or chromatin regulation. Most recently, one of the human members has been shown to be a histone demethylase, and the jmjC domain is essential for the demethylase activity. Meanwhile, more and more evidence indicating that the jumonji family proteins play important roles during development is accumulating. Many proteins in the jumonji family may regulate chromatin and gene expression, and control development through various signaling pathways. Here, we highlight the roles of jmj and jumonji family proteins in chromatin regulation and development. Developmental Dynamics 235: 2449 -2459, 2006.

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A receptor for phosphatidylserine-specific clearance of apoptotic cells

Cited by 1,364 publications

References 30 publications

Hemin-induced suicidal erythrocyte death

Hemin-induced suicidal erythrocyte death

Clearance of dying autophagic cells of different origin by professional and non-professional phagocytes

Roles of jumonji and jumonji family genes in chromatin regulation and development

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