Retinoic Acid Induced Suicidal Erythrocyte Death

Abed, Majed; Herrmann, Tabea; Alzoubi, Kousi; Pakladok, Tatsiana; Läng, Florian

doi:10.1159/000113761

Cited by 66 publications

(19 citation statements)

References 107 publications

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“…Some of these diseases may cause eryptosis by stimulating the formation of hemin. Furthermore, several eryptosis-triggering xenobiotics and endogeneous substances have been identified, such as cordycepin [50], methylglyoxal [54], amyloid peptides [53], lipopetides [71] retinoic acid [55], paclitaxel [44], amantadine [23], chlorpromazine [1], ciglitazone [58], cyclosporine [56], Bay-5884 [65], curcumin [4], valinomycin [64], listeriolysin [25], aluminum [57], copper [46], bismuth [13], tin [52], cadmium [68], selenium [67], vanadate [27], gold [69], and arsenic [51]. At least in theory, some of those substances may be effective through stimulation of hemin formation.…”

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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“…Eryptosis may further be stimulated by ceramide (acylsphingosine) [76], prostaglandin E 2 [64], platelet activating factor [92], anti-A IgG antibodies [93], hemolysin from Vibrio parahaemolyticus [94], listeriolysin [95], paclitaxel [96], amantadine [97], azathioprine [98], amiodarone [99], retinoic acid [100], ciglitazone [101], chlorpromazine [58], peptidoglycan [102], cyclosporine [60], methylglyoxal [59], amyloid peptides [103], anandamide [104], Bay-Y5884 [105], curcumin [106], arsenic [107], methyldopa [108], valinomycin [109], aluminium [110], mercury [111], lead [112], gold [113], selenium [114], vanadium [115], cadmium [116], tin [117], and copper [118].…”

Section: Suicidal Erythrocyte Deathmentioning

confidence: 99%

Suicide for Survival - Death of Infected Erythrocytes as a Host Mechanism to Survive Malaria

Föller

Bobbala²,

Koka³

et al. 2009

Cell Physiol Biochem

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The pathogen of malaria, Plasmodium, enters erythrocytes and thus escapes recognition by the immune system. The pathogen induces oxidative stress to the host erythrocyte, which triggers eryptosis, the suicidal death of erythrocytes. Eryptosis is characterized by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling with phosphatidylserine exposure at the cell surface. Phosphatidylserine-exposing erythrocytes are identified by macrophages which engulf and degrade the eryptotic cells. To the extent that infected erythrocytes undergo eryptosis prior to exit of Plasmodiaand subsequent infection of other erythrocytes, the premature eryptosis may protect against malaria. Accordingly, any therapeutical intervention accelerating suicidal death of infected erythrocytes has the potential to foster elimination of infected erythrocytes, delay the development of parasitemia and favorably influence the course of malaria. Eryptosis is stimulated by a wide variety of triggers including osmotic shock, oxidative stress, energy depletion and a wide variety of xenobiotics. Diseases associated with accelerated eryptosis include sepsis, haemolytic uremic syndrome, malaria, sickle-cell anemia, beta-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, phosphate depletion, iron deficiency and Wilson’s disease. Among the known stimulators of eryptosis, paclitaxel, chlorpromazine, cyclosporine, curcumin, PGE₂ and lead have indeed been shown to favourably influence the course of malaria. Moreover, sickle-cell trait, beta-thalassemia trait, glucose-6-phosphate dehydrogenase (G6PD)-deficiency and iron deficiency confer some protection against a severe course of malaria. Importantly, counteracting Plasmodia by inducing eryptosis is not expected to generate resistance of the pathogen, as the proteins involved in suicidal death of the host cell are not encoded by the pathogen and thus cannot be modified by mutations of its genes.

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“…Phosphatidylserine exposure in erythrocytes could further be elicited by ligation of specific surface antigens, such as glycophorin-C [14], of CD47, 382 the critical RBC antigenic marker that exhibits an inhibitory role in macrophage activation [15], and of the death receptor CD95/Fas [16]. Moreover, eryptosis is triggered by paclitaxel [17], amantadine [18], azathioprine [19], retinoic acid [20], chlorpromazine [21], cyclosporine [22], methylglyoxal [23], amyloid peptides [24], anandamide [25], Bay-Y5884 [26] and curcumin [27]. Mechanisms underlying eryptosis may not only affect circulating erythrocytes but may contribute to the limitation of erythrocytes during storage [28][29][30].…”

Section: Introductionmentioning

confidence: 99%

Lipopeptides in the Triggering of Erythrocyte Cell Membrane Scrambling

Wang

Mahmud²,

Föller³

et al. 2008

Cell Physiol Biochem

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Sepsis is paralleled by anemia, an effect partially resulting from eryptosis, the suicidal death of erythrocytes. Eryptosis is characterized by cell membrane scrambling with phosphatidylserine exposure at the erythrocyte surface. Pathogen-induced eryptosis may partially result from interaction of bacterial cell wall components such as lipoproteins with the erythrocyte cell membrane. The present study explored, whether the synthetic lipopeptide Pam3CSK4 mimicking the acylated amino terminus of bacterial lipoproteins triggers eryptosis. According to annexin-V-binding in FACS analysis, Pam3CSK4 (1 µg/ml) stimulated phosphatidylserine exposure, an effect significantly blunted in the nominal absence of Ca 2+ . According to Fluo3 fluorescence, Pam3CSK4 increased cytosolic Ca 2+ activity and moderately stimulated erythrocytic ceramide formation, both major triggers of eryptosis. In conclusion, bacterial lipoproteins participate in the stimulation of erythrocyte cell membrane scrambling by bacterial cell wall components. Thus, lipoproteindependent suicidal erythrocyte death may contribute to the pleotropic effects of sepsis.

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Retinoic Acid Induced Suicidal Erythrocyte Death

Cited by 66 publications

References 107 publications

Hemin-induced suicidal erythrocyte death

Hemin-induced suicidal erythrocyte death

Suicide for Survival - Death of Infected Erythrocytes as a Host Mechanism to Survive Malaria

Lipopeptides in the Triggering of Erythrocyte Cell Membrane Scrambling

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