Vanadate-Induced Suicidal Erythrocyte Death

Föller, Michael; Sopjani, Mentor; Mahmud, Hasan; Läng, Florian

doi:10.1159/000119704

Cited by 56 publications

(34 citation statements)

References 98 publications

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“…Further substances reported to stimulate eryptosis and to be enhanced in renal insufficiency are vanadate [47] and methylglyoxal [7] . Along those lines, iron deficiency, which contributes to anemia in chronic renal failure [4,5] is a known trigger of eryptosis [64].…”

Section: Discussionmentioning

confidence: 99%

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The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death

Ahmed

Langer

Abed

et al. 2013

Kidney Blood Press Res

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Background: Anemia is a major complication of end stage renal disease. The anemia is mainly the result of impaired formation of erythrocytes due to lack of erythropoietin and iron deficiency. Compelling evidence, however, points to the contribution of accelerated erythrocyte death, which decreases the life span of circulating erythrocytes. Erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by cell membrane scrambling with phosphatidylserine-exposure at the erythrocyte surface. Triggers of eryptosis include increase of cytosolic Ca²⁺-activity ([Ca²⁺]_i). Erythrocytes could be sensitized to cytosolic Ca²⁺ by ceramide. In end stage renal disease, eryptosis may possibly be stimulated by uremic toxins. The present study explored, whether the uremic toxin acrolein could trigger eryptosis. Methods: Cell volume was estimated from forward scatter, phosphatidylserine-exposure from annexin-V-binding, hemolysis from hemoglobin release, [Ca²⁺]_i from Fluo3-fluorescence, and ceramide from fluorescent antibodies. Results: A 48 h exposure to acrolein (30 － 50 µM) did not significantly modify [Ca²⁺]_i but significantly decreased forward scatter and increased annexin-V-binding. Acrolein further triggered slight, but significant hemolysis and increased ceramide formation in erythrocytes. Acrolein (50 µM) induced annexin-V-binding was significantly blunted in the nominal absence of extracellular Ca²⁺. Acrolein augmented the annexin-V-binding following treatment with Ca²⁺ ionophore ionomycin (1 µM). Conclusion: Acrolein stimulates suicidal erythrocyte death or eryptosis, an effect at least in part due to stimulation of ceramide formation with subsequent sensitisation of the erythrocytes to cytosolic Ca²⁺.

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Section: Discussionmentioning

confidence: 99%

“…Little is known, however, about mechanisms stimulating eryptosis in end stage renal disease. Eryptosis is known to be stimulated by vanadate [47] and methylglyoxal [7], both substances increased in uremic plasma [7,47]. Other uremic toxins have, to the best of our knowledge, not been tested.…”

Section: Introductionmentioning

confidence: 99%

The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death

Ahmed

Langer

Abed

et al. 2013

Kidney Blood Press Res

Self Cite

150

123

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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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“…Suicidal erythrocyte death could be triggered by ligation of specific surface antigens, such as glycophorin-C (41), the thrombospondin-1 receptor CD47 (42) and the death receptor CD95/Fas (43). Further stimulators of eryptosis include ceramide (acylsphingosine) (44), prostaglandin E 2 (45), platelet activating factor (46), anti A IgG antibodies (47), hemolysin from Vibrio parahaemolyticus (48), listeriolysin (49), paclitaxel (50), amantadine (51), azathioprine (52), retinoic acid (53), chlorpromazine (54), cyclosporine (55), methylglyoxal (56), amyloid peptides (57), anandamide (58), Bay-Y5884 (59), curcumin (60), valinomycin (61), aluminium (62), mercury (63), lead (64), gold (65), vanadium (66) and copper (67).…”

Section: Triggers Of Eryptosismentioning

confidence: 99%