Stimulation of Suicidal Erythrocyte Death by Fumagillin

Zbidah, Mohanad; Lupescu, Adrian; Jilani, Kashif; Läng, Florian

doi:10.1111/bcpt.12033

Cited by 68 publications

(46 citation statements)

References 77 publications

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“…Accelerated suicidal erythrocyte death may contribute to the anemia of several clinical disorders and eryptosis may be triggered by a wide variety of xenobiotics [22,23,24,25,26,27,28,29,30,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45]. …”

Section: Introductionmentioning

confidence: 99%

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: 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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“…Eryptosis may be stimulated by a wide variety of xenobiotics [15,31,32,33,34,35,36,37,38,39,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66] and excessive eryptosis is further observed in several clinical conditions including diabetes, renal insufficiency, hemolytic uremic syndrome, sepsis, malaria, sickle cell disease, Wilson's disease, iron deficiency, malignancy, phosphate depletion, and metabolic syndrome [15]. …”

Section: Introductionmentioning

confidence: 99%

Stimulation of Erythrocyte Cell Membrane Scrambling by Gedunin

Lupescu¹,

Bissinger²,

Warsi³

et al. 2014

Cell Physiol Biochem

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Background/Aims: Gedunin, an inhibitor of heat shock protein HSP90, triggers apoptosis of tumor cells and is thus effective against malignancy. Moreover, the drug has antimalarial potency. In analogy to apoptosis of nucleated cells, erythrocytes may enter suicidal death or eryptosis, which is characterized by cell shrinkage and by phosphatidylserine translocation to the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca²⁺-activity ([Ca²⁺]_i). The present study explored whether gedunin stimulates eryptosis. Methods: Forward scatter was determined to estimate cell volume, annexin V binding to identify phosphatidylserine-exposing erythrocytes, hemoglobin release to depict hemolysis, and Fluo3-fluorescence to quantify [Ca²⁺]_i. Results: A 48 h exposure of human erythrocytes to gedunin significantly increased [Ca²⁺]_i (12 µM), significantly decreased forward scatter (24 µM) and significantly increased annexin-V-binding (12 µM). The effect of gedunin (24 µM) on annexin-V-binding was virtually abrogated by removal of extracellular Ca²⁺. Conclusion: Gedunin stimulates suicidal erythrocyte death or eryptosis, an effect mainly if not exclusively due to stimulation of Ca²⁺ entry.

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“…Eryptosis is triggered by a myriad of xenobiotics [26,40,41,42,43,44,45,46,47,48,49,50,51,52,53,54,55,56,57,58,59,60,61,62,63,64,65,66,67,68,69,70,71,72,73,74] and excessive eryptosis is observed in a wide variety of clinical conditions, such as sepsis, malaria, sickle cell disease, Wilson's disease, iron deficiency, malignancy, metabolic syndrome, diabetes, renal insufficiency, hemolytic uremic syndrome, hyperphosphatemia and phosphate depletion [24,75]. …”

Section: Introductionmentioning

confidence: 99%

Stimulation of Eryptosis by Cryptotanshinone

Bissinger

Lupescu

Zelenak

et al. 2014

Cell Physiol Biochem

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Background/Aims: Cryptotanshinone, a component of Salvia miltiorrhiza Bunge roots, may trigger suicidal death or apoptosis of tumor cells and has thus been recommended for the prevention and treatment of malignancy. On the other hand, Cryptotanshinone has been shown to counteract apoptosis of neurons and hepatocytes. Similar to apoptosis of nucleated cells, erythrocytes may enter eryptosis, a suicidal death characterized by cell shrinkage and phosphatidylserine translocation to the erythrocyte surface. Eryptosis may be triggered by increase of cytosolic Ca²⁺-activity ([Ca²⁺]_i). The present study explored whether Cryptotanshinone stimulates eryptosis. Methods: Forward scatter was taken as measure of cell volume, annexin V binding for identification of phosphatidylserine-exposing erythrocytes and Fluo3-fluorescence for determination of [Ca²⁺]_i. Results: A 48 h exposure of human erythrocytes to Cryptotanshinone (10 µM) was followed by significant decrease of forward scatter, significant increase of the percentage annexin-V-binding cells and significant increase of [Ca²⁺]_i. The effect of Cryptotanshinone (1 µM) on annexin-V-binding was virtually abrogated by removal of extracellular Ca²⁺. Conclusion: Cryptotanshinone is a powerful stimulator of suicidal erythrocyte death or eryptosis, which is effective mainly, if not exclusively, by stimulation of Ca²⁺ entry.

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Stimulation of Suicidal Erythrocyte Death by Fumagillin

Cited by 68 publications

References 77 publications

The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death

The Uremic Toxin Acrolein Promotes Suicidal Erythrocyte Death

Stimulation of Erythrocyte Cell Membrane Scrambling by Gedunin

Stimulation of Eryptosis by Cryptotanshinone

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