Eryptosis in autoimmune haemolytic anaemia

Bartolmäs, Thilo; Mayer, Beate; Balola, Abdelwahab Hassan Ahmed; Salama, Abdulgabar

doi:10.1111/ejh.12976

Cited by 24 publications

(34 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Several inbitors of eryptosis have been identified [88][89][90][91]. Eryptosis is enhanced in several clinical conditions including iron deficiency [33], dehydration [33], hyperphosphatemia [33], vitamin D excess [33], chronic kidney disease (CKD) [92][93][94][95][96][97], hemolytic-uremic syndrome [98], autoimmune hemolytic anemia [99], diabetes [33], hypertension and dyslipidemia [100], hepatic failure [101], malignancy [102][103][104], arteritis [105], systemic lupus erythematosus [106], sepsis [107,108], malaria [33,109,110], sickle-cell disease [33], beta-thalassemia [33], Hb-C and G6PD-deficiency [33], Wilsons disease [107], as well as advanced age [33]. Eryptosis is fostered by storage for transfusion [41,42,58,111].…”

Section: Introductionmentioning

confidence: 99%

Taurolidine Sensitivity of Eryptosis, the Suicidal Erythrocyte Death

Fink

Bhuyan

Zacharopoulou

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: The taurine derivative Taurolidine is effective against diverse bacteria and tumor growth. In the treatment of cancer, the substance is effective in part by triggering suicidal death or apoptosis of tumor cells. The Taurolidine-induced apoptosis involves mitochondria. Erythrocytes lack mitochondria but are nevertheless able to enter suicidal erythrocyte death or eryptosis, which is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling of eryptosis includes increase of cytosolic Ca²⁺ activity ([Ca²⁺]_i), oxidative stress and ceramide. The present study explores, whether Taurolidine induces eryptosis and, if so, which cellular mechanisms are involved. Methods: Phosphatidylserine exposure at the cell surface was estimated using annexin-V-binding, cell volume using forward scatter, [Ca²⁺]_i using Fluo3-fuorescence, reactive oxygen species (ROS) formation using 2’,7’-dichlorodihydrofuorescein (DCF)-dependent fluorescence, and ceramide abundance using specific antibodies. Results: A 48 hours exposure of human erythrocytes to Taurolidine (60 µg/ml) significantly enhanced the percentage of annexin-V-binding cells, significantly decreased forward scatter and significantly increased Fluo3-fluorescence and ceramide abundance, but not DCF-fluorescence. The effect of Taurolidine on annexin-V-binding was virtually abrogated by removal of extracellular Ca²⁺. Conclusion: Taurolidine triggers cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part due to Ca²⁺ entry and paralleled by increase of ceramide abundance.

show abstract

Section: Introductionmentioning

confidence: 99%

Taurolidine Sensitivity of Eryptosis, the Suicidal Erythrocyte Death

Fink

Bhuyan

Zacharopoulou

et al. 2018

Cell Physiol Biochem

View full text Add to dashboard Cite

show abstract

“…26 It is, therefore, tempting to speculate that reduction in surface SA contributes to enhanced agedependent susceptibility of erythrocytes to eryptosis. Accelerated clearance of injured eryptotic erythrocytes has been propounded to be essential in the pathogenesis of anemia in several clinical conditions such as chronic kidney disease, 42 hepatic failure, 31,43 iron deficiency, 20 autoimmune hemolytic anemia, 44 arteritis, 45 calcitriol excess, 46 malignancy, 47 and advanced age. 48 Eryptosis is further elicited by a myriad of clinically-used and other biologically-active agents 22,23,25 and modulates erythrocyte survival during transfusionrelated storage.…”

Section: Discussionmentioning

confidence: 99%

Bacterial neuraminidase‐mediated erythrocyte desialylation provokes cell surface aminophospholipid exposure

Qadri

Donkor

Nazy

et al. 2018

European J of Haematology

View full text Add to dashboard Cite

show abstract

“…Это делает слой менее текучим по сравнению с теми, которые находятся в составе фосфатидилэтаноламина и фосфатидилсерина внутренней поверхности. Во-вторых, отрицательно заряженный фосфатидилсерин, взаимодействующий с регуляторными и структурными белками, при нарушении асимметрии приводит к экспонированию фосфатидилсерина на наружной поверхности, что является сигналом к эриптозу [49,50,82,254], а также к изменению соотношения зарядов на внутренней и внешней сторонах бислоя мембраны эритроцита. Таким образом, aссимметрия фосфолипидов определяет текучесть мембраны (fragility) и вносит важный вклад в поддержание механических свойств мембраны [95,236].…”

Section: ãëèêîôîðèíunclassified

Eryptosis (quasi-apoptosis) the human red blood cells. Its role in medicinal therapy

Vaschenko

Иванович²,

Vilyaninov

et al. 2019

Rev Clin Pharm Drug Ther

View full text Add to dashboard Cite

In the course of circulation erythrocytes can test damages, which compromises their integrity and thus triggers suicidal erythrocyte death or eryptosis. This mechanism is characterised by cell shrinkage, cell membrane blebbing, and cell membrane phospholipid scrambling after phosphatidylserine exposure on the cell surface that is identified by macrophages, which engulf and degrade the eryptotic cells. The term eryptosis also includes typical mechanisms, which contribute to the triggering of this process, such as oxidative stress, Ca2+ entry with an increase in cytosolic Ca2+ activity and the activation of p38 kinase, which is a kinase expressed in human erythrocytes and activated after hyperosmotic shock. Enhanced eryptosis has been observed in several clinical conditions such as diabetes, renal insufficiency, haemolytic uremic syndrome, sepsis, mycoplasma infection, malaria, iron deficiency, sickle cell anaemia, beta-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, hereditary spherocytosis, paroxysmal nocturnal haemoglobinuria, Wilson’s disease, myelodysplastic syndrome, and phosphate depletion. Therefore, eryptosis may be considered as a useful mechanism of removal of defective erythrocytes to prevent haemolysis. Moreover, the clearance of infected erythrocytes in diseases such as malaria may counteract parasitemia. Indeed it is known that sickle-cell trait, beta-thalassemia trait, G6PD-deficiency and iron deficiency confer some protection against a severe course of malaria. Importantly, strategies to control Plasmodium infection by inducing eryptosis are 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. However, excessive eryptosis could compromise microcirculation and lead to anemia. Besides, adhesion of eryptosis erythrocytes to a vascular wall also can lead to microcirculation infringement.Thus, modern representations about eryptosis expand our knowledge about the programmed death of blood cells and is more directed to create new therapeutic schemes of treatment of patients.

show abstract

Eryptosis in autoimmune haemolytic anaemia

Cited by 24 publications

References 32 publications

Taurolidine Sensitivity of Eryptosis, the Suicidal Erythrocyte Death

Taurolidine Sensitivity of Eryptosis, the Suicidal Erythrocyte Death

Bacterial neuraminidase‐mediated erythrocyte desialylation provokes cell surface aminophospholipid exposure

Eryptosis (quasi-apoptosis) the human red blood cells. Its role in medicinal therapy

Contact Info

Product

Resources

About