Deoxygenation-Induced Non-Electrolyte Pathway in Red Cells from Sickle Cell Patients

Browning, Joseph A.; Robinson, Hannah; Ellory, J. C.; Gibson, John S.

doi:10.1159/000099204

Cited by 27 publications

(24 citation statements)

References 52 publications

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“…Eryptosis participates in the pathophysiology of several clinical conditions, including sepsis [119], hemolytic uremic syndrome [120], renal insuficiency [121], malaria [10], sickle-cell anemia [122,123], beta-thalassemia [80], glucose-6-phosphate dehydrogenase (G6PD)-deficiency [80], phosphate depletion [124], and Wilson's disease [118]. Enhanced eryptosis in sepsis [119] and hemolytic uremic syndrome [120] is secondary to the capability of serum from respective patients to trigger eryptosis.…”

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

154

161

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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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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

154

161

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“…P sickle has the characteristics of a nonspecific cation channel [34]. An anion permeability is controversial, whilst, more recently, it has been proposed as permeable under certain conditions to nonelectrolytes [49]. The main effect of P sickle is probably the increased Ca 2+ entry [49, 50] and possibly the Mg 2+ loss [45].…”

Section: Altered Membrane Transport In Homozygous Hbss Cellsmentioning

confidence: 99%

“…An anion permeability is controversial, whilst, more recently, it has been proposed as permeable under certain conditions to nonelectrolytes [49]. The main effect of P sickle is probably the increased Ca 2+ entry [49, 50] and possibly the Mg 2+ loss [45]. Raised intracellular Ca 2+ has several roles which include phospholipid scrambling [51].…”

Section: Altered Membrane Transport In Homozygous Hbss Cellsmentioning

confidence: 99%

The Properties of Red Blood Cells from Patients Heterozygous for HbS and HbC (HbSC Genotype)

Hannemann

Weiss

Rees

et al. 2011

Anemia

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Sickle cell disease (SCD) is one of the commonest severe inherited disorders, but specific treatments are lacking and the pathophysiology remains unclear. Affected individuals account for well over 250,000 births yearly, mostly in the Tropics, the USA, and the Caribbean, also in Northern Europe as well. Incidence in the UK amounts to around 12–15,000 individuals and is increasing, with approximately 300 SCD babies born each year as well as with arrival of new immigrants. About two thirds of SCD patients are homozygous HbSS individuals. Patients heterozygous for HbS and HbC (HbSC) constitute about a third of SCD cases, making this the second most common form of SCD, with approximately 80,000 births per year worldwide. Disease in these patients shows differences from that in homozygous HbSS individuals. Their red blood cells (RBCs), containing approximately equal amounts of HbS and HbC, are also likely to show differences in properties which may contribute to disease outcome. Nevertheless, little is known about the behaviour of RBCs from HbSC heterozygotes. This paper reviews what is known about SCD in HbSC individuals and will compare the properties of their RBCs with those from homozygous HbSS patients. Important areas of similarity and potential differences will be emphasised.

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“…The present short review compiles the present knowledge on mechanisms regulating, triggering and inhibiting the suicidal erythrocyte death or eryptosis. For a more detailed discussion of mechanisms involved, the reader is referred to earlier, more extensive reviews [5][6][7][11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Ceramide in Suicidal Death of Erythrocytes

Läng

Gulbins²,

Lang³

et al. 2010

Cell Physiol Biochem

214

274

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The suicidal death of erythrocytes or eryptosis is characterized by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling resulting in phosphatidylserine exposure at the cell surface. Eryptosis is stimulated in a wide variety of diseases including sepsis, haemolytic uremic syndrome, malaria, sickle-cell anemia, beta-thalassemia, glucose-6-phosphate dehydrogenase (G6PD)-deficiency, phosphate depletion, iron deficiency and Wilson’s disease. Moreover, eryptosis is elicited by osmotic shock, oxidative stress, energy depletion as well as a wide variety of endogenous mediators and xenobiotics. Excessive eryptosis is observed in erythrocytes lacking the cGMP-dependent protein kinase type I (cGKI) or the AMP-activated protein kinase AMPK. Inhibitors of eryptosis include erythropoietin, nitric oxide NO, catecholamines and high concentrations of urea. Eryptosis-triggering diseases and chemicals are partially effective by stimulating the formation of ceramide, which in turn fosters cell membrane scrambling. Accordingly, ceramide-induced eryptosis participates in the pathophysiology of several diseases and contributes to the effects of a large number of xenobiotics. The mechanisms underlying ceramide formation in erythrocytes are, however, still ill defined. In case of osmotic cell shrinkage, ceramide formation is apparently due to activation of phospholipase 2, leading to formation of platelet activating factor PAF and PAF-dependent stimulation of ceramide formation, which possibly involves acid sphingomyelinase. Additional experiments are needed to conclusively define the ceramide-generating enzyme and the ceramide-dependent cellular events eventually leading to suicidal erythrocyte death.

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Deoxygenation-Induced Non-Electrolyte Pathway in Red Cells from Sickle Cell Patients

Cited by 27 publications

References 52 publications

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

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

The Properties of Red Blood Cells from Patients Heterozygous for HbS and HbC (HbSC Genotype)

Ceramide in Suicidal Death of Erythrocytes

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