Erythrocyte programmed cell death

  title={Erythrocyte programmed cell death},
  author={Michael F{\"o}ller and Stephan M Huber and Florian Lang},
  journal={IUBMB Life},
Eryptosis, the suicidal death of erythrocytes, is characterised by cell shrinkage, membrane blebbing and cell membrane phospholipid scrambling with phosphatidylserine exposure at the cell surface. Phosphatidylserine‐exposing erythrocytes are recognised by macrophages, which engulf and degrade the affected cells. Reported triggers of eryptosis include osmotic shock, oxidative stress, energy depletion, ceramide, prostaglandin E2, platelet activating factor, hemolysin, listeriolysin, paclitaxel… 

Methods Employed in Cytofluorometric Assessment of Eryptosis, the Suicidal Erythrocyte Death

The present synopsis describes the experimental procedures required for the analysis of phosphatidylserine exposure at the cell surface with annexin-V, cell volume with forward scatter, cytosolic Ca2+ activity ([Ca2+]i) with Fluo3, oxidative stress with 2′,7′-dichlorodihydrofuorescein diacetate (DCFDA), and ceramide abundance with specific antibodies.

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

Modern representations about eryptosis expand the authors' knowledge about the programmed death of blood cells and is more directed to create new therapeutic schemes of treatment of patients.

Eryptosis, a Window to Systemic Disease

The case is made that analysis of enhanced eryptosis may direct to the pathophysiology of systemic disease, including drug side effects, sepsis, haemolytic uremic syndrome, Wilson´s disease, phosphate depletion and a rare condition caused by a mutation in GLUT1 turning the carrier into a cation channel.

Induction of Suicidal Erythrocyte Death by Novobiocin

Whether novobiocin elicits eryptosis is explored, an effect at least in part due to entry of extracellular Ca2+ and formation of ceramide is found and removal ofextracellularCa2+ virtually abrogated the increase of annexin-V-binding following novobocin exposure.

Eryptosis: An Erythrocyte's Suicidal Type of Cell Death

Eryptosis ensures healthy erythrocyte quantity in circulation whereas excessive eryptosis may set an environment for the clinical presence of pathophysiological conditions including anaemia.

Enhanced Apoptotic Death of Erythrocytes Induced by the Mycotoxin Ochratoxin A

Ochratoxin A triggers suicidal erythrocyte death or eryptosis, an effect partially but not fully due to stimulation of Ca2+-entry, which may lead to anemia.

Silver ion‐induced suicidal erythrocyte death

The present study explored the effect of AgNO3 on eryptosis, the suicidal death of erythrocytes, cells devoid of mitochondria, and found an effect attributed to ATP depletion, PKC activation and decrease of cellular NO.

Anti-Eryptotic Activity of Food-Derived Phytochemicals and Natural Compounds

This review addresses and collates the existing ex vivo and animal studies on the inhibition of eryptosis by food-derived phytochemicals and natural compounds including phenolic compounds (PC), alkaloids, and other substances that could be a therapeutic and/or co-adjuvant option in eryPTotic-driven disorders, especially if they are introduced through the diet.

Effect of Dermaseptin on Erythrocytes

This study explored whether dermaseptin modifies [Ca2+]i and elicits eryptosis, an effect at least partially due to entry of extracellular Ca2+.



Amyloid Induced Suicidal Erythrocyte Death

The present observations disclose a novel action of Aβ 1-42, which may well contribute to the pathophysiological effects of amyloid peptides, such as vascular complications in Alzheimer''s disease.

Mechanisms of Suicidal Erythrocyte Death

Erythrocyte shrinkage and phosphatidylserine exposure (‘eryptosis’) mimic features of apoptosis in nucleated cells which however, involves several mechanisms lacking in erythrocytes.

Induction of Suicidal Erythrocyte Death by Listeriolysin from Listeria monocytogenes

Listeriolysin triggers suicidal death of erythrocytes, an effect at least partially due to depletion of intracellular K+ and could well contribute to the pathophysiology of L. monocytogenes infection.

Cation channels trigger apoptotic death of erythrocytes

Osmotic and oxidative stress open Ca2-permeable cation channels in erythrocytes, thus increasing cytosolic Ca2+ activity and triggering ery Throcyte apoptosis.

Programmed cell death in mature erythrocytes: a model for investigating death effector pathways operating in the absence of mitochondria

It is reported that mature erythrocytes can undergo a rapid self-destruction process sharing several features with apoptosis, including cell shrinkage, plasma membrane microvesiculation, phosphatidylserine externalization, and leading to ERYthrocyte disintegration, or, in the presence of macrophages, to macrophage ingestion of dying ery Throcytes.

Suicidal erythrocyte death in sepsis

A novel pathophysiological mechanism leading to anemia and derangement of microcirculation during sepsis is disclosed, including exposure to plasma from septic patients triggers phosphatidylserine exposure leading to adherence to the vascular wall and clearance from circulating blood.

Inhibition of suicidal erythrocyte death by nitric oxide

In conclusion, nitric oxide participates in the regulation of erythrocyte survival, an effect partially mimicked by cGMP and paralleled by alterations of protein nitrosylation and thioredoxin activity.

Curcumin Induced Suicidal Erythrocyte Death

A proeryptotic effect of Curcumin is disclosed which may affect the life span of circulating erythrocytes and that of eryptosis and phosphatidylserine exposing cells are phagocytosed and thus rapidly cleared from circulating blood.

Involvement of ceramide in hyperosmotic shock-induced death of erythrocytes

It is shown that ceramide and Ca2+ entry through cation channels concert to trigger erythrocyte death during osmotic shock, with ceramide is blunted but not abolished in the absence of Ca2+.