Eryptosis, a Window to Systemic Disease

Läng, Florian; Gulbins, Erich; Lerche, Holger; Huber, Stephan M.; Kempe, Daniela S.; Föller, Michael

doi:10.1159/000185448

Cited by 223 publications

(344 citation statements)

References 135 publications

(80 reference statements)

Supporting

Mentioning

329

Contrasting

Unclassified

Order By: Relevance

“…Erythrocytes are very sensitive to ROS due to the high poly-unsaturated fatty acids (PUFAs) content in the membrane [25]. The pool of ROS can induce oxidative stress and eventually trigger apoptosis that impairs the function of erythrocytes [24,26] and leads to a wide variety of further diseases or clinical conditions [27]. Thus, it is important to protect erythrocytes against oxidative stress and apoptosis.…”

Section: Introductionmentioning

confidence: 99%

The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

Jiang

Liu

et al. 2016

Free Radical Biology and Medicine

View full text Add to dashboard Cite

a b s t r a c tThe present study explored the apoptosis pathways in hydroxyl radicals ( • OH)-induced carp erythrocytes. Carp erythrocytes were treated with the caspase inhibitors in physiological carp saline (PCS) or Ca 2 þ -free PCS in the presence of 40 μM FeSO 4 /20 μM H 2 O 2 . The results showed that the generation of reactive oxygen species (ROS), the release of cytochrome c and DNA fragmentation were caspase-dependent, and Ca 2 þ was involved in calpain activation and phosphatidylserine (PS) exposure in • OH-induced carp erythrocytes. Moreover, the results suggested that caspases were involved in PS exposure, and Ca 2 þ was involved in DNA fragmentation in • OH-induced fish erythrocytes. These results demonstrated that there might be two apoptosis pathways in fish erythrocytes, one is the caspase and cytochrome c-dependent apoptosis that is similar to that in mammal nucleated cells, the other is the Ca 2 þ -involved apoptosis that was similar to that in mammal non-nucleated erythrocytes. So, fish erythrocytes may be used as a model for studying oxidative stress and apoptosis in mammal cells. Furthermore, the present study investigated the effects of glutamine (Gln)'s metabolites [alanine (Ala), citrulline (Cit), proline (Pro) and their combination (Ala 10 Pro 4 Cit 1 )] on the pathways of apoptosis in fish erythrocytes. The results displayed that Ala, Cit, Pro and Ala 10 Pro 4 Cit 1 effectively suppressed ROS generation, cytochrome c release, activation of caspase-3, caspase-8 and caspase-9 at the physiological concentrations, prevented Ca 2 þ influx, calpain activation, PS exposure, DNA fragmentation and the degradation of the cytoskeleton and oxidation of membrane and hemoglobin (Hb) and increased activity of anti-hydroxyl radical (AHR) in • OH-induced carp erythrocytes. Ala 10 Pro 4 Cit 1 produced a synergistic effect of inhibited oxidative stress and apoptosis in fish erythrocytes. These results demonstrated that Ala, Cit, Pro and their combination can protect mammal erythrocytes and nucleated cells against oxidative stress and apoptosis. The studies supported the use of Gln, Ala, Cit and Pro as oxidative stress and apoptosis inhibitors in mammal cells and the hypothesis that the inhibited effects of Gln on oxidative stress and apoptosis are at least partly dependent on that of its metabolites in mammalian.

show abstract

Section: Introductionmentioning

confidence: 99%

The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

Jiang

Liu

et al. 2016

Free Radical Biology and Medicine

View full text Add to dashboard Cite

show abstract

“…Hemin-induced damage of erythrocytes is considered to be largely due to hemolysis [48,49,59,70]. However, several conditions leading to hemolysis have recently been shown to trigger eryptosis, the suicidal death of erythrocytes [40]. Hallmarks of eryptosis are scrambling of the erythrocyte membrane and cell shrinkage [40].…”

Section: Introductionmentioning

confidence: 99%

“…However, several conditions leading to hemolysis have recently been shown to trigger eryptosis, the suicidal death of erythrocytes [40]. Hallmarks of eryptosis are scrambling of the erythrocyte membrane and cell shrinkage [40]. The cell membrane scrambling leads to exposure of phosphatidylserine at their surface, which is apparent from annexin V-binding of the erythrocytes [40].…”

Section: Introductionmentioning

confidence: 99%

“…Hallmarks of eryptosis are scrambling of the erythrocyte membrane and cell shrinkage [40]. The cell membrane scrambling leads to exposure of phosphatidylserine at their surface, which is apparent from annexin V-binding of the erythrocytes [40]. Cell shrinkage is apparent from a decrease of forward scatter in fluorescence-activated cell sorter (FACS) analysis [40].…”

Section: Introductionmentioning

confidence: 99%

“…The cell membrane scrambling leads to exposure of phosphatidylserine at their surface, which is apparent from annexin V-binding of the erythrocytes [40]. Cell shrinkage is apparent from a decrease of forward scatter in fluorescence-activated cell sorter (FACS) analysis [40]. Eryptosis is stimulated by increase in cytosolic Ca 2+ activity [5,11,12,19,41].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Hemin-induced suicidal erythrocyte death

2009

Self Cite

View full text Add to dashboard Cite

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.

show abstract

Microbial Inhibitors of Apoptosis

H��cker¹

2009

Encyclopedia of Life Sciences

View full text Add to dashboard Cite

Infection with microbial agents (bacteria, fungi, viruses and parasites) is a challenge to a host cell. The host cell's response to infection is complex and entails changes in the activity of a number of intracellular signalling pathways, commonly including the apoptotic machinery. Microbes, if they have evolved the capacity to infect mammals or other complex hosts, have to be able to deal with such defence systems. The lifestyle of microbes varies substantially – viruses, for instance, depend on an intact cell, whereas many bacteria grow on surfaces and are not sensitive to host cell apoptosis. What we know about microbial interference with host cell apoptosis is in accordance with these lifestyles. Viruses often directly target and inhibit the apoptosis machinery with specific proteins whereas other microbes frequently also interfere with host apoptosis but more indirectly. Key concepts: Microbes (bacteria, fungi, viruses and parasites) can vary widely in terms of growth requirements and intimacy of association with host cells. Apoptosis is commonly induced in cells infected with microbes. In infections with obligate intracellular agents, apoptosis can be a defence mechanism of the host cell. A number of viruses carry genes whose products can directly interfere with the host cell's apoptosis apparatus. Many cells become activated when encountering microbial agents, and this activation may entail the triggering of pro‐survival pathways in the host cell. Activation of antiapoptotic pathways in immune cells by microbial components is a regulatory mechanism of the immune response.

show abstract

Eryptosis, a Window to Systemic Disease

Cited by 223 publications

References 135 publications

The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

The metabolites of glutamine prevent hydroxyl radical-induced apoptosis through inhibiting mitochondria and calcium ion involved pathways in fish erythrocytes

Hemin-induced suicidal erythrocyte death

Microbial Inhibitors of Apoptosis

Contact Info

Product

Resources

About