[Signal pathways of eryptosis-review].
Erythrocytes are devoid of nuclei and mitochondria which are the crucial elements of apoptosis, so their programmed suicidal death is called eryptosis. Eryptosis is characterized by cell shrinkage, membrane blebbing, activation of proteases, and phosphatidylserine exposure. Prostaglandin E(2) (PGE(2)) activates nonselective cation channels that increase cytosolic Ca(2+) activity and platelet-activating factor (PAF) activates a sphingomyelinase which lead to formation of ceramide. Either can lead to membrane scrambling with subsequent phosphatidylserine exposure. Exposed phosphatidylserine is recognized by macrophages that engulf and degrade the injured cells. As such, eryptosis can clear the injured red blood cells and avoid the release of hemoglobin. The signaling of eryptosis includes PGE(2), cation channels, PAF, ceramide, protein kinase C, and in some instances, caspases. In this review, the PGE(2), PAF and protein kinase pathways, erythrocyte surface receptor-mediated effects, oxidative stress and caspase effects, the inhibitory factors of eryptosis and the clinical eryptosis-related diseases are discussed.
Bao
Guo-Qiang
GQ
Beijing Institute of Transfusion Medicine, Academy of Military Medical Sciences, Beijing 100850, China. baogq@nic.bmi.ac.cn
Ju
Ai-Zhong
AZ
D017209:Apoptosis / Q000502:physiology*; D015232:Dinoprostone / Q000378:metabolism; D004912:Erythrocytes / Q000378:metabolism* / Q000502:physiology*; D006801:Humans; D010972:Platelet Activating Factor / Q000378:metabolism; D015398:Signal Transduction
D010972:Platelet Activating Factor; D015232:Dinoprostone