Signal pathways of eryptosis-review / 中国实验血液学杂志
Journal of Experimental Hematology
;
(6): 1097-1100, 2009.
Artículo
en Chino
| WPRIM
| ID: wpr-343340
ABSTRACT
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.
Texto completo:
Disponible
Índice:
WPRIM (Pacífico Occidental)
Asunto principal:
Fisiología
/
Factor de Activación Plaquetaria
/
Dinoprostona
/
Transducción de Señal
/
Apoptosis
/
Eritrocitos
/
Metabolismo
Límite:
Humanos
Idioma:
Chino
Revista:
Journal of Experimental Hematology
Año:
2009
Tipo del documento:
Artículo
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