Studying Mechanisms of Eryptosis

Abstract

Cellular stress leads to activation of erythrocyte cation channels with subsequent Ca2+ entry and stimulates a sphingomyelinase with subsequent formation of ceramide. Both signaling molecules then activate the death program of erythrocytes (eryptosis) which is characterized by phosphatidylserine exposure, cellular shrinkage, membrane blebbing and activation of death-inducing proteases. Some of the mediators accounting for activation of the erythrocyte death machinery, i. e. prostaglandin E2 (PGE2) and platelet activating factor (PAF), have been described and the respective signaling cascades disclosed. The present article outlines and discusses the methods which have been used to analyze erythrocyte death pathways. Furthermore, some of the pathophysiological implications of eryptosis signaling are delineated and the methods to screen for eryptosis defects in those conditions are presented. Needless to say that further research will be required to fully understand the mechanisms leading to suicidal red blood cell death and to elucidate the role of eryptosis during anemic complications.