作者: Daiana M. Vota , Romina E. Maltaneri , Shirley D. Wenker , Alcira B. Nesse , Daniela C. Vittori
DOI: 10.1007/S12013-012-9408-4
关键词:
摘要: Eryptosis is a process by which mature erythrocytes can undergo self-destruction sharing several features with apoptosis. Premature programmed erythrocyte death may be induced different agents. In this study, we compared mechanisms involved in two eryptotic models (oxidative stress and cell calcium overload) so as to distinguish whether they share signaling pathways could prevented erythropoietin (Epo). Phosphatidylserine (PS) translocation increased content were common signs exposed sodium nitrite plus hydrogen peroxide or ionophore A23187 (CaI), while ROS decreased GSH levels detected the oxidative model. Protein kinase activation seemed an outstanding feature eryptosis stress, whereas phosphatase was favored CaI Cell morphology membrane protein modifications also differential between both models. Epo able prevent imbalance, thus blunting PS translocation. However, hormone intracellular influx reason why it not completely counteract induction of eryptosis. Instead, unable inhibit externalization The explain action upon