We are analyzing https://link.springer.com/article/10.1007/s12013-012-9408-4.

Title:
Differential Erythropoietin Action upon Cells Induced to Eryptosis by Different Agents | Cell Biochemistry and Biophysics
Description:
Eryptosis is a process by which mature erythrocytes can undergo self-destruction sharing several features with apoptosis. Premature programmed erythrocyte death may be induced by 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 and could be prevented by erythropoietin (Epo). Phosphatidylserine (PS) translocation and increased calcium content were common signs in erythrocytes exposed to sodium nitrite plus hydrogen peroxide or calcium ionophore A23187 (CaI), while increased ROS and decreased GSH levels were detected in the oxidative model. Protein kinase activation seemed to be an outstanding feature in eryptosis induced by oxidative stress, whereas phosphatase activation was favored in the CaI model. Cell morphology and membrane protein modifications were also differential signs between both models. Epo was able to prevent cell oxidative imbalance, thus blunting PS translocation. However, the hormone favored intracellular calcium influx which could be the reason why it could not completely counteract the induction of eryptosis. Instead, Epo was unable to inhibit PS externalization in the CaI model. The different mechanisms involved in the eryptotic models may explain the differential action of Epo upon erythrocytes induced to eryptosis by different agents.
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Keywords {🔍}

article, google, scholar, cas, pubmed, cell, erythrocytes, human, journal, erythropoietin, death, oxidative, eryptosis, biochemistry, cells, erythrocyte, calcium, vittori, research, induced, nesse, blood, content, protein, membrane, lang, red, privacy, cookies, vota, daniela, apoptosis, stress, access, phosphotyrosine, publish, search, differential, action, agents, daiana, maltaneri, wenker, alcira, mechanisms, epo, cai, model, phosphatase, role,

Topics {✒️}

month download article/chapter eosin-5-maleimide p-tyr n-acetyl-cysteine rhepo hyperosmotic shock-induced death cell calcium overload full article pdf privacy choices/manage cookies red blood cells protein kinase activation article cell biochemistry erythrocyte oxidative damage membrane protein modifications calcium ionophore a23187 erythroid cells induced free radical metabolism programmed cell death phosphotyrosine phosphatases acting oxidative stress human erythroid cells phosphatidylserine dcfh-da decreased gsh levels ut-7 cell line differential erythropoietin action integral membrane proteins increased calcium content action abbreviations pmsf related subjects long term ingestion biochimica biophysica acta clinica chimica acta calderón-salinas human erythrocyte ghosts suicidal erythrocyte death calpain inhibitor inhibit ps externalization conditions privacy policy erythrocyte cation channels check access instant access peroxynitrite-induced senescence european economic area share signaling pathways chronic fatigue syndrome calpain-catalyzed cleavage accepting optional cookies human erythrocytes incubated chronic kidney disease oxidative damage blunting ps translocation author information authors

Questions {❓}

Erythrocyte aging: a more than superficial resemblance to apoptosis?
Erythrocyte vesiculation: A self-protective mechanism?
Is erythropoietin a survival factor for red blood cells?

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         description:Eryptosis is a process by which mature erythrocytes can undergo self-destruction sharing several features with apoptosis. Premature programmed erythrocyte death may be induced by 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 and could be prevented by erythropoietin (Epo). Phosphatidylserine (PS) translocation and increased calcium content were common signs in erythrocytes exposed to sodium nitrite plus hydrogen peroxide or calcium ionophore A23187 (CaI), while increased ROS and decreased GSH levels were detected in the oxidative model. Protein kinase activation seemed to be an outstanding feature in eryptosis induced by oxidative stress, whereas phosphatase activation was favored in the CaI model. Cell morphology and membrane protein modifications were also differential signs between both models. Epo was able to prevent cell oxidative imbalance, thus blunting PS translocation. However, the hormone favored intracellular calcium influx which could be the reason why it could not completely counteract the induction of eryptosis. Instead, Epo was unable to inhibit PS externalization in the CaI model. The different mechanisms involved in the eryptotic models may explain the differential action of Epo upon erythrocytes induced to eryptosis by different agents.
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      description:Eryptosis is a process by which mature erythrocytes can undergo self-destruction sharing several features with apoptosis. Premature programmed erythrocyte death may be induced by 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 and could be prevented by erythropoietin (Epo). Phosphatidylserine (PS) translocation and increased calcium content were common signs in erythrocytes exposed to sodium nitrite plus hydrogen peroxide or calcium ionophore A23187 (CaI), while increased ROS and decreased GSH levels were detected in the oxidative model. Protein kinase activation seemed to be an outstanding feature in eryptosis induced by oxidative stress, whereas phosphatase activation was favored in the CaI model. Cell morphology and membrane protein modifications were also differential signs between both models. Epo was able to prevent cell oxidative imbalance, thus blunting PS translocation. However, the hormone favored intracellular calcium influx which could be the reason why it could not completely counteract the induction of eryptosis. Instead, Epo was unable to inhibit PS externalization in the CaI model. The different mechanisms involved in the eryptotic models may explain the differential action of Epo upon erythrocytes induced to eryptosis by different agents.
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