Eryptosis: Ally or Enemy

Title:Eryptosis: Ally or Enemy

Volume: 24 Issue: 9

Author(s): Marilena Briglia, Maria Antonia Rossi and Caterina Faggio*

Affiliation:

• Department of Chemical, Biological, Pharmaceutical and Environmental Sciences, University of Messina, Viale Ferdinando Stagno d`Alcontres 31, 98166 S.Agata-Messina,Italy

Keywords: Eryptosis, malaria, anaemia, beta-thalassemia, cytosolic Ca2+, diabetes.

Abstract: Prior to senescence, erythrocytes may experience injury, which compromises their integrity and thus triggers suicidal erythrocyte death or eryptosis. This mechanism is characterised by cell shrinkage, cell membrane blebbing, and cell membrane phospholipid scrambling after phosphatidylserine exposure on the cell surface that is identified by macrophages, which engulf and degrade the eryptotic cells. The term eryptosis also includes typical mechanisms, which contribute to the triggering of this process, such as oxidative stress, Ca2+ entry with an increase in cytosolic Ca2+ activity ([Ca ]i) and the activation of p38 kinase, which is a kinase expressed in human erythrocytes and activated after hyperosmotic shock. Enhanced eryptosis has been observed in several clinical conditions such as diabetes, renal insufficiency, haemolytic uremic syndrome, sepsis, mycoplasma infection, malaria, iron deficiency, sickle cell anaemia, beta-thalassemia, glucose-6-phosphate dehydrogenase-(G6PD) deficiency, hereditary spherocytosis, paroxysmal nocturnal haemoglobinuria, Wilson's disease, myelodysplastic syndrome, and phosphate depletion. Therefore, eryptosis may be considered as a useful mechanism of removal of defective erythrocytes to prevent haemolysis. Moreover, the clearance of infected erythrocytes in diseases such as malaria may counteract parasitemia. Indeed it is known that sickle-cell trait, beta-thalassemia trait, glucose-6-phosphate dehydrogenase (G6PD)- deficiency and iron deficiency confer some protection against a severe course of malaria. Importantly, strategies to control Plasmodium infection by inducing eryptosis are not expected to generate resistance of the pathogen, as the proteins involved in suicidal death of the host cell are not encoded by the pathogen and thus cannot be modified by mutations of its genes. However, excessive eryptosis could compromise microcirculation and lead to anemia.

Cite this article as:

Briglia Marilena, Rossi Maria Antonia and Faggio Caterina*, Eryptosis: Ally or Enemy, Current Medicinal Chemistry 2017; 24 (9) . https://dx.doi.org/10.2174/0929867324666161118142425