Eryptosis (quasi-apoptosis) the human red blood cells. Its role in medicinal therapy

Abstract

In the course of circulation erythrocytes can test damages, 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 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, 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. Besides, adhesion of eryptosis erythrocytes to a vascular wall also can lead to microcirculation infringement.Thus, modern representations about eryptosis expand our knowledge about the programmed death of blood cells and is more directed to create new therapeutic schemes of treatment of patients.

Usnic Acid and Usnea barbata (L.) F.H. Wigg. Dry Extracts Promote Apoptosis and DNA Damage in Human Blood Cells through Enhancing ROS Levels

“…They can express caspase-3 and caspase-8 [ 53 ], but they do not display other elements of the apoptotic machinery, such as Apaf-1, cytochrome c , and caspases-2, -6, -7 and -9 [ 54 ]. Klatt et al (2018) reported that significant receptors belonging to the tumor necrosis factors (TNF) family (CD95 [ 55 ] and Fas [ 56 ]) signaling in RBCs are known to induce a particular type of programmed cell death, similar to the apoptotic death of nucleated cells named eryptosis [ 57 ], by caspase-3 activation, leading to cell shrinkage and cell membrane scrambling [ 58 ] with PS externalization [ 59 ]. The major trigger of eryptosis is the increase of cytosolic Ca 2+ activity resulting from Ca 2+ entry through Ca 2+ -permeable unselective cation channels (permeable to both Na + and Ca 2+ ) [ 60 ].…”

Генерація Активних Форм Кисню В Еритроцитах Пацієнтів Із Політравмою Та Станом Відміни Алкоголю, Ускладненим Алкогольним Делірієм

“…За своєю суттю підвищення АФК в еритроцитах призводить до ериптозу -процесу, що нагадує апоптоз ядровмісних клітин. Цей процес відбувається шляхом зморщування клітин, переміщення молекул фосфоліпідів з одного боку цитоплазматичної мембрани в інший, що призводить до зміни властивостей та функціональної активності еритроцитів [8]. Скремблювання фосфоліпідів клітинних мембран еритроцитів під час ериптозу зумовлює транслокацію фосфатидилсерину на зовнішній бік цитоплазматичної мембрани.…”