Erythrocyte: Programmed Cell Death

DANIELA VITTORI; DAIANA VOTA; ALCIRA NESSE

Anemia

Intech

Año: 2012; p. 21 - 38

Erythrocytes are produced by a complex and finely regulated process of erythropoiesis. Itstarts with a pluripotential stem cell that, in addition of its self replication capacity, can giverise to separate cell lineages. Erythropoiesis passes from the stem cell through themultipotent progenitor CFU-GEMM (colony-forming unit granulocyte erythroid monocyteand megakaryocyte), and then BFU-E (burst-forming unit erythroid) and CFU-E (colonyforming unit eryhtroid), to the first recognizable erythrocyte precursor in the bone marrow,the pronormoblast. This cell gives rise to a series of progressively smaller normoblasts withincreasing content of hemoglobin. The nucleus is finally extruded from the late normoblastleading to mature red blood cell through the reticulocyte stage. Erythropoiesis ends with themature circulating red cell, which is a non-nucleated biconcave disc, performing its functionof oxygen delivery. In this process, the glycoprotein hormone erythropoietin has beenknown as the major humoral regulator of red cell production. It is now well established thaterythropoietin stimulates erythropoiesis, at least in part, by protecting erythroblasts fromapoptosis.Human mature erythrocytes are terminally differentiated cells that are devoid ofmitochondria, as well as of nucleus and other organelles. In circulation, the red cell isconstantly tested for its capacity to undergo marked cellular deformation. This ability tochange its shape is essential for optimal cell function, since the resting diameter of thehuman red cell far exceeds that of the capillaries and splenic endothelial slits through whichit must pass (Mohandas & Groner, 1989). A two dimensional network of proteins interactingbetween transmembrane location and cytoplasmic surface of the plasma membrane givesthe red blood cell its properties of elasticity and flexibility that allows the success of thisjourney.The mature erythrocyte is unable to self-repair and has no capacity to synthesize proteins.Therefore, its lifespan is finite and is shortened further when the cell?s environment becomeshostile or when the erythrocyte?s ability to cope with damaging extracellular influencesbecomes impaired. The erythrocyte limited lifespan implies that, as in other cells, life anddeath are well regulated for erythrocytes, in spite of their lack of capacity for proteinsynthesis (Bosman et al., 2005).In the present review, we aim to show updated information concerning erythrocyte death inorder to contribute to the understanding of the physiopathological relationship of thisprocess with the development of anemia.