Changes

Upon the secretion of erythropoietin by the peritubular fibroblasts into systemic circulation, the hormone travels in the bloodstream until it reaches the bone marrow. EPO stimulates the production of mature erythrocytes by mediating the survival, proliferation and differentiation of unipotent erythroid progenitor cells , called erythroblasts. When EPO binds onto erythropoietin receptors in the bone marrow, the JACK2 (Janus Kinase 2) cascade is initiated, thereby protecting the erythroid progenitor cells from apoptosis . Thus, the viability of the erythroblasts is preserved, and this is of great importance because these progenitor cells are the precursors to the mature erythrocytes. Consequently, the erythroblast can undergo maturation. The progenitor cell loses its nucleus, and most of its intracellular membranes are degraded; the now non-nucleated form of the cell, termed a reticulocyte, then loses its lysosomes, thus preventing any further synthesis of oxygen. At this stage, the cell is an erythrocyte and can enter circulation. It is clear, therefore, that reduced EPO secretion can lead to ischaemia. During chronic renal disease, EPO secretion is significantly surpressed. The application of genetic engineering and the use of recombinant DNA, however, have allowed the in vitro production of EPO, known as Harish Recombinant EPO (rhEPO). rhEPO has shown great promise in treating and preventing ischaemia in patients suffering from chronic renal disease.

Upon the secretion of erythropoietin by the peritubular fibroblasts into systemic circulation, the hormone travels in the bloodstream until it reaches the bone marrow. EPO stimulates the production of mature erythrocytes by mediating the survival, proliferation and differentiation of unipotent erythroid progenitor cells , called erythroblasts. When EPO binds onto erythropoietin receptors in the bone marrow, the JACK2 (Janus Kinase 2) cascade is initiated, thereby protecting the erythroid progenitor cells from apoptosis . Thus, the viability of the erythroblasts is preserved, and this is of great importance because these progenitor cells are the precursors to the mature erythrocytes. Consequently, the erythroblast can undergo maturation. The progenitor cell loses its nucleus, and most of its intracellular membranes are degraded; the now non-nucleated form of the cell, termed a reticulocyte, then loses its lysosomes, thus preventing any further synthesis of oxygen. At this stage, the cell is an erythrocyte and can enter circulation. It is clear, therefore, that reduced EPO secretion can lead to ischaemia. During chronic renal disease, EPO secretion is significantly surpressed. The application of genetic engineering and the use of recombinant DNA, however, have allowed the in vitro production of EPO, known as Harish Recombinant EPO (rhEPO). rhEPO has shown great promise in treating and preventing ischaemia in patients suffering from chronic renal disease.