Abstract
Human red blood cells (RBCs) are normally phagocytized by macrophages of splenic and hepatic sinusoids at 120 days of age. The destruction of RBCs is ultimately controlled by antagonist effects of phosphatidylserine (PS) and CD47 on the phagocytic activity of macrophages. In this work, we introduce a conceptual model that explains RBC lifespan as a consequence of the dynamics of these molecules. Specifically, we suggest that PS and CD47 define a molecular algorithm that sets the timing of RBC phagocytosis. We show that significant changes in RBC lifespan described in the literature can be explained as alternative outcomes of this algorithm when it is executed in different conditions of oxygen availability. The theoretical model introduced here provides a unified framework to understand a variety of empirical observations regarding RBC biology. It also highlights the role of RBC lifespan as a key element of RBC homeostasis.
Highlights
The population of red blood cells (RBCs) in the organism must remain within definite limits in order to ensure the oxygenation of body tissues and to maintain adequate values of blood pressure and viscosity
We suggest that neocytolysis and erythrophagocytosis should not be considered as independent mechanisms, but as alternative outcomes of the algorithm of RBC lifespan determination
We postulate that quantitate aspects of these dynamics explain how RBC lifespan variations are related to oxygen homeostasis
Summary
The population of red blood cells (RBCs) in the organism must remain within definite limits in order to ensure the oxygenation of body tissues and to maintain adequate values of blood pressure and viscosity This is achieved by means of homeostatic mechanisms that control the ratio between cell production and destruction and compensate any unbalance between oxygen supply and demand by increasing or reducing the number of circulating RBCs [1,2]. Higher sensitivities to OS correlate with shorter lifespans [20] This observation has been interpreted as evidence of an active mechanism that would set RBC lifespan by fine-tuning the expression of genes that confer resistance to OS in erythroid precursors [16,20]. We will show that these phenomena emerge as alternative outcomes of the same mechanisms working under different conditions of oxygen availability
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