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Computational modeling and analysis of iron release from macrophages
Alka A Potdar1, Joydeep Sarkar2, Nupur K Das3
1Department of Biomedical Engineering, Case Western Reserve University, Cleveland, Ohio, United States of America; Department of Cellular and Molecular Medicine, Cleveland Clinic, Cleveland, Ohio, United States of America.
Plos Computational Biology
|July 4, 2014
Summary
Iron release from macrophages is crucial for whole-body iron metabolism. A new facilitated-transport model, involving ferroportin (FPN), ceruloplasmin (Cp), and apo-transferrin (Tf), better explains iron release than passive diffusion.
Area of Science:
- Cellular Biology
- Biochemistry
- Physiology
Background:
- Macrophage iron release is a key process in whole-body iron homeostasis.
- Iron is recycled from phagocytosed erythrocytes for erythropoiesis.
- The current passive-gradient model for iron release has limitations.
Purpose of the Study:
- To investigate the detailed mechanism of iron release from macrophages.
- To elucidate the roles of ceruloplasmin (Cp), ferroportin (FPN), and apo-transferrin (Tf) in macrophage iron efflux.
- To quantitatively analyze and compare the passive-gradient and facilitated-transport models of iron release.
Main Methods:
- Experimental investigations of macrophage iron release.
- Mathematical modeling to analyze iron transport mechanisms.
- Quantitative comparison of experimental data with model simulations.
Main Results:
- The passive-gradient model could not adequately explain macrophage iron release.
- A facilitated-transport model involving FPN, Cp, and Tf accurately predicts cellular iron efflux.
- Intracellular FPN transports iron to the membrane, extracellular Cp oxidizes it, and apo-Tf binds the ferric ion.
Conclusions:
- The facilitated-transport model provides a more accurate mechanism for macrophage iron release.
- This model is essential for developing physiologically relevant whole-body iron metabolism models.
- Understanding this process is critical for managing iron homeostasis and related disorders.
