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Updated: Nov 20, 2025

Proliferation and Differentiation of Murine Myeloid Precursor 32D/G-CSF-R Cells
Published on: February 21, 2018
Dietary magnesium restriction affects hematopoiesis and triggers neutrophilia by increasing STAT-3 expression and
Fabiana da Silva Lima1, Edson Naoto Makiyama2, Araceli Aparecida Hastreiter2
1Department of Food and Experimental Nutrition, Faculty of Pharmaceutical Sciences, University of São Paulo, São Paulo, Brazil.
Background & Aims:
Magnesium (Mg2+) is able to modulate the differentiation and proliferation of cells. Mg2+ restriction can trigger neutrophilia, but the processes that result in this change have yet to be investigated and are not fully understood. Hematopoiesis is a complex process that is regulated by many factors, including cytokines and growth factors, and is strongly influenced by nutrient availability. In this context, our objective was to investigate the impact of the short-term restriction of dietary Mg2+ on bone marrow hematopoietic and peripheral blood cells, especially in processes related to granulocyte differentiation and proliferation.
Methods:
Male C57BL/6 mice were fed a Mg2+ restricted diet (50 mg Mg2+/kg diet) for 4 weeks. Cell blood count and bone marrow cell count were evaluated. Bone marrow cells were also characterized by flow cytometry. Gene expression and cytokine production were evaluated, and a colony-forming cell assay related to granulocyte differentiation and proliferation was performed.
Results:
Short-term dietary restriction of Mg2+ resulted in peripheral neutrophilia associated with an increased number of granulocytic precursors in the bone marrow. Additionally, Mg2+ restriction resulted in an increased number of granulocytic colonies formed in vitro. Moreover, the Mg2+ restricted group showed increased expression of CSF3 and CEBPα genes as well as increased production of G-CSF in association with increased expression of STAT3 protein.
Conclusion:
Short-term dietary restriction of Mg2+ induces granulopoiesis by increasing G-CSF production and activating the CEBPα and STAT-3 pathways, resulting in neutrophilia in peripheral blood.
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