Related Experiment Video
Updated: Jun 10, 2026

Lentiviral-mediated Knockdown During Ex Vivo Erythropoiesis of Human Hematopoietic Stem Cells
Published on: July 16, 2011
In vitro cytotoxicity of deferoxamine on human marrow haematopoietic progenitors
Z Estrov1, A Cohen, E W Gelfand
1Division of Hematology, Department of Pediatrics, The Hospital for Sick Children, University of Toronto, Toronto, Canada M5G 1X8; Division of Immunology/Rheumatology, Department of Pediatrics, The Hospital for Sick Children, University of Toronto, Toronto, Canada M5G 1X8.
Abstract:
Deferoxamine (DFO), a widely used clinical chelator of ferric iron, was found to inhibit human bone-marrow (BM) stem-cell colony formation as measured by assays on the proliferation of the haematopoietic progenitor cell populations: the granulocyte-macrophage, colony forming unit in culture (CFU-C) lineage and the erythroid lineages-erythroid colony forming unit (CFU-E) and erythroid burst forming unit (BFU-E). DFO (5-20 mum) markedly reduced the proliferation of CFU-C, CFU-E and BFU-E in a dose-dependent fashion, whereas ferrioxamine, the chelated form of DFO, had no effect on colony growth. CFU-E and BFU-E colonies were more sensitive than CFU-C to the growth-inhibitory effect of DFO. The removal of either adherent cells or T lymphocytes or both from the BM did not affect the inhibitory properties of DFO, indicating that DFO interacts directly with the haematopoietic progenitor cells rather than through another cell population. These in vitro findings suggest that DFO may cause myelosuppression if administered to patients whose plasma iron levels are normal or low.
Insights
Deferoxamine (DFO) inhibits human bone marrow stem cell colony formation, affecting key blood cell lineages. This suggests DFO may cause myelosuppression in patients with normal or low iron levels.
Area of Science:
- Hematology
- Stem Cell Biology
- Pharmacology
Background:
- Deferoxamine (DFO) is a clinical chelator for ferric iron.
- Bone marrow (BM) stem cells are crucial for hematopoiesis.
- Understanding DFO's effects on stem cells is important for patient safety.
Purpose of the Study:
- To investigate the in vitro effects of DFO on human bone marrow stem cell proliferation.
- To determine if DFO directly impacts hematopoietic progenitor cells.
Main Methods:
- Assays were used to measure colony formation of granulocyte-macrophage (CFU-C), erythroid colony forming unit (CFU-E), and erythroid burst forming unit (BFU-E).
- DFO's effects were tested in a dose-dependent manner.
- Experiments involved removing adherent cells or T lymphocytes to assess DFO's interaction site.
Main Results:
- DFO significantly inhibited CFU-C, CFU-E, and BFU-E proliferation in a dose-dependent manner.
- Ferrioxamine, the chelated form of DFO, did not affect colony growth.
- Erythroid progenitor cells (CFU-E, BFU-E) were more sensitive to DFO than CFU-C.
- DFO's inhibitory effects were independent of adherent cells or T lymphocytes, indicating direct action on progenitor cells.
Conclusions:
- DFO directly inhibits human bone marrow stem cell proliferation in vitro.
- The findings suggest a potential risk of myelosuppression with DFO administration in patients with normal or low plasma iron levels.

