Abstract
Galectin-3 (gal-3) is a β-galactoside binding protein present in multivalent complexes with an extracellular matrix and with cell surface glycoconjugates. In this context, it can deliver a variety of intracellular signals to modulate cell activation, differentiation and survival. In the hematopoietic system, it was demonstrated that gal-3 is expressed in myeloid cells and surrounding stromal cells. Furthermore, exogenous and surface gal-3 drive the proliferation of myeloblasts in a granulocyte-macrophage colony-stimulating factor (GM-CSF)-dependent manner. Here, we investigated whether gal-3 regulates the formation of myeloid bone marrow compartments by studying galectin-3 -/- mice (gal-3 -/-) in the C57BL/6 background. The bone marrow histology of gal-3 -/- mice was significantly modified and the myeloid compartments drastically disturbed, in comparison with wild-type (WT) animals. In the absence of gal-3, we found reduced cell density and diaphyseal disorders containing increased trabecular projections into the marrow cavity. Moreover, myeloid cells presented limited capacity to differentiate into mature myeloid cell populations in gal-3 -/- mice and the number of hematopoietic multipotent progenitors was increased relative to WT animals. In addition, bone marrow stromal cells of these mice had reduced levels of GM-CSF gene expression. Taken together, our data suggest that gal-3 interferes with hematopoiesis, controlling both precursors and stromal cells and favors terminal differentiation of myeloid progenitors rather than proliferation.
Original language | English (US) |
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Pages (from-to) | 427-437 |
Number of pages | 11 |
Journal | Cell and Tissue Research |
Volume | 346 |
Issue number | 3 |
DOIs | |
State | Published - Dec 2011 |
Keywords
- Galectin-3
- Hematopoiesis
- Myeloid differentiation
ASJC Scopus subject areas
- Pathology and Forensic Medicine
- Cell Biology
- Histology