TY - JOUR
T1 - The bone marrow compartment is modified in the absence of galectin-3
AU - Brand, C.
AU - Oliveira, F. L.
AU - Ricon, L.
AU - Fermino, M. L.
AU - Boldrini, L. C.
AU - Hsu, D. K.
AU - Liu, Fu-Tong
AU - Chammas, R.
AU - Borojevic, R.
AU - Farina, M.
AU - El-Cheikh, M. C.
PY - 2011/12
Y1 - 2011/12
N2 - 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.
AB - 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.
KW - Galectin-3
KW - Hematopoiesis
KW - Myeloid differentiation
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U2 - 10.1007/s00441-011-1276-5
DO - 10.1007/s00441-011-1276-5
M3 - Article
C2 - 22120666
AN - SCOPUS:84856740977
VL - 346
SP - 427
EP - 437
JO - Zeitschrift für Zellforschung und mikroskopische Anatomie (Vienna, Austria : 1948)
JF - Zeitschrift für Zellforschung und mikroskopische Anatomie (Vienna, Austria : 1948)
SN - 0302-766X
IS - 3
ER -