Galectin-3 inhibits granulocyte-macrophage colony-stimulating factor (GM-CSF)-driven rat bone marrow cell proliferation and GM-CSF-induced gene transcription

• Published in: Immunobiology (1979) 1997-06, Vol.197 (1), p.97-109
• Main Authors: Krugluger, Walter, Frigeri, Luciano G., Lucas, Trevor, Schmer, Michael, Förster, Othmar, Liu, Fu-Tong, Boltz-Nitulescu, George
• Format: Article
• Language: English
• Subjects: Animals; Antigens, Differentiation - genetics; Antigens, Differentiation - metabolism; Antigens, Differentiation - pharmacology; Bone Marrow - drug effects; Bone Marrow - metabolism; Bone Marrow Cells; Cell Division - drug effects; Galectin 3; Gene Expression Regulation - drug effects; Granulocyte-Macrophage Colony-Stimulating Factor - physiology; Polymerase Chain Reaction; Protein Binding - genetics; Rats; Rats, Inbred Lew; Recombinant Proteins - metabolism; Transcription, Genetic - drug effects
• ISSN: 0171-2985; 1878-3279
• DOI: 10.1016/S0171-2985(97)80060-5

The expression of galectin-3 (formerly known as IgE-binding protein or Mac-2) in rat bone marrow (BM) was investigated by FACS, immunocytochemical and immunoblot analysis. The functional significance of rat recombinant galectin-3 on mouse recombinant granulocyte-macrophage colony-stimulating factor (GM-CSF)-driven proliferation of macrophage progenitors and gene transcription was further examined. Immunocytochemical analysis of in situ BM sections demonstrated galectin-3 in myelopoietic cells and surrounding stroma, whereas erythropoietic and lymphopoietic environments essentially lacked galectin-3 expression. FACS analysis demonstrated that incubation of freshly isolated BMC with lactose, a competing ligand for galectin-3 binding to glycoconjugates, decreased binding of antigalectin antibodies to cells primarily expressing the myeloid antigen recognized by mAb His-54. Similarly, lectin-mediated binding of exogenous galectin-3 to myeloid lineage cells was also demonstrated. Immunoblot analysis of BM eluates demonstrated galectin-3 both in the extracellular matrix and in a lactose elutable form, bound to the surface of BMC. [ 3H]Thymidine incorporation studies on BMC cultured in the presence of galectin-3 demonstrated suppression of GM-CSF-induced proliferation by galectin-3. In addition, differential display analysis of immediate early gene expression in BMC cultured in the presence of galectin-3 revealed a 76.2% inhibition of GM-CSF-induced gene transcription by galectin-3 assessed by the number of PCR-fragments generated. Our data suggest a role for galectin-3 in the organization of myelopoietic compartments in rat BM and regulation of the action of growth factors on myelopoietic precursor cells.