Mouse anti-Human Galectin-3 Monoclonal antibody, clone 10D5

Background/Aim: The effects of O-linked P-Nacetyl-D-glucosamine (O-GlcNAc) transferase (OGT) and O-GlcNAcase (OGA) inhibitors on galectin gene expression profiles were examined in MCF7, HT-29, and HL-60 cancer cell lines. Materials and Methods: Cell cultures were treated for 24 h with OGA inhibitor thiamet G or OGT inhibitor 2-acetamido-1,3,4,6-tetra-O-acetyl-2-deoxy-5-thio-a-D- glucopyranose, and global O-GlcNAc levels and expression of galectin genes were determined using an immunodot blot assay and real-time quantitative polymerase chain reaction. Results: Two galectin genes, LGALS3 in MCF7 cells and LGALSJ2 in HL-60 cells, were up-regulated by O-GlcNAc, whereas other cell-specific galectins were unresponsive to changes in O-GlcNAc level. Of interest, basal levels of O-GlcNAc in resting HL-60 and HT-29 cells were significantly higher than those in cells differentiated into neutrophilic or enterocytic lineages, respectively. Conclusion: O-GlcNAcmediated signaling pathways may be involved in regulating the expression of only a limited number of galectin genes. Additional O-GlcNAc-dependent mechanisms may work at the protein level (galectin secretion and intracellular localization) and warrant further investigation.

Background and Purpose: Galectin-3, a P-galactoside binding lectin, acts as a strong pro-inflammatory signal. Many immunomodulatory drugs affect signaling pathways that comprise transcription factors involved in the regulation of galectin-3 gene (LGALS3) expression. The aim of our study was to investigate the effects of steroidal anti-inflammatory drugs (hydrocortisone - HC and dexamethasone - Dex) on the expression of galectin-3, both at the mRNA and the protein level. Materials and Methods: The human monocytic cell line THP-1 was exposed to various concentrations of HC (0.1, 1, 5 and 10 mu M) and Dex (0.1, 1, 10 and 100 nM) during 1, 3, 5,24, 48 or 72 hrs. Relative RT-PCR method and GeneScan analysis software were used for assessing galectin-3 mRNA level and chemiluminescent-western blot analysis for measuring galectin-3 level. Results: The results showed that both drugs in all applied concentrations halved the galectin-3 mRNA level already after I h of exposure. The decrease continued and after 72 hours the mRNA level dropped to 3.8-15.4% of the initial value. The protein expression of galectin-3 did not follow the same pattern; although both drugs in all applied concentration provoked the reduction in galectin-3 level, the decrease was observed not until 48 and 72 hours of exposure, when galectin-3 level fell to 7176 to 38% of the initial value, respectively. Conclusion: Steroidal anti-inflammatory drugs cause the reduction in both gene and protein expression of galectin-3, but the intensity of changes and the time of their appearance strongly depend on the type and concentration of the drug.