Bone formation, mineralization and remodelling is dependent on the activity of osteoblasts and osteoclasts. While many genes support bone development, their specific functions in the different stages of cell differentiation and maturation are often unknown. Galectin-1 (LGALS1) has roles in tumour angiogenesis and immune regulation but also enhances osteoblast differentiation of MSCs. This study aimed to elucidate the role of LGALS1 in the osteogenesis of Saos2 cells. We demonstrated that Saos2 cells have a gene expression profile representing a mature osteoblast stage that shifts to an osteocyte-like profile under osteogenic conditions. We modulated LGALS1 using stable transfection to overexpress LGALS1 and lentiviral transduction of a short-hairpin RNA to knockdown LGALS1. LGALS1 overexpression significantly reduced cell viability under basal culture conditions and significantly reduced mineralisation after 21 of osteogenic culture. Knockdown of LGALS1 also significantly reduced cell viability under basal culture but following osteogenic culture a significant increase in mineralization was observed. No effect on collagen deposition was seen following either knockdown or overexpression, suggesting that LGALS1 is involved in negatively regulating mineralisation. Osteogenic gene expression demonstrated few significant changes when LGALS1 was overexpressed. In contrast, knocking down LGALS1 resulted in many significant changes in osteogenic gene expression under both basal and osteogenic culture conditions. However, there was no clear correlation between the effect on gene expression and the increase in mineralisation. This study demonstrated a novel role of LGALS1 in mature osteoblast-like cells. Further investigation into the regulatory pathways is warranted.
Ross et al. (Wed,) studied this question.