Finally, syndecan-2 functions as an inhibitor of Wnt-β-catenin–T-cell factor signaling pathway, activating glycogen synthase kinase 3 and then decreasing the Wnt-dependent production of Wnt ligands and R-spondin. However, syndecan-2 specifically promoted the vasculature characterized by high expression of CD31 and Endomucin in 6-week-old transgenic mice, but this was reduced in 12-week-old transgenic mice. Indeed, syndecan-2 overexpression increased apoptosis of mesenchymal precursors within the bone marrow. Increased proteoglycan expression at the bone surface resulted in decreased osteoblastic and osteoclastic precursors in bone marrow. Osteoblast activity was not modified in the transgenic mice, but bone formation was decreased in 4-month-old transgenic mice because of reduced osteoblast number. Syndecan-2 overexpression reduced the expression of receptor activator of NF- kB ligand (RANKL) in bone marrow cells and strongly inhibited bone resorption. Bone mass was increased in these transgenic mice. We used a transgenic mouse model with high syndecan-2 expression in osteoblasts to enrich the bone surface with cellular GAGs. Syndecan-2 is a membrane heparan sulfate proteoglycan that is associated with osteoblastic differentiation. The osteogenic properties of matrix glycosaminoglycans (GAGs) have been explored however, the functions of GAGs at the surface of bone-forming cells are less documented. Stimulating bone formation is an important challenge for bone anabolism in osteoporotic patients or to repair bone defects.
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