osteoclast precursor

This has the effect of inhibiting the differentiation of the osteoclast precursor into a mature osteoclast.

During the maturation of osteoclast precursors, groups of podosomes form higher ordered ring structures which ultimately coalesce into a band about the cell periphery.

These membrane bound proteins are produced by neighbouring stromal cells and osteoblasts, thus requiring direct contact between these cells and osteoclast precursors.

M-CSF is essential for macrophage maturation, but formation of osteoclasts also requires contact between osteoclast precursors and stromal cells or osteoblasts [ 23].

In the present study, we demonstrate that early exposure to RANKL renders osteoclast precursors resistant to the effects of IFN-γ, including inhibition of osteoclastogenesis.

In osteoclast precursors, RANKL induced increasing TRAP expression until virtually 100% of mononuclear cells were highly TRAP-positive.

Surface RANKL on osteoblasts as well as secreted RANKL provide necessary signals for osteoclast precursors to differentiate into osteoclasts.

Conclusion We have demonstrated, using in vitro methods, that osteoclast precursors exposed to RANKL for 1-2 days can be rendered resistant to maximal osteoclast-inhibitory doses of IFN-γ.

More specifically, miR-223 expression suppresses the differentiation of osteoclast precursors into osteoclast thus making it a potential viable therapeutic target for a range of bone metabolic disorders with excess osteoclast activity.

His work was the first to show that the human osteoclast shares specific surface antigens with macrophages and that the mononuclear human osteoclast precursor circulates in the (CD14+) monocyte fraction.

Dock5 has been identified as a crucial signalling protein in osteoclasts, and suppression of Dock5 expression with shRNA has been shown to inhibit survival and differentiation of osteoclast precursor cells.

OPG binding to RANKL on osteoblast/stromal cells, blocks the RANKL-RANK ligand interaction between osteoblast/stromal cells and osteoclast precursors.

These data may help explain the contradictory findings regarding the effects of IFN-γ as an inhibitor of osteoclastogenesis, and also suggest a model of erosive disease in the presence of IFN-γ whereby osteoclast precursors are exposed to RANKL before they enter the IFN-γ-rich environment.