Abstract
Receptor activator of NF-κB ligand (RANKL)/ Receptor activator of NF-κB (RANK) engaged activation of p38 Mitogen-activated protein kinase (p38), extracellular signal-regulated kinase (ERK1/2) on an osteoclast precursor cells. Phosphatidylinositol 3-kinase (PI 3-K) is critical to activation of cellular functions, which is activation of cell viability. However, It is not clarified about the relation of these kinase in the cascade of soluble RANKL (sRANKL) differentiation signaling.
We investigated the role of PI 3-K on RANKL-mediated mouse leukemic monocyte cell line RAW264 cells differentiation into osteoclast cells. LY294002 blocked the differentiation into osteoclast cells induced by sRANKL in a dose dependent manner. Western analysis has shown that the posphorylation of p38 and ERK1/2 were blocked by LY294002 in a dose dependent manner.
These results suggest that RANKL/RANK mediated phosphorylation of p38 and ERK1/2 and a differentiation into osteoclast cells depend on PI 3-K.
