Inflammatory processes play a role in osteoclastogenesis. C-reactive protein (CRP), an acute phase reactant that reflects different degree of inflammation. More recently, accumulating evidence suggest that CRP is not only an inflammatory marker but also direct cause of diseases. Therefore, we examined the direct effects of CRP on osteoclast formation using RAW 264.7 cells. CRP significantly inhibited RANKL-induced TRAP-positive multinucleated cell formation in RAW 264.7 cell cultures in a dose-dependent manner (1 ug/ml to 30 ug/ml). We observed suppression of ERK and p38 MAPKs induced by RANKL in western blotting after CRP treatment in RAW 264.7 cells. Furthermore, CRP increased TNFa and IFNb expression in RAW 264.7 cells. OxPAPC, inhibitor of toll-like receptor signaling, decreased CRP-induced TLR signaling and expression of TNFα and IFNβ. Furthermore, OxPAPC reduced CRP-induced inhibition of TRAP-positive multinucleated cell formation. These data indicated that CRP may have a direct role on osteoclastogenesis via MAPK and TLR-dependent pathway.
17 May 2014 - 20 May 2014