RANKL cytokine enhances TNF-induced osteoclastogenesis independently of TNF receptor associated factor (TRAF) 6 by degrading TRAF3 in osteoclast precursors.

ABSTRACT: Cytokines, including receptor activator of nuclear factor κB ligand (RANKL) and TNF, induce increased osteoclast (OC) formation and bone loss in postmenopausal osteoporosis and inflammatory arthritides. RANKL and TNF can independently induce OC formation in vitro from WT OC precursors via TNF receptor-associated factor (TRAF) adaptor proteins, which bind to their receptors. Of these, only TRAF6 is required for RANKL-induced osteoclastogenesis in vitro However, the molecular mechanisms involved remain incompletely understood. Here we report that RANKL induced the formation of bone-resorbing OCs from TRAF6^-/- OC precursors when cultured on bone slices but not on plastic. The mechanisms involved increased TNF production by TRAF6^-/- OC precursors resulting f

SUBMITTER: Yao Z 

PROVIDER: S-EPMC5473222 | biostudies-literature | 2017 Jun

REPOSITORIES: biostudies-literature