SLAT Negatively Regulates RANKL-Induced Osteoclast Differentiation (original) (raw)

“…Its regulation mechanism is reported to act through its differential regulation of transforming growth factor (TGF)‐β and bone morphogenetic protein (BMP) bioavailability in bone, where both TGF‐β and BMP signaling pathways play a critical role in bone development. Differentially expressed in FDCP 6 homolog ( DEF6 ) at 6p21.31 modulates RANKL‐induced osteoclast differentiation in vitro and in vivo . DEF6 deficiency enables TNF‐alpha alone to induce osteoclastogenesis in the absence of RANKL, and it markedly enhances TNF‐α–induced osteoclastogenesis and bone resorption .…”

Section: Resultsmentioning

“…Although the mechanisms that contribute to the bone resorption in these mice with complex autoimmunity have not been fully elucidated, these data suggest potential involvement of Def6 in pathologic bone resorption. Def6 was reported to modulate RANKL-induced osteoclast differentiation in vitro (41). However, the role of Def6 in vivo especially bone erosion in inflammatory conditions and the underlying molecular mechanisms have not been delineated.…”

Section: Introductionmentioning

“…Murine osteoclasts were prepared from bone marrow cells as previously described ( Youn et al, 2013 ). Murine bone marrow cells were cultured in α-MEM (HyClone Laboratories) containing 10% FBS (HyClone Laboratories) with M-CSF (20 ng/ml) for 3 days.…”

Section: Methodsmentioning