Abstract
RANKL-RANK signaling regulates osteoblast differentiation and bone formation
Highlights
TNFRSF11A) drives osteoclast development as the crucial signaling pathway.[1–3] accumulating evidence implies that osteoblastic receptor activator of nuclear factor-kappaB ligand (RANKL) regulates osteoblastogenesis.[4–6] The studies “RANKL signaling in bone marrow mesenchymal stem cells negatively regulates osteoblastic bone formation” by Chen et al in the current issue of Bone Research, and “Coupling of bone resorption and formation by RANKL reverse signalling” by Yuki Ikeuchi et al in Nature (2018;561:195–200) reveal that RANKLRANK signaling regulates osteoblastogenesis in addition to its role in osteoclastogenesis
Chen et al demonstrate that RANK is expressed in bone marrow mesenchymal stem cells (BMSCs) and is decreased during osteogenic differentiation
This study reveals that RANKL forward signaling in BMSCs functions as a negative regulator in osteoblast differentiation and bone formation (Fig. 1)
Summary
TNFRSF11A) drives osteoclast development as the crucial signaling pathway.[1–3] accumulating evidence implies that osteoblastic RANKL regulates osteoblastogenesis.[4–6] The studies “RANKL signaling in bone marrow mesenchymal stem cells negatively regulates osteoblastic bone formation” by Chen et al in the current issue of Bone Research, and “Coupling of bone resorption and formation by RANKL reverse signalling” by Yuki Ikeuchi et al in Nature (2018;561:195–200) reveal that RANKLRANK signaling regulates osteoblastogenesis in addition to its role in osteoclastogenesis. Chen et al demonstrate that RANK is expressed in bone marrow mesenchymal stem cells (BMSCs) and is decreased during osteogenic differentiation. RANK silencing significantly promotes, while overexpression suppresses, the osteoblast differentiation of Mice with a conditional knock-out of RANK in MSCs (Prx1-Cre: RANKflox/flox) show a significant increase of osteoblast differentiation and bone formation.
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