RANKL from Bone Marrow Adipocytes Regulates Osteoclast Formation and Bone Loss in Mice
Posted 12 Sep 2020
bioRxiv DOI: 10.1101/2020.09.12.294348
Posted 12 Sep 2020
Receptor activator of NF-κB ligand (RANKL) is essential for osteoclast formation. The cellular source of RANKL for osteoclastogenesis has not been fully uncovered. Bone marrow (BM) adipocytes derived from bone marrow mesenchymal stromal cells (BMSCs) express RANKL. Here we demonstrated that the AdipoqCre could target bone marrow adipocytes. We crossed the AdipoqCre mice with ranklfl/fl mice to conditionally delete RANKL from BM adipocytes. Conditional deletion of RANKL increased cancellous bone mass in the long bones of growing and adult mice by reducing the formation of trabecular osteoclasts and inhibiting bone resorption but did not affect cortical bone thickness or resorption of calcified cartilage. AdipoqCre ; ranklfl/fl mice exhibited resistance to estrogen deficiency and rosiglitazone (ROS) induced trabecular bone loss but showed bone loss induced by unloading. BM adipocytes therefore represent an essential source of RANKL for the formation of trabecula osteoclasts and resorption of cancellous bone during remodeling. ### Competing Interest Statement The authors have declared no competing interest.
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