Bone marrow adipoq+ cell population controls bone mass via sclerostin in mice
Huanqing Gao, Yiming Zhong, Sixiong Lin, Qinnan Yan, Xuenong Zou, Guozhi Xiao
Abstract
The comorbidity of obesity and osteoporosis illustrates the communication and coordination of adipose and bone tissues. Leptin and adiponectin derived from adipocytes regulate osteoblast formation and function to impact bone mass through direct and indirect mechanisms. 1 It is known that bone marrow adipocytes (BMA) can control bone mass by modulating the bone morphogenetic protein (BMP) and other signaling pathways. BMAs can secret soluble factors, which impact osteoblasts, osteoclasts, and osteocytes. 2 Sclerostin is a potent inhibitor of bone acquisition that antagonizes Wnt/β-catenin signaling. Deleting sclerostin was recently reported to protect against cardiovascular disease. 3 Furthermore, neutralizing monoclonal antibodies against sclerostin increase bone mass and are utilized to treat osteoporosis. Previous studies revealed that global ablation of sclerostin increased both trabecular and cortical bone mass 4 and that sclerostin produced by the osteocytes located in the bone matrix negatively regulated bone mass in mice. 5 However, it is not known whether sclerostin derived from other cell types also contributes to bone formation.