Journal
BONE RESEARCH
Volume 6, Issue -, Pages -Publisher
SPRINGERNATURE
DOI: 10.1038/s41413-018-0012-0
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Funding
- Excellent Young Scientist Foundation of the National Natural Science Foundation of China [81522012]
- National Natural Science Foundation of China [81670807, 81600699, 81702237, 81701383, 81400858]
- Thousand Youth Talents Plan of China [D1119003]
- Hunan Youth Talent Project [2016RS3021]
- Innovation Driven Project of Central South University [2016CX028]
- Youth Foundation of Xiangya Hospital in Central South University [2016Q10]
- Fundamental Research Funds for the Central Universities of Central South University [2017zzts032, 2017zzts014]
- Hunan Province Natural Science Foundation of China [2017JJ3501]
- China Postdoctoral Science Foundation [2017M612596]
- Natural Science Foundation for Distinguished Yong Scholars of Guangdong Province [2016A030306051]
- National Basic Research Program of China (973 Program) [2014CB942903]
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Osteoporosis is a frequent complication of chronic inflammatory diseases and increases in the pro-inflammatory cytokines make an important contribution to bone loss by promoting bone resorption and impairing bone formation. Omentin-1 is a newly identified adipocytokine that has anti-inflammatory effects, but little is known about the role of omentin-1 in inflammatory osteoporosis. Here we generated global omentin-1 knockout (omentin-1-/-) mice and demonstrated that depletion of omentin-1 induces inflammatory bone loss-like phenotypes in mice, as defined by abnormally elevated pro-inflammatory cytokines, increased osteoclast formation and bone tissue destruction, as well as impaired osteogenic activities. Using an inflammatory cell model induced by tumor necrosis factor-alpha (TNF-alpha), we determined that recombinant omentin-1 reduces the production of proinflammatory factors in the TNF-alpha-activated macrophages, and suppresses their anti-osteoblastic and pro-osteoclastic abilities. In the magnesium silicate-induced inflammatory osteoporosis mouse model, the systemic administration of adenoviral-delivered omentin-1 significantly protects from osteoporotic bone loss and inflammation. Our study suggests that omentin-1 can be used as a promising therapeutic agent for the prevention or treatment of inflammatory bone diseases by downregulating the proinflammatory cytokines.
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