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Omentin-1 prevents inflammation-induced osteoporosis by downregulating the pro-inflammatory cytokines #MMPMID29619269
Rao SS; Hu Y; Xie PL; Cao J; Wang ZX; Liu JH; Yin H; Huang J; Tan YJ; Luo J; Luo MJ; Tang SY; Chen TH; Yuan LQ; Liao EY; Xu R; Liu ZZ; Chen CY; Xie H
Bone Res 2018[]; 6 (ä): ä PMID29619269show ga
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-? (TNF-?), we determined that recombinant omentin-1 reduces the production of pro-inflammatory factors in the TNF-?-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 pro-inflammatory cytokines.