1. Omentin-1 attenuates arterial calcification and bone loss in osteoprotegerin-deficient mice by inhibition of RANKL expression.
- Author
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Xie, Hui, Xie, Ping-Li, Wu, Xian-Ping, Chen, San-Mei, Zhou, Hou-De, Yuan, Ling-Qing, Sheng, Zhi-Feng, Tang, Si-Yuan, Luo, Xiang-Hang, and Liao, Er-Yuan
- Subjects
ADIPOKINES ,CALCIFICATION ,TUMOR necrosis factors ,LABORATORY mice ,GENE expression ,ADIPOSE tissues ,OBESITY ,VASCULAR smooth muscle ,BONE metabolism - Abstract
Aims Omentin-1 (also known as intelectin-1) is a recently identified visceral adipose tissue-derived cytokine that is inversely related to obesity. Our previous study showed that omentin-1 inhibits osteoblastic differentiation of calcifying vascular smooth muscle cells (CVSMCs) in vitro. This study was undertaken to investigate the effects of omentin-1 on arterial calcification and bone metabolism in vivo. Methods and results In vitro, omentin-1 stimulated production of osteoprotegerin (OPG) and inhibited production of receptor activator for nuclear factor κB ligand (RANKL) in both CVSMCs and osteoblasts. In vivo, adenovirus-mediated over-expression of omentin-1 attenuated arterial calcification and bone loss in OPG−/− mice. All these in vitro and in vivo actions were abrogated by blockade of the PI3K–Akt signalling pathway. Furthermore, omentin-1 reduced serum levels of RANKL, tartarate-resistant acid phosphatase-5b and osteocalcin, all of which are increased dramatically in OPG−/− mice. Conclusion These data suggest that omentin-1 ameliorates arterial calcification and bone loss in vivo through the regulation of the RANK signalling pathway. [ABSTRACT FROM PUBLISHER]
- Published
- 2011
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