期刊
CARDIOVASCULAR RESEARCH
卷 92, 期 2, 页码 296-306出版社
OXFORD UNIV PRESS
DOI: 10.1093/cvr/cvr200
关键词
Omentin-1; Arterial calcification; Bone; Osteoprotegerin; Receptor activator for nuclear factor kappa B ligand
资金
- China National Natural Scientific Foundation [81000122, 81070696, 81070246, 30872708]
- Science and Technology Project of Changsha City [K1009020-31]
- Hunan Provincial Natural Scientific Foundation [100JJ1007]
- Central South University [2010QZZD025]
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 kappa B 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.
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