期刊
BONE RESEARCH
卷 6, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41413-018-0035-6
关键词
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资金
- National Natural Science Foundation (NNSF) Key Research Program in Aging [91749204]
- National Natural Science Foundation of China [81871099, 31370958, 81701364, 81771491, 81501052]
- Shanghai Municipal Science and Technology Commission Key Program [15411950600, 18431902300]
- Municipal Human Resources Development Program for Outstanding Leaders in Medical Disciplines in Shanghai [2017BR011]
RANKL signaling is essential for osteoclastogenesis. Its role in osteoblastic differentiation and bone formation is unknown. Here we demonstrate that RANK is expressed at an early stage of bone marrow mesenchymal stem cells (BMSCs) during osteogenic differentiation in both mice and human and decreased rapidly. RANKL signaling inhibits osteogenesis by promoting beta-catenin degradation and inhibiting its synthesis. In contrast, RANKL signaling has no significant effects on adipogenesis of BMSCs. Interestingly, conditional knockout of rank in BMSCs with Prx1-Cre mice leads to a higher bone mass and increased trabecular bone formation independent of osteoclasts. In addition, rank(flox/flox): Prx1-Cre mice show resistance to ovariectomy-(OVX) induced bone loss. Thus, our results reveal that RANKL signaling regulates both osteoclasts and osteoblasts by inhibition of osteogenic differentiation of BMSCs and promotion of osteoclastogenesis.
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