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首页> 外文期刊>Journal of bone and mineral research: the official journal of the American Society for Bone and Mineral Research >Circadian Clock Regulates Bone Resorption in Mice
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Circadian Clock Regulates Bone Resorption in Mice

机译：昼夜节奏调节小鼠的骨吸收

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The circadian clock controls many behavioral and physiological processes beyond daily rhythms. Circadian dysfunction increases the risk of cancer, obesity, and cardiovascular and metabolic diseases. Although clinical studies have shown that bone resorption is controlled by circadian rhythm, as indicated by diurnal variations in bone resorption, the molecular mechanism of circadian clock-dependent bone resorption remains unknown. To clarify the role of circadian rhythm in bone resorption, aryl hydrocarbon receptor nuclear translocator-like (Bmal1), a prototype circadian gene, was knocked out specifically in osteoclasts. Osteoclast-specific Bmal1-knockout mice showed a high bone mass phenotype due to reduced osteoclast differentiation. A cell-based assay revealed that BMAL1 upregulated nuclear factor of activated T cells, cytoplasmic, calcineurin-dependent 1 (Nfatc1) transcription through its binding to an E-box element located on the Nfatc1 promoter in cooperation with circadian locomotor output cycles kaput (CLOCK), a heterodimer partner of BMAL1. Moreover, steroid receptor coactivator (SRC) family members were shown to interact with and upregulate BMAL1: CLOCK transcriptional activity. Collectively, these data suggest that bone resorption is controlled by osteoclastic BMAL1 through interactions with the SRC family and binding to the Nfatc1 promoter. (C) 2016 American Society for Bone and Mineral Research.
机译：昼夜钟控制每天节奏的许多行为和生理过程。昼夜功能障碍增加了癌症，肥胖和心血管和代谢疾病的风险。虽然临床研究表明，骨吸收受昼夜节律控制，如骨吸收的昼夜变化所示，昼夜时钟依赖性骨吸收的分子机制仍然未知。为了澄清昼夜节律在骨吸收中的作用，芳基烃受体核转移仪样（BMAL1），一种原型昼夜基因，特别是在破骨细胞中敲出。由于降低的破骨细胞分化，骨核醛特异性BMAL1敲除小鼠显示出高骨质量表型。基于细胞的测定显示，通过其与位于NFATC1启动子的E-Box元素的结合，BMA11上调活化的T细胞，细胞质，钙磷素依赖性1（NFATC1）转录的核因子，其与位于NFATC1启动子的E-Box元素配合，与昼夜运动输出周期Kaput（时钟），BMA1的异二聚体伴侣。此外，类固醇受体共粘膜（SRC）家族成员被证明与BMA11：时钟转录活动相互作用。总的来说，这些数据表明，通过与SRC系列的相互作用和与NFATC1启动子结合来控制骨吸收的骨吸收控制。 （c）2016年美国骨骼和矿物学学会。

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