Deficiency of circadian clock protein BMAL1 in mice results in a low bone mass phenotype
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- 作者：William E. Samsaa ; samsa.william@gmail.com" class="auth_mail" title="E-mail the corresponding author ; Amit Vasanjib ; avasanji@image-iq.com" class="auth_mail" title="E-mail the corresponding author ; Ronald J. Midurab ; midurar@ccf.org" class="auth_mail" title="E-mail the corresponding author ; Roman V. Kondratova ; r.kondratov@csuohio.edu" class="auth_mail" title="E-mail the corresponding author
- 关键词：BMAL1 ; Brain and Muscle ARNT-Like Protein 1 ; MSCs ; Mesenchymal Stem Cells ; CLOCK ; Circadian Locomotor Output Cycles Kaput ; Per1 ; Period 1 ; Per2 ; Period 2 ; Cry1 ; Cryptochrome 1 ; Cry2 ; Cryptochrome 2 ; Rev-Erb α ; Nuclear Receptor Subfamily 1 ; Group D ; Member 1 ; CCGs ; Clock Controlled Genes ; Micro-CT ; Micro Computed Tomography ; ROI ; Region of Interest ; Tb.Th. ; Trabecular Thickness ; Tb.N. ; Trabecular Number ; BV/TV ; Bon Volume per Tissue Volume ; BMD ; Bone Mineral Density ; BMC ; Bone Mineral Content ; AR
- 刊名：Bone
- 出版年：2016
- 出版时间：March 2016
- 年：2016
- 卷：84
- 期：Complete
- 页码：194-203
- 全文大小：1149 K
文摘
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The circadian clock regulates organismal bone physiology.
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A circadian clock deficient mouse model exhibits a low bone mass phenotype and what appears to be accelerated bone aging
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The circadian clock regulates mesenchymal stem cell osteoblastogenesis in vivo and in vitro.
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Extends findings on circadian control of bone homeostasis to show that BMAL1 deficiency causes a low bone mass phenotype.