Circadian Clock Regulates Bone Resorption in Mice

ABSTRACT 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,...

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Published inJournal of bone and mineral research Vol. 31; no. 7; pp. 1344 - 1355
Main Authors Xu, Cheng, Ochi, Hiroki, Fukuda, Toru, Sato, Shingo, Sunamura, Satoko, Takarada, Takeshi, Hinoi, Eiichi, Okawa, Atsushi, Takeda, Shu
Format Journal Article
LanguageEnglish
Published United States Oxford University Press 01.07.2016
Subjects
Animals
ARNTL Transcription Factors - genetics
ARNTL Transcription Factors - metabolism
BMAL1
Bone Resorption - genetics
Bone Resorption - metabolism
Cell Differentiation - physiology
CIRCADIAN CLOCK
Circadian Clocks - physiology
CLOCK Proteins - genetics
CLOCK Proteins - metabolism
Mice
Mice, Knockout
NFATC Transcription Factors - genetics
NFATC Transcription Factors - metabolism
NFATC1
Osteoclasts - metabolism
src-Family Kinases - genetics
src-Family Kinases - metabolism
SRCS FAMILY
CIRCADIAN CLOCK
NFATC1
SRCS FAMILY
BMAL1
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Abstract ABSTRACT 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. © 2016 American Society for Bone and Mineral Research.
AbstractList 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. © 2016 American Society for Bone and Mineral Research.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. © 2016 American Society for Bone and Mineral Research.
ABSTRACT 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. © 2016 American Society for Bone and Mineral Research.
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. © 2016 American Society for Bone and Mineral Research.
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. .
Author Sato, Shingo
Xu, Cheng
Sunamura, Satoko
Takeda, Shu
Ochi, Hiroki
Takarada, Takeshi
Fukuda, Toru
Hinoi, Eiichi
Okawa, Atsushi
Author_xml – sequence: 1
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  surname: Xu
  fullname: Xu, Cheng
  organization: Tokyo Medical and Dental University
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  surname: Ochi
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  organization: Japan Science and Technology Agency
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  fullname: Fukuda, Toru
  organization: Japan Science and Technology Agency
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  surname: Sato
  fullname: Sato, Shingo
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  surname: Sunamura
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  givenname: Takeshi
  surname: Takarada
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  organization: Tokyo Medical and Dental University
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  givenname: Shu
  surname: Takeda
  fullname: Takeda, Shu
  organization: Japan Science and Technology Agency
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Snippet ABSTRACT The circadian clock controls many behavioral and physiological processes beyond daily rhythms. Circadian dysfunction increases the risk of cancer,...
The circadian clock controls many behavioral and physiological processes beyond daily rhythms. Circadian dysfunction increases the risk of cancer, obesity, and...
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SubjectTerms Animals
ARNTL Transcription Factors - genetics
ARNTL Transcription Factors - metabolism
BMAL1
Bone Resorption - genetics
Bone Resorption - metabolism
Cell Differentiation - physiology
CIRCADIAN CLOCK
Circadian Clocks - physiology
CLOCK Proteins - genetics
CLOCK Proteins - metabolism
Mice
Mice, Knockout
NFATC Transcription Factors - genetics
NFATC Transcription Factors - metabolism
NFATC1
Osteoclasts - metabolism
src-Family Kinases - genetics
src-Family Kinases - metabolism
SRCS FAMILY
Title Circadian Clock Regulates Bone Resorption in Mice
URI https://onlinelibrary.wiley.com/doi/abs/10.1002%2Fjbmr.2803
https://www.ncbi.nlm.nih.gov/pubmed/26841172
https://www.proquest.com/docview/1801533245
https://www.proquest.com/docview/1802477031
https://www.proquest.com/docview/1808686025
Volume 31
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