PMID- 25615839
OWN - NLM
STAT- MEDLINE
DCOM- 20160104
LR  - 20190223
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 10
IP  - 1
DP  - 2015
TI  - Aryl hydrocarbon receptors in osteoclast lineage cells are a negative regulator 
      of bone mass.
PG  - e0117112
LID - 10.1371/journal.pone.0117112 [doi]
LID - e0117112
AB  - Aryl hydrocarbon receptors (AhRs) play a critical role in various pathological 
      and physiological processes. Although recent research has identified AhRs as a 
      key contributor to bone metabolism following studies in systemic AhR knockout 
      (KO) or transgenic mice, the cellular and molecular mechanism(s) in this process 
      remain unclear. In this study, we explored the function of AhR in bone metabolism 
      using AhR(RANKDeltaOc/DeltaOc) (RANK(Cre/+);AhR(flox/flox)) mice. We observed enhanced 
      bone mass together with decreased resorption in both male and female 12 and 
      24-week-old AhR(RANKDeltaOc/DeltaOc) mice. Control mice treated with 3-methylcholanthrene 
      (3MC), an AhR agonist, exhibited decreased bone mass and increased bone 
      resorption, whereas AhR(CtskDeltaOc/DeltaOc) (Ctsk(Cre/+);AhR(flox/flox)) mice injected 
      with 3MC appeared to have a normal bone phenotype. In vitro, bone marrow-derived 
      macrophages (BMDMs) from AhR(RANKDeltaOc/DeltaOc) mice exhibited impaired 
      osteoclastogenesis and repressed differentiation with downregulated expression of 
      B lymphocyte-induced maturation protein 1 (Blimp1), and cytochrome P450 genes 
      Cyp1b1 and Cyp1a2. Collectively, our results not only demonstrated that AhR in 
      osteoclast lineage cells is a physiologically relevant regulator of bone 
      resorption, but also highlighted the need for further studies on the skeletal 
      actions of AhR inhibitors in osteoclast lineage cells commonly associated with 
      bone diseases, especially diseases linked to environmental pollutants known to 
      induce bone loss.
FAU - Yu, Tai-yong
AU  - Yu TY
AD  - Division of Integrative Pathophysiology, Proteo-Science Center, Graduate School 
      of Medicine, Ehime University, Ehime 791-0295, Japan; Laboratory of Epigenetic 
      Skeletal Diseases, Institute of Molecular and Cellular Biosciences, The 
      University of Tokyo, Tokyo 113-0032, Japan.
FAU - Pang, Wei-jun
AU  - Pang WJ
AD  - College of Animal Science and Technology, Northwest A&F University, Yangling, 
      Shaanxi Province, 712100, P.R. China.
FAU - Yang, Gong-she
AU  - Yang GS
AD  - College of Animal Science and Technology, Northwest A&F University, Yangling, 
      Shaanxi Province, 712100, P.R. China.
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150123
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
RN  - 0 (Ahr protein, mouse)
RN  - 0 (Basic Helix-Loop-Helix Transcription Factors)
RN  - 0 (Receptors, Aryl Hydrocarbon)
SB  - IM
MH  - Animals
MH  - Basic Helix-Loop-Helix Transcription Factors/*genetics/*metabolism
MH  - Bone Density
MH  - Bone Resorption
MH  - Cells, Cultured
MH  - Female
MH  - Femur/*physiology
MH  - Gene Knockout Techniques
MH  - Male
MH  - Mice
MH  - Mice, Transgenic
MH  - Osteoclasts/*metabolism
MH  - Receptors, Aryl Hydrocarbon/*genetics/*metabolism
PMC - PMC4304837
COIS- Competing Interests: The authors have declared that no competing interests exist.
EDAT- 2015/01/24 06:00
MHDA- 2016/01/05 06:00
PMCR- 2015/01/23
CRDT- 2015/01/24 06:00
PHST- 2014/07/16 00:00 [received]
PHST- 2014/12/19 00:00 [accepted]
PHST- 2015/01/24 06:00 [entrez]
PHST- 2015/01/24 06:00 [pubmed]
PHST- 2016/01/05 06:00 [medline]
PHST- 2015/01/23 00:00 [pmc-release]
AID - PONE-D-14-31874 [pii]
AID - 10.1371/journal.pone.0117112 [doi]
PST - epublish
SO  - PLoS One. 2015 Jan 23;10(1):e0117112. doi: 10.1371/journal.pone.0117112. 
      eCollection 2015.