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Aryl Hydrocarbon Receptors in Osteoclast Lineage Cells Are a Negative Regulator of Bone Mass

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)... Full description

Journal Title: PLoS ONE Jan 23, 2015, Vol.10(1)
Main Author: Yu, Tai-Yong
Other Authors: Pang, Wei-Jun , Yang, Gong-She
Format: Electronic Article Electronic Article
Language: English
Subjects:
Quelle: Cengage Learning, Inc.
ID: ISSN: 1932-6203
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recordid: gale_ofa422547723
title: Aryl Hydrocarbon Receptors in Osteoclast Lineage Cells Are a Negative Regulator of Bone Mass
format: Article
creator:
  • Yu, Tai-Yong
  • Pang, Wei-Jun
  • Yang, Gong-She
subjects:
  • Genetic Engineering – Physiological Aspects
  • Cytochrome P-450 – Physiological Aspects
  • Bone Density – Physiological Aspects
ispartof: PLoS ONE, Jan 23, 2015, Vol.10(1)
description: 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.sup.RANK[DELTA]Oc/[DELTA]Oc (RANK.sup.Cre/+ ;AhR.sup.flox/flox) mice. We observed enhanced bone mass together with decreased resorption in both male and female 12 and 24-week-old AhR.sup.RANK[DELTA]Oc/[DELTA]Oc mice. Control mice treated with 3-methylcholanthrene (3MC), an AhR agonist, exhibited decreased bone mass and increased bone resorption, whereas AhR.sup.Ctsk[DELTA]Oc/[DELTA]Oc (Ctsk.sup.Cre/+ ;AhR.sup.flox/flox) mice injected with 3MC appeared to have a normal bone phenotype. In vitro, bone marrow-derived macrophages (BMDMs) from AhR.sup.RANK[DELTA]Oc/[DELTA]Oc 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.
language: eng
source: Cengage Learning, Inc.
identifier: ISSN: 1932-6203
fulltext: fulltext
issn:
  • 1932-6203
  • 19326203
url: Link


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titleAryl Hydrocarbon Receptors in Osteoclast Lineage Cells Are a Negative Regulator of Bone Mass
creatorYu, Tai-Yong ; Pang, Wei-Jun ; Yang, Gong-She
ispartofPLoS ONE, Jan 23, 2015, Vol.10(1)
identifierISSN: 1932-6203
subjectGenetic Engineering – Physiological Aspects ; Cytochrome P-450 – Physiological Aspects ; Bone Density – Physiological Aspects
descriptionAryl 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.sup.RANK[DELTA]Oc/[DELTA]Oc (RANK.sup.Cre/+ ;AhR.sup.flox/flox) mice. We observed enhanced bone mass together with decreased resorption in both male and female 12 and 24-week-old AhR.sup.RANK[DELTA]Oc/[DELTA]Oc mice. Control mice treated with 3-methylcholanthrene (3MC), an AhR agonist, exhibited decreased bone mass and increased bone resorption, whereas AhR.sup.Ctsk[DELTA]Oc/[DELTA]Oc (Ctsk.sup.Cre/+ ;AhR.sup.flox/flox) mice injected with 3MC appeared to have a normal bone phenotype. In vitro, bone marrow-derived macrophages (BMDMs) from AhR.sup.RANK[DELTA]Oc/[DELTA]Oc 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.
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titleAryl Hydrocarbon Receptors in Osteoclast Lineage Cells Are a Negative Regulator of Bone Mass.
descriptionAryl 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.sup.RANK[DELTA]Oc/[DELTA]Oc (RANK.sup.Cre/+ ;AhR.sup.flox/flox) mice. We observed enhanced bone mass together with decreased resorption in both male and female 12 and 24-week-old AhR.sup.RANK[DELTA]Oc/[DELTA]Oc mice. Control mice treated with 3-methylcholanthrene (3MC), an AhR agonist, exhibited decreased bone mass and increased bone resorption, whereas AhR.sup.Ctsk[DELTA]Oc/[DELTA]Oc (Ctsk.sup.Cre/+ ;AhR.sup.flox/flox) mice injected with 3MC appeared to have a normal bone phenotype. In vitro, bone marrow-derived macrophages (BMDMs) from AhR.sup.RANK[DELTA]Oc/[DELTA]Oc 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.
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abstractAryl 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.sup.RANK[DELTA]Oc/[DELTA]Oc (RANK.sup.Cre/+ ;AhR.sup.flox/flox) mice. We observed enhanced bone mass together with decreased resorption in both male and female 12 and 24-week-old AhR.sup.RANK[DELTA]Oc/[DELTA]Oc mice. Control mice treated with 3-methylcholanthrene (3MC), an AhR agonist, exhibited decreased bone mass and increased bone resorption, whereas AhR.sup.Ctsk[DELTA]Oc/[DELTA]Oc (Ctsk.sup.Cre/+ ;AhR.sup.flox/flox) mice injected with 3MC appeared to have a normal bone phenotype. In vitro, bone marrow-derived macrophages (BMDMs) from AhR.sup.RANK[DELTA]Oc/[DELTA]Oc 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.
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atitleAryl Hydrocarbon Receptors in Osteoclast Lineage Cells Are a Negative Regulator of Bone Mass
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date2015-01-23