Evidence map›Paper›PMID 24333171›Full record

ArticleBone2014

Estrogen receptor α in osteocytes regulates trabecular bone formation in female mice.

Shino Kondoh, Kazuki Inoue, Katsuhide Igarashi, Hiroe Sugizaki, Yuko Shirode-Fukuda, Erina Inoue, Taiyong Yu, Jun K Takeuchi, Jun Kanno, Lynda F Bonewald and 1 more

Abstract read
In one paragraph

Article in Bone, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
66citing papers in PubMed, 4 pooled it
4.0field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

66 citing papers in PubMed, 4 syntheses or guidelines pooled it, 113 citations in OpenAlex.

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  10. Aromatase in adipose tissue exerts an osteoprotective function in male mice via phosphate regulation.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
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6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Shino KondohLaboratory of Epigenetic Skeletal Diseases, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Kazuki InoueLaboratory of Epigenetic Skeletal Diseases, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan; Division of Integrative Pathophysiology, Proteo-Science Center, Graduate School of Medicine, Ehime University, Ehime, Japan; Department of Biological Resources, Integrated Center for Science, Ehime University, Ehime, Japan.
Katsuhide IgarashiDivision of Cellular & Molecular Toxicology, Biological Safety Research Center, National Institute of Health Sciences, Tokyo, Japan.
Hiroe SugizakiDivision of Cardiovascular Regeneration, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Yuko Shirode-FukudaLaboratory of Epigenetic Skeletal Diseases, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Erina InoueLaboratory of Epigenetic Skeletal Diseases, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan.
Taiyong YuLaboratory of Epigenetic Skeletal Diseases, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan; Division of Integrative Pathophysiology, Proteo-Science Center, Graduate School of Medicine, Ehime University, Ehime, Japan.
Jun K TakeuchiDivision of Cardiovascular Regeneration, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan; JST PRESTO, Japan.
Jun KannoDivision of Cellular & Molecular Toxicology, Biological Safety Research Center, National Institute of Health Sciences, Tokyo, Japan.
Lynda F BonewaldDepartment of Oral Biology, School of Dentistry, University of Missouri at Kansas City, Kansas City, MO, USA.
Yuuki ImaiLaboratory of Epigenetic Skeletal Diseases, Institute of Molecular and Cellular Biosciences, The University of Tokyo, Tokyo, Japan; Division of Integrative Pathophysiology, Proteo-Science Center, Graduate School of Medicine, Ehime University, Ehime, Japan. Electronic address: y-imai@m.ehime-u.ac.jp.
The University of Tokyo · JPNational Institute of Health Sciences · JPUniversity of Missouri–Kansas City · US

Funding

Transgenic CoreP01AR046798 · NIAMS · UNIVERSITY OF TEXAS HLTH SCI CTR SAN ANT · PI BONEWALD, LYNDA F · 2001 to 2010
$10.5M
NIAMS NIH HHS P01 AR046798
6 · The paper itself

Abstract

Estrogens are well known steroid hormones necessary to maintain bone health. In addition, mechanical loading, in which estrogen signaling may intersect with the Wnt/β-catenin pathway, is essential for bone maintenance. As osteocytes are known as the major mechanosensory cells embedded in mineralized bone matrix, osteocyte ERα deletion mice (ERα(ΔOcy/ΔOcy)) were generated by mating ERα floxed mice with Dmp1-Cre mice to determine the role of ERα in osteocytes. Trabecular bone mineral density of female, but not male ERα(ΔOcy/ΔOcy) mice was significantly decreased. Bone formation parameters in ERα(ΔOcy/ΔOcy) were significantly decreased while osteoclast parameters were unchanged. This suggests that ERα in osteocytes exerts osteoprotective function by positively controlling bone formation. To identify potential targets of ERα, gene array analysis of Dmp1-GFP osteocytes sorted by FACS from ERα(ΔOcy/ΔOcy) and control mice was performed. Gene expression microarray followed by gene ontology analyses revealed that osteocytes from ERα(ΔOcy/ΔOcy) highly expressed genes categorized in 'Secreted' when compared to control osteocytes. Among them, expression of Mdk and Sostdc1, both of which are Wnt inhibitors, was significantly increased without alteration of expression of the mature osteocyte markers such as Sost and β-catenin. Moreover, hindlimb suspension experiments showed that trabecular bone loss due to unloading was greater in ERα(ΔOcy/ΔOcy) mice without cortical bone loss. These data suggest that ERα in osteocytes has osteoprotective functions in trabecular bone formation through regulating expression of Wnt antagonists, but conversely plays a negative role in cortical bone loss due to unloading.

Indexed as

OsteogenesisAdaptor Proteins, Signal TransducingAnimalsBone and BonesBone Morphogenetic ProteinsCells, CulturedEstrogen Receptor alphaFemaleGene DeletionGene Expression ProfilingGene TargetingIntercellular Signaling Peptides and ProteinsMaleMiceMidkineOsteoblastsAdaptor Proteins, Signal TransducingBone Morphogenetic ProteinsEstrogen Receptor alphaIntercellular Signaling Peptides and ProteinsMdk protein, mouseMidkineSostdc1 protein, mouseBone formationEstrogenEstrogen receptor αOsteocyteWnt signaling

Identifiers

PMID24333171
PMCPMC3944732
OpenAlexW2136445754

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.