Evidence map›Paper›PMID 25193158›Full record

ArticleBone2014

Disruption of glucocorticoid signaling in chondrocytes delays metaphyseal fracture healing but does not affect normal cartilage and bone development.

Jinwen Tu, Holger Henneicke, Yaqing Zhang, Shihani Stoner, Tegan L Cheng, Aaron Schindeler, Di Chen, Jan Tuckermann, Mark S Cooper, Markus J Seibel and 1 more

Abstract read
PubMed Full text at PMC Publisher
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 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
2.8field-weighted citation impact, top 10% 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

14 citing papers in PubMed, 33 citations in OpenAlex.

  1. Article
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  6. Review
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  8. Review
  9. Induced global deletion of glucocorticoid receptor impairs fracture healing.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2018
    Article
  10. Review
  11. Article
  12. Review
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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 5 institutions in 3 countries.

Jinwen TuBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, Australia.
Holger HenneickeBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, Australia.
Yaqing ZhangBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, Australia.
Shihani StonerBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, Australia.
Tegan L ChengOrthopaedic Research & Biotechnology Unit, The Children's Hospital at Westmead, Sydney, Australia.
Aaron SchindelerOrthopaedic Research & Biotechnology Unit, The Children's Hospital at Westmead, Sydney, Australia.
Di ChenTissue Department of Biochemistry, Rush University Medical Center, USA.
Jan TuckermannInstitute of General Zoology and Endocrinology, University of Ulm, Ulm, Germany.
Mark S CooperDepartment of Endocrinology & Metabolism, Concord Hospital, Sydney, Australia.
Markus J SeibelBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, Australia; Department of Endocrinology & Metabolism, Concord Hospital, Sydney, Australia.
Hong ZhouBone Research Program, ANZAC Research Institute, University of Sydney, Sydney, Australia. Electronic address: h.zhou@sydney.edu.au.
The University of Sydney · AUChildren's Hospital at Westmead · AUConcord Repatriation General Hospital · AURush University Medical Center · USUniversität Ulm · DE

Funding

The Mechanism through which TGF-Beta Maintains Chondrocytes in Proliferating StagR01AR054465 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2007 to 2018
$2.7M
Beta-Catenin Signaling and Pathogenesis of OsteoarthritisR01AR055915 · NIAMS · UNIVERSITY OF ROCHESTER · PI CHEN, DI · 2009 to 2013
$1.7M
NIAMS NIH HHS R01 AR054465NIAMS NIH HHS R01 AR055915
6 · The paper itself

Abstract

States of glucocorticoid excess are associated with defects in chondrocyte function. Most prominently there is a reduction in linear growth but delayed healing of fractures that require endochondral ossification to also occur. In contrast, little is known about the role of endogenous glucocorticoids in chondrocyte function. As glucocorticoids exert their cellular actions through the glucocorticoid receptor (GR), we aimed to elucidate the role of endogenous glucocorticoids in chondrocyte function in vivo through characterization of tamoxifen-inducible chondrocyte-specific GR knockout (chGRKO) mice in which the GR was deleted at various post-natal ages. Knee joint architecture, cartilage structure, growth plates, intervertebral discs, long bone length and bone micro-architecture were similar in chGRKO and control mice at all ages. Analysis of fracture healing in chGRKO and control mice demonstrated that in metaphyseal fractures, chGRKO mice formed a larger cartilaginous callus at 1 and 2 week post-surgery, as well as a smaller amount of well-mineralized bony callus at the fracture site 4 week post-surgery, when compared to control mice. In contrast, chondrocyte-specific GR knockout did not affect diaphyseal fracture healing. We conclude that endogenous GC signaling in chondrocytes plays an important role during metaphyseal fracture healing but is not essential for normal long bone growth.

Indexed as

AnimalsBone DevelopmentCartilageChondrocytesFracture HealingGlucocorticoidsImmunohistochemistryMiceMice, Inbred C57BLMice, KnockoutSignal TransductionGlucocorticoidsCartilageChondrocyteDiaphyseal fractureGlucocorticoidsGrowthMetaphyseal fracture

Identifiers

PMID25193158
PMCPMC4284102
OpenAlexW2085626537

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.