Evidence map›Paper›PMID 25333900›Full record

ArticleNature communications2014

Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts.

Johannes Keller, Philip Catala-Lehnen, Antje K Huebner, Anke Jeschke, Timo Heckt, Anja Lueth, Matthias Krause, Till Koehne, Joachim Albers, Jochen Schulze and 23 more

Open access · hybridAbstract read
In one paragraph

Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers.

0numbers the graph read from it
0cells of the map it votes in
91citing papers in PubMed
7.1field-weighted citation impact, top 2% 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

91 citing papers in PubMed, 202 citations in OpenAlex.

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  12. Cxcl9-deficiency attenuates the progression of post-traumatic osteoarthritis in mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  16. Sphingosine-1-phosphate promotes osteogenesis by stimulating osteoblast growth and neovascularization in a vascular endothelial growth factor-dependent manner.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024
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31 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

33 authors at 8 institutions in 2 countries.

Johannes KellerDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Philip Catala-LehnenDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Antje K Huebner1] Department of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany [2] Institute of Human Genetics, University Hospital Jena, 07743 Jena, Germany.
Anke JeschkeDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Timo HecktDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Anja LuethInstitute of Nutritional Science, University of Potsdam, 14469 Potsdam, Germany.
Matthias KrauseDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Till KoehneDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Joachim AlbersDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Jochen SchulzeDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Sarah SchillingDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Michael HaberlandDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Hannah DenningerDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Mona NevenDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Irm Hermans-BorgmeyerCenter for Molecular Neurobiology, University of Hamburg, 20251 Hamburg, Germany.
Thomas StreichertInstitute of Clinical Chemistry, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Stefan BreerDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Florian BarvencikDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Bodo LevkauInstitute of Pathophysiology, University Hospital Essen, 45122 Essen, Germany.
Birgit Rathkolb1] Institute of Molecular Animal Breeding and Biotechnology, Gene Center, Ludwig-Maximilian-University, 81377 Munich, Germany [2] German Mouse Clinic, Institute of Experimental Genetics, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Eckhard WolfInstitute of Molecular Animal Breeding and Biotechnology, Gene Center, Ludwig-Maximilian-University, 81377 Munich, Germany.
Julia Calzada-WackGerman Mouse Clinic, Institute of Pathology, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Frauke NeffGerman Mouse Clinic, Institute of Pathology, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Valerie Gailus-DurnerGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Helmut FuchsGerman Mouse Clinic, Institute of Experimental Genetics, Helmholtz Center Munich, 85764 Neuherberg, Germany.
Martin Hrabĕ de Angelis1] German Mouse Clinic, Institute of Experimental Genetics, Helmholtz Center Munich, 85764 Neuherberg, Germany [2] Center of Life and Food Sciences Weihenstephan, Technische Universität München, 85354 Freising, Germany [3] German Center for Diabetes Research, 85764 Neuherberg, Germany.
Susanne KlutmannDepartment of Nuclear Medicine, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Elena TsourdiDepartment of Medicine III, Dresden University Medical Center, 01307 Dresden, Germany.
Lorenz C HofbauerDepartment of Medicine III, Dresden University Medical Center, 01307 Dresden, Germany.
Burkhard KleuserInstitute of Nutritional Science, University of Potsdam, 14469 Potsdam, Germany.
Jerold ChunScripps Research Institute, La Jolla, California 92937, USA.
Thorsten SchinkeDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Michael AmlingDepartment of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, 20246 Hamburg, Germany.
Universität Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEHelmholtz Zentrum München · DELudwig-Maximilians-Universität München · DETU Dresden · DEUniversity of Potsdam · DEEssen University Hospital · DEScripps Research Institute · US

Funding

Receptor-mediated S1P signaling in the embryonic brainR01DA019674 · NIDA · SCRIPPS RESEARCH INSTITUTE, THE · PI CHUN, JEROLD · 2006 to 2010
$1.9M
Targeting S1P receptors to prevent hearing lossR21DC009505 · NIDCD · SCRIPPS RESEARCH INSTITUTE, THE · PI CHUN, JEROLD · 2009 to 2010
$520k
NIDA NIH HHS DA019674NIDA NIH HHS R01 DA019674NIDCD NIH HHS DC009505NIDCD NIH HHS R21 DC009505
6 · The paper itself

Abstract

The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signalling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P3. Finally, pharmacologic treatment with the nonselective S1P receptor agonist FTY720 causes increased bone formation in wild-type, but not in S1P3-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts.

Indexed as

OsteogenesisAllelesAnimalsBone and BonesCalcitoninCollagenasesCrosses, GeneticFemaleLysophospholipidsMiceMice, Inbred C57BLMice, TransgenicOsteoblastsOsteoclastsOsteoporosisPhenotypeCalcitoninCollagenasesLysophospholipidsReceptors, CalcitoninSphingosinesphingosine 1-phosphate

Identifiers

PMID25333900
PMCPMC4205484
OpenAlexW1980751002

What OpenQuestion holds

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Registered trials

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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.