Evidence map›Paper›PMID 24211207›Full record

ArticleBiochemical and biophysical research communications2013

Sclerostin deficient mice rapidly heal bone defects by activating β-catenin and increasing intramembranous ossification.

Meghan E McGee-Lawrence, Zachary C Ryan, Lomeli R Carpio, Sanjeev Kakar, Jennifer J Westendorf, Rajiv Kumar

Abstract read
In one paragraph

Article in Biochemical and biophysical research communications, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.7field-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

30 citing papers in PubMed, 56 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Review
  5. Hormone sensitive lipase ablation promotes bone regeneration.Biochimica et biophysica acta. Molecular basis of disease · 2022
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Osteocytic connexin 43 channels affect fracture healing.Journal of cellular physiology · 2019
    Article
  11. Article
  12. Article
  13. Article
  14. Cellular biology of fracture healing.Journal of orthopaedic research : official publication of the Orthopaedic Research Society · 2019
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Review
  20. Review
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

6 authors at 2 institutions in 1 country.

Meghan E McGee-LawrenceDepartment of Orthopedic Surgery, Mayo Clinic College of Medicine, Mayo Clinic, 200 1st St., Southwest, Rochester, MN 55905, USA.
Zachary C Ryan
Lomeli R Carpio
Sanjeev Kakar
Jennifer J Westendorf
Rajiv Kumar
Mayo Clinic · USWinnMed · US

Funding

Musculoskeletal Research Training ProgramT32AR056950 · NIAMS · MAYO CLINIC ROCHESTER · PI Jennifer J Westendorf · 2009 to 2026
$7.0M
Runx2 and Axin2 Interactions During Bone FormationR01DE020194 · NIDCR · MAYO CLINIC ROCHESTER · PI WESTENDORF, JENNIFER J · 2010 to 2014
$2.1M
Structure of Sclerostin Protein ComplexesR21AR060869 · NIAMS · MAYO CLINIC ROCHESTER · PI KUMAR, RAJIV · 2011 to 2012
$390k
Relationship between Hdac3 suppression and Wnt signaling in osteoblastsF32AR060140 · NIAMS · MAYO CLINIC ROCHESTER · PI MCGEE-LAWRENCE, MEGHAN E. · 2010 to 2011
$99k
NIAMS NIH HHS AR60869NIAMS NIH HHS F32 AR060140NIAMS NIH HHS F32 AR60140NIAMS NIH HHS R21 AR060869NIAMS NIH HHS T32 AR056950NIDCR NIH HHS R01 DE020194
6 · The paper itself

Abstract

We investigated the influence of the osteocyte protein, sclerostin, on fracture healing by examining the dynamics and mechanisms of repair of single-cortex, stabilized femoral defects in sclerostin knockout (Sost(-/-); KO) and sclerostin wild-type (Sost(+/+); WT) mice. Fourteen days following generation of bone defects, Sost KO mice had significantly more bone in the healing defect than WT mice. The increase in regenerating bone was due to an increase in the thickness of trabecularized spicules, osteoblast numbers and surfaces within the defect. Enhanced healing of bone defects in Sost KO mice was associated with significantly more activated β-catenin expression than observed in WT mice. The findings were similar to those observed in Axin2(-/-) mice, in which β-catenin signaling is known to be enhanced to facilitate bone regeneration. Taken together, these data indicate that enhanced β-catenin signaling is present in Sost(-/-) mice that demonstrate accelerated healing of bone defects, suggesting that modulation of β-catenin signaling in bone could be used to promote fracture repair.

Indexed as

Adaptor Proteins, Signal TransducingAnimalsAxin Proteinbeta CateninFracture HealingGlycoproteinsIntercellular Signaling Peptides and ProteinsMaleMiceMice, KnockoutOsteoblastsOsteogenesisSignal TransductionAdaptor Proteins, Signal TransducingAxin2 protein, mouseAxin Proteinbeta CateninCTNNB1 protein, mouseGlycoproteinsIntercellular Signaling Peptides and ProteinsSost protein, mouseFracture healingIntramembranous ossificationOsteoblastSclerostinWntβ-Catenin

Identifiers

PMID24211207
PMCPMC3876417
OpenAlexW2038416884

What OpenQuestion holds

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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.