Evidence map›Paper›PMID 27111560›Full record

ArticleBritish journal of pharmacology2016

Antagonizing midkine accelerates fracture healing in mice by enhanced bone formation in the fracture callus.

Melanie Haffner-Luntzer, Aline Heilmann, Anna Elise Rapp, Robin Roessler, Thorsten Schinke, Michael Amling, Anita Ignatius, Astrid Liedert

Open access · hybridAbstract read
In one paragraph

Article in British journal of pharmacology, 2016. 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
2.1field-weighted citation impact, top 12% 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, 31 citations in OpenAlex.

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  4. Therapeutic approaches to activate the canonical Wnt pathway for bone regeneration.Journal of tissue engineering and regenerative medicine · 2022
    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

8 authors at 1 institution in 1 country.

Melanie Haffner-LuntzerInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.ORCID 0000-0002-3333-2613
Aline HeilmannInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Anna Elise RappInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Robin RoesslerInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Thorsten SchinkeInstitute of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Michael AmlingInstitute of Osteology and Biomechanics, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Anita IgnatiusInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Astrid LiedertInstitute of Orthopedic Research and Biomechanics, University Medical Center Ulm, Ulm, Germany.
Universität Hamburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

background and purposePrevious findings suggest that the growth and differentiation factor midkine (Mdk) is a negative regulator of osteoblast activity and bone formation, thereby raising the possibility that a specific Mdk antagonist might improve bone formation during fracture healing. EXPERIMENTAL APPROACH: In the present study, we investigated the effects of a monoclonal anti-Mdk antibody (Mdk-Ab) on bone healing using a standardized femur osteotomy model in mice. Additional in vitro experiments using chondroprogenitor and preosteoblastic cells were conducted to analyse the effects of recombinant Mdk and Mdk-Ab on differentiation markers and potential binding partners in these cells. KEY

resultsWe demonstrated that treatment with Mdk-Ab accelerated bone healing in mice based on increased bone formation in the fracture callus. In vitro experiments using preosteoblastic cells showed that Mdk-Ab treatment abolished the Mdk-induced negative effects on the expression of osteogenic markers and Wnt/β-catenin target proteins, whereas the differentiation of chondroprogenitor cells was unaffected. Phosphorylation analyses revealed an important role for the low-density lipoproteinLDL receptor-related protein 6 in Mdk signalling in osteoblasts. CONCLUSIONS AND IMPLICATIONS: We conclude that Mdk-Ab treatment may be a potential novel therapeutic strategy to enhance fracture healing in patients with orthopaedic complications such as delayed healing or non-union formation.

Indexed as

AnimalsAntibodies, MonoclonalBony CallusCytokinesFemaleFracture HealingMiceMice, Inbred C57BLMidkineOsteogenesisAntibodies, MonoclonalCytokinesMidkine

Identifiers

PMID27111560
PMCPMC4919577
OpenAlexW2344407059

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.