Evidence map›Paper›PMID 29463853›Full record

ArticleScientific reports2018

Spina bifida-predisposing heterozygous mutations in Planar Cell Polarity genes and Zic2 reduce bone mass in young mice.

Isabel R Orriss, Stuart Lanham, Dawn Savery, Nicholas D E Greene, Philip Stanier, Richard Oreffo, Andrew J Copp, Gabriel L Galea

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.7field-weighted citation impact, top 25% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. The Function and Regulation of celsr1a in Skeletal Age-associated Homeostasis and Repair in Zebrafish.The journals of gerontology. Series A, Biological sciences and medical sciences · 2025
    Article
  2. Article
  3. Neuron-Specific Deletion ofFrontiers in genetics · 2022
    Article
  4. Article
  5. Article
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 4 institutions in 2 countries.

Isabel R OrrissDepartment of Comparative Biomedical Sciences, Royal Veterinary College, Camden, London, NW1 0TU, UK.
Stuart LanhamBone and Joint Research Group, Centre for Human Development, Stem Cells and Regeneration, Human Development and Health, Institute of Developmental Sciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.
Dawn SaveryDevelopmental Biology of Birth Defects, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Nicholas D E GreeneDevelopmental Biology of Birth Defects, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Philip StanierDevelopmental Biology of Birth Defects, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.
Richard OreffoBone and Joint Research Group, Centre for Human Development, Stem Cells and Regeneration, Human Development and Health, Institute of Developmental Sciences, Faculty of Medicine, University of Southampton, Southampton, SO16 6YD, UK.ORCID 0000-0001-5995-6726
Andrew J CoppDevelopmental Biology of Birth Defects, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK.ORCID 0000-0002-2544-9117
Gabriel L GaleaDevelopmental Biology of Birth Defects, UCL GOS Institute of Child Health, 30 Guilford Street, London, WC1N 1EH, UK. g.galea@ucl.ac.uk.ORCID 0000-0003-2515-1342
University College London · GBUniversity of Southampton · GBInstitute of Child Health · GRRoyal Veterinary College · GB

Funding

Biotechnology and Biological Sciences Research Council BB/G010579/1Biotechnology and Biological Sciences Research Council BB/LO21072/1British Heart Foundation PG/15/13/31296Medical Research Council G0801124Medical Research Council J003794Medical Research Council K022741Wellcome Trust 087525Wellcome Trust 107474/Z/15/Z
6 · The paper itself

Abstract

Fractures are a common comorbidity in children with the neural tube defect (NTD) spina bifida. Mutations in the Wnt/planar cell polarity (PCP) pathway contribute to NTDs in humans and mice, but whether this pathway independently determines bone mass is poorly understood. Here, we first confirmed that core Wnt/PCP components are expressed in osteoblasts and osteoclasts in vitro. In vivo, we performed detailed µCT comparisons of bone structure in tibiae from young male mice heterozygous for NTD-associated mutations versus WT littermates. PCP signalling disruption caused by Vangl2 (Vangl2

Indexed as

Cell PolarityMutationAnimalsBone and BonesHeterozygoteMaleMiceMice, Inbred C57BLMice, KnockoutNerve Tissue ProteinsNeural Tube DefectsPAX3 Transcription FactorReceptors, G-Protein-CoupledSpinal DysraphismTranscription FactorsCelsr1 protein, mouseLtap protein, mouseNerve Tissue ProteinsPax3 protein, mousePAX3 Transcription FactorReceptors, G-Protein-CoupledTranscription FactorsZic2 protein, mouse

Identifiers

PMID29463853
PMCPMC5820290
OpenAlexW2794017676

What Socratic holds

Textmetadata
LicenceCC BY
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 Socratic graph.