Evidence map›Paper›PMID 30414510›Full record

ArticleBone2019

Deletion of nicotinic acetylcholine receptor alpha9 in mice resulted in altered bone structure.

Lisa Baumann, Vivien Kauschke, Anna Vikman, Lutz Dürselen, Gabriela Krasteva-Christ, Marian Kampschulte, Christian Heiss, Kathleen T Yee, Douglas E Vetter, Katrin Susanne Lips

Open access · hybridAbstract read
In one paragraph

Article in Bone, 2019. 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
0.5field-weighted citation impact, top 36% 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, 21 citations in OpenAlex.

  1. Trial
  2. Review
  3. Neural Orchestration of Mandibular Development.International dental journal · 2026
    Review
  4. Review
  5. Article
  6. Article
  7. Bidirectional Interaction Between the Brain and Bone in Traumatic Brain Injury.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Review
  8. Review
  9. Crosstalk between bone and brain in Alzheimer's disease: Mechanisms, applications, and perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024
    Review
  10. Article
  11. Article
  12. α9-Containing Nicotinic Receptors in Cancer.Frontiers in cellular neuroscience · 2021
    Review
  13. Article
  14. 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

10 authors at 5 institutions in 2 countries.

Lisa BaumannExperimental Trauma Surgery, Justus-Liebig-University Giessen, Aulweg 128, 35392 Giessen, Germany. Electronic address: Lisa.Baumann@med.uni-giessen.de.
Vivien KauschkeExperimental Trauma Surgery, Justus-Liebig-University Giessen, Aulweg 128, 35392 Giessen, Germany. Electronic address: Vivien.Kauschke@chiru.med.uni-giessen.de.
Anna VikmanInstitute of Orthopaedic Research and Biomechanics, Center for Trauma Research, Ulm University Medical Centre, Helmholtzstrasse 14, 89081 Ulm, Germany.
Lutz DürselenInstitute of Orthopaedic Research and Biomechanics, Center for Trauma Research, Ulm University Medical Centre, Helmholtzstrasse 14, 89081 Ulm, Germany. Electronic address: Lutz.Duerselen@uni-ulm.de.
Gabriela Krasteva-ChristInstitute of Anatomy and Cell Biology, Saarland University, Kirrberger Straße, 66421 Homburg, Germany. Electronic address: Gabriela.Krasteva-Christ@uks.eu.
Marian KampschulteLaboratory of Experimental Radiology, Justus-Liebig-University Giessen, Schubertstrasse 81, 35392 Giessen, Germany. Electronic address: Marian.Kampschulte@radiol.med.uni-giessen.de.
Christian HeissDepartment of Trauma, Hand, and Reconstructive Surgery Giessen, University Hospital of Giessen-Marburg, Rudolf-Buchheim-Str. 7, 35392 Giessen, Germany. Electronic address: Christian.Heiss@chiru.med.uni-giessen.de.
Kathleen T YeeDepartment of Neurobiology and Anatomical Sciences, University Mississippi Medical Center, Jackson, MS, USA. Electronic address: kyee@umc.edu.
Douglas E VetterDepartment of Neurobiology and Anatomical Sciences, University Mississippi Medical Center, Jackson, MS, USA. Electronic address: dvetter@umc.edu.
Katrin Susanne LipsExperimental Trauma Surgery, Justus-Liebig-University Giessen, Aulweg 128, 35392 Giessen, Germany. Electronic address: Katrin.S.Lips@chiru.med.uni-giessen.de.
University of Giessen · DEHelmholtz-Institute Ulm · DEUniversity of Mississippi Medical Center · USSaarland University · DEUniversitätsklinikum Gießen und Marburg · DE

Funding

Center for Psychiatric NeuroscienceP30GM103328 · NIGMS · UNIVERSITY OF MISSISSIPPI MED CTR · PI STOCKMEIER, CRAIG ALLEN · 2013 to 2017
$5.5M
An investigation into cochlear HPA like signalingR21DC015124 · NIDCD · UNIVERSITY OF MISSISSIPPI MED CTR · PI VETTER, DOUGLAS E · 2016 to 2017
$419k
NIDCD NIH HHS R21 DC015124NIGMS NIH HHS P30 GM103328
6 · The paper itself

Abstract

Alterations in bone strength and structure were found in knockout (KO) mouse strains with deletion of several acetylcholine receptors. Interestingly, the expression of the nicotinic acetylcholine receptors (nAChR) subunit α10 was down-regulated in osteogenic differentiated mesenchymal stem cells of patients with osteoporosis whereas the expression of subunit α9 was not altered. Since nAChR subunits α9 and α10 are often combined in a functional receptor, we analyzed here the bone of adult female KO mice with single deletion of either nAChR alpha9 (α9KO) or alpha10 (α10KO). Biomechanical testing showed a significant decrease of bending stiffness and maximal breaking force in α9KO compared to their corresponding wild type mice. Furthermore, an increase in trabecular pattern factor (Tb.Pf) and structure model index (SMI) was detected by μCT in α9KO indicating reduced bone mass. On the mRNA level a decrease of Collagen 1α1 and Connexin-43 was measured by real-time RT-PCR in α9KO while no alteration of osteoclast markers was detected in either mouse strain. Using electron microcopy we observed an increase in the number of osteocytes that showed signs of degeneration and cell death in the α9KO compared to their wild type mice, while α10KO showed no differences. In conclusion, we demonstrate alterations in bone strength, structure and bio-marker expression in α9KO mice which imply the induction of osteocyte degeneration. Thus, our data suggest that nAChR containing the α9 subunit might be involved in the homeostasis of osteocytes and therefore in bone mass regulation.

Indexed as

Gene DeletionAlkaline PhosphataseAnimalsAnimals, NewbornBone and BonesCancellous BoneCortical BoneFemaleFemurMice, Inbred C57BLMice, KnockoutOsteoblastsOsteoclastsOsteocytesReceptors, NicotinicAlkaline PhosphataseChrna9 protein, mouseReceptors, NicotinicBending stiffnessCollagen 1α1Connexin-43Micro-CTnAChR α10Non-neuronal cholinergic system

Identifiers

PMID30414510
PMCPMC6492625
OpenAlexW2899815924

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.