Evidence map›Paper›PMID 33856623›Full record

ArticlePurinergic signalling2021

Bone phenotype of P2X4 receptor knockout mice: implication of a P2X7 receptor mutation?

Maria Ellegaard, Tanja Hegner, Ming Ding, Lauriane Ulmann, Niklas Rye Jørgensen

Open access · greenAbstract read
In one paragraph

Article in Purinergic signalling, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.8field-weighted citation impact, top 30% 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

6 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Animal Models for the Investigation of P2X7 Receptors.International journal of molecular sciences · 2023
    Review
  6. 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

5 authors at 4 institutions in 2 countries.

Maria EllegaardDepartment of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.
Tanja HegnerDepartment of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark.
Ming DingInstitute of Clinical Research, University of Southern Denmark, Odense, Denmark.
Lauriane UlmannIGF, Univ Montpellier, CNRS, INSERM, Montpellier, France.
Niklas Rye JørgensenDepartment of Clinical Biochemistry, Rigshospitalet, Copenhagen, Denmark. niklas.rye.joergensen@regionh.dk.ORCID 0000-0001-9624-5210
Rigshospitalet · DKCentre National de la Recherche Scientifique · FRUniversity of Copenhagen · DKUniversity of Southern Denmark · DK

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Transgenic and knockout animal models are widely used to investigate the role of receptors, signaling pathways, and other peptides and proteins. Varying results are often published on the same model from different groups, and much effort has been put into understanding the underlying causes of these sometimes conflicting results. Recently, it has been shown that a P2X4R knockout model carries a so-called passenger mutation in the P2X7R gene, potentially affecting the interpretation of results from studies using this animal model. We therefore report this case to raise awareness about the potential pitfalls using genetically modified animal models, especially within P2 receptor research. Although purinergic signaling has been recognized as an important contributor to the regulation of bone remodeling, the process that maintains the bone quality during life, little is known about the role of the P2X4 receptor (P2X4R) in regulation of bone remodeling in health and disease. To address this, we analyzed the bone phenotype of P2rx4tm1Rass (C57BL/6J) knockout mice and corresponding wildtype using microCT and biomechanical testing. Overall, we found that the P2X4R knockout mice displayed improved bone microstructure and stronger bones in an age- and gender-dependent manner. While cortical BMD, trabecular BMD, and bone volume were higher in the 6-month-old females and 3-month-old males, this was not the case for the 3-month-old females and the 6-month-old males. Bone strength was only affected in the females. Moreover, we found that P2X4R KO mice carried the P2X7 receptor 451P wildtype allele, whereas the wildtype mice carried the 451L mutant allele. In conclusion, this study suggests that P2X4R could play a role in bone remodeling, but more importantly, it underlines the potential pitfalls when using knockout models and highlights the importance of interpreting results with great caution. Further studies are needed to verify any specific effects of P2X4R on bone metabolism.

Indexed as

AnimalsAnimals, Genetically ModifiedBone and BonesBone DensityBone RemodelingFemaleMaleMiceMice, Inbred C57BLMice, KnockoutMutationPhenotypeReceptors, Purinergic P2X4Receptors, Purinergic P2X7Signal TransductionX-Ray MicrotomographyReceptors, Purinergic P2X4Receptors, Purinergic P2X7Bone metabolismBone structureKnockout miceP2X4 purinergic receptorP2X7 purinergic receptor

Identifiers

PMID33856623
PMCPMC8155156
OpenAlexW3153063786

What OpenQuestion holds

Textmetadata
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.