Evidence map›Paper›PMID 22927401›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2012

Regulation of beta catenin signaling and parathyroid hormone anabolic effects in bone by the matricellular protein periostin.

Nicolas Bonnet, Simon J Conway, Serge L Ferrari

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 83 papers.

0numbers the graph read from it
0cells of the map it votes in
83citing papers in PubMed
7.2field-weighted citation impact, top 2% 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

83 citing papers in PubMed, 143 citations in OpenAlex.

  1. Trial
  2. Identification and characterization of POSTNJournal of orthopaedic translation · 2026
    Article
  3. Mechanisms underlying the waning of osteoanabolic therapy effects in osteoporosis.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2026
    Review
  4. Article
  5. Review
  6. Article
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Review
  14. PeriostinBone research · 2024
    Article
  15. Article
  16. Article
  17. Review
  18. Review
  19. Periostin in Osteoporosis and Cardiovascular Disease.Journal of the Endocrine Society · 2023
    Review
  20. Article

23 more citing papers are in PubMed but not listed here.

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

3 authors at 2 institutions in 3 countries.

Nicolas BonnetDivision of Bone Diseases, Department of Rehabilitation and Geriatrics, World Health Organization Collaborating Center for Osteoporosis Prevention, Geneva University Hospital and Faculty of Medicine, Geneva 14, Switzerland. nicolas.bonnet@unige.ch
Simon J Conway
Serge L Ferrari
World Health Organization · CHIndiana University School of Medicine

Funding

NEURAL-CREST RELATED HEART DEFECTSR01HL060714 · NHLBI · MEDICAL COLLEGE OF GEORGIA (MCG) · PI CONWAY, SIMON JAMES · 1998 to 2017
$4.7M
NHLBI NIH HHS HL60714NHLBI NIH HHS R01 HL060714
6 · The paper itself

Abstract

Periostin (Postn) is a matricellular protein preferentially expressed by osteocytes and periosteal osteoblasts in response to mechanical stimulation and parathyroid hormone (PTH). Whether and how periostin expression influences bone anabolism, however, remains unknown. We investigated the skeletal response of adult Postn(-/-) and Postn(+/+) mice to intermittent PTH. Compared with Postn(+/+), Postn(-/-) mice had a lower bone mass, cortical bone volume, and strength response to PTH. PTH-stimulated bone-forming indices were all significantly lower in Postn(-/-) mice, particularly at the periosteum. Furthermore, in vivo stimulation of Wnt-β-catenin signaling by PTH, as evaluated in TOPGAL reporter mice, was inhibited in the absence of periostin (TOPGAL;Postn(-/-) mice). PTH stimulated periostin and inhibited MEF2C and sclerostin (Sost) expression in bone and osteoblasts in vitro. Recombinant periostin also suppressed Sost expression, which was mediated through the integrin αVβ3 receptor, whereas periostin-blocking antibody prevented inhibition of MEF2C and Sost by PTH. In turn, administration of a Sost-blocking antiboby partially restored the PTH-mediated increase in bone mass in Postn(-/-) mice. In addition, primary osteoblasts from Postn(-/-) mice showed a lower proliferation, mineralization, and migration, both spontaneously and in response to PTH. Osteoblastic gene expression levels confirmed a defect of Postn(-/-) osteoblast differentiation with and without PTH, as well as an increased osteoblast apoptosis in the absence of periostin. These data elucidate the complex role of periostin on bone anabolism, through the regulation of Sost, Wnt-β-catenin signaling, and osteoblast differentiation.

Indexed as

Adaptor Proteins, Signal TransducingAnabolic AgentsAnimalsbeta CateninBlotting, WesternCell Adhesion MoleculesGene Expression RegulationGlycoproteinsImmunohistochemistryIntegrin alphaVbeta3Intercellular Signaling Peptides and ProteinsMEF2 Transcription FactorsMiceMice, KnockoutMyogenic Regulatory FactorsOsteoblastsAdaptor Proteins, Signal TransducingAnabolic Agentsbeta CateninCell Adhesion MoleculesGlycoproteinsIntegrin alphaVbeta3Intercellular Signaling Peptides and ProteinsMef2c protein, mouseMEF2 Transcription FactorsMyogenic Regulatory FactorsParathyroid HormonePostn protein, mouseSost protein, mouse

Identifiers

PMID22927401
PMCPMC3443161
OpenAlexW2128777779

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.