Evidence map›Paper›PMID 25605327›Full record

ArticleMolecular and cellular biology2015

Loss of osteoblast Runx3 produces severe congenital osteopenia.

Omri Bauer, Amnon Sharir, Ayako Kimura, Shay Hantisteanu, Shu Takeda, Yoram Groner

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
2.4field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 58 citations in OpenAlex.

  1. Article
  2. Article
  3. Regulation of Skeletal Development and Maintenance by Runx2 and Sp7.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Article
  6. Review
  7. Runt-related transcription factors in human carcinogenesis: a friend or foe?Journal of cancer research and clinical oncology · 2023
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Whole Aspect of Runx2 Functions in Skeletal Development.International journal of molecular sciences · 2022
    Review
  13. Review
  14. Article
  15. Review
  16. Article
  17. Article
  18. Transcriptomic analysis of bone and fibrous tissue morphogenesis during digit tip regeneration in the adult mouse.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
    Article
  19. Article
  20. 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

6 authors at 2 institutions in 2 countries.

Omri BauerDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Amnon SharirDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Ayako KimuraDepartment of Orthopedics, Tokyo Medical and Dental University, Tokyo, Japan.
Shay HantisteanuDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel.
Shu TakedaDepartment of Orthopedics, Tokyo Medical and Dental University, Tokyo, Japan.
Yoram GronerDepartment of Molecular Genetics, Weizmann Institute of Science, Rehovot, Israel Yoram.Groner@weizmann.ac.il.
Weizmann Institute of Science · ILTokyo Medical and Dental University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Congenital osteopenia is a bone demineralization condition that is associated with elevated fracture risk in human infants. Here we show that Runx3, like Runx2, is expressed in precommitted embryonic osteoblasts and that Runx3-deficient mice develop severe congenital osteopenia. Runx3-deficient osteoblast-specific (Runx3(fl/fl)/Col1α1-cre), but not chondrocyte-specific (Runx3(fl/fl)/Col1α2-cre), mice are osteopenic. This demonstrates that an osteoblastic cell-autonomous function of Runx3 is required for proper osteogenesis. Bone histomorphometry revealed that decreased osteoblast numbers and reduced mineral deposition capacity in Runx3-deficient mice cause this bone formation deficiency. Neonatal bone and cultured primary osteoblast analyses revealed a Runx3-deficiency-associated decrease in the number of active osteoblasts resulting from diminished proliferation and not from enhanced osteoblast apoptosis. These findings are supported by Runx3-null culture transcriptome analyses showing significant decreases in the levels of osteoblastic markers and increases in the levels of Notch signaling components. Thus, while Runx2 is mandatory for the osteoblastic lineage commitment, Runx3 is nonredundantly required for the proliferation of these precommitted cells, to generate adequate numbers of active osteoblasts. Human RUNX3 resides on chromosome 1p36, a region that is associated with osteoporosis. Therefore, RUNX3 might also be involved in human bone mineralization.

Indexed as

AnimalsApoptosisBone and BonesBone DevelopmentBone Diseases, MetabolicCells, CulturedCore Binding Factor Alpha 3 SubunitGene DeletionGene Expression Regulation, DevelopmentalHumansMiceMice, KnockoutOsteoblastsOsteogenesisTranscriptomeCore Binding Factor Alpha 3 Subunit

Identifiers

PMID25605327
PMCPMC4355527
OpenAlexW2112274246

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.