Evidence map›Paper›PMID 21297990›Full record

ArticlePloS one2011

Interaction of TGFβ and BMP signaling pathways during chondrogenesis.

Bettina Keller, Tao Yang, Yuqing Chen, Elda Munivez, Terry Bertin, Bernhard Zabel, Brendan Lee

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% 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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. A synthetic, closed-looped gene circuit for the autonomous regulation of RUNX2 activity during chondrogenesis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2024
    Article
  6. Review
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  16. Axial mechanical loading toBone reports · 2021
    Article
  17. Review
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  20. Article

5 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

7 authors at 3 institutions in 2 countries.

Bettina KellerDepartment of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America.
Tao Yang
Yuqing Chen
Elda Munivez
Terry Bertin
Bernhard Zabel
Brendan Lee
Baylor College of Medicine · USHoward Hughes Medical Institute · USUniversity Medical Center Freiburg · DE

Funding

THE SKELETAL DYSPLASIASP01HD022657 · NICHD · CEDARS-SINAI MEDICAL CENTER · PI LEE, BRENDAN · 1987 to 2011
$17.0M
Project 3: Collagen post-translational modification and cross-linking in OIP01HD070394 · NICHD · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN · 2011 to 2020
$13.4M
Mouse mutations that model human craniofacial/limb abnormalitiesP01ES011253 · NIEHS · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN HL · 2001 to 2005
$5.4M
Transcriptional Regulation of Craniofacial SkeletogenesisR01DE016990 · NIDCR · BAYLOR COLLEGE OF MEDICINE · PI LEE, BRENDAN · 2005 to 2009
$1.6M
Howard Hughes Medical InstituteNICHD NIH HHS HD22657NICHD NIH HHS P01 HD022657NICHD NIH HHS P01 HD070394NIDCR NIH HHS DE016990NIDCR NIH HHS R01 DE016990NIEHS NIH HHS ES11253NIEHS NIH HHS P01 ES011253
6 · The paper itself

Abstract

TGFβ and BMP signaling pathways exhibit antagonistic activities during the development of many tissues. Although the crosstalk between BMP and TGFβ signaling pathways is well established in bone development, the relationship between these two pathways is less well defined during cartilage development and postnatal homeostasis. We generated hypomorphic mouse models of cartilage-specific loss of BMP and TGFβ signaling to assess the interaction of these pathways in postnatal growth plate homeostasis. We further used the chondrogenic ATDC5 cell line to test effects of BMP and TGFβ signaling on each other's downstream targets. We found that conditional deletion of Smad1 in chondrocytes resulted in a shortening of the growth plate. The addition of Smad5 haploinsufficiency led to a more severe phenotype with shorter prehypertrophic and hypertrophic zones and decreased chondrocyte proliferation. The opposite growth plate phenotype was observed in a transgenic mouse model of decreased chondrocytic TGFβ signaling that was generated by expressing a dominant negative form of the TGFβ receptor I (ΔTβRI) in cartilage. Histological analysis demonstrated elongated growth plates with enhanced Ihh expression, as well as an increased proliferation rate with altered production of extracellular matrix components. In contrast, in chondrogenic ATDC5 cells, TGFβ was able to enhance BMP signaling, while BMP2 significantly reduces levels of TGF signaling. In summary, our data demonstrate that during endochondral ossification, BMP and TGFβ signaling can have antagonistic effects on chondrocyte proliferation and differentiation in vivo. We also found evidence of direct interaction between the two signaling pathways in a cell model of chondrogenesis in vitro.

Indexed as

ChondrogenesisAnimalsBone Morphogenetic Protein 1Bone Morphogenetic Protein 2Bone Morphogenetic ProteinsCartilageCell DifferentiationCell ProliferationGrowth PlateMiceModels, AnimalReceptor Cross-TalkSignal TransductionSmad ProteinsTransforming Growth Factor betaBmp1 protein, mouseBmp2 protein, mouseBone Morphogenetic Protein 1Bone Morphogenetic Protein 2Bone Morphogenetic ProteinsSmad ProteinsTransforming Growth Factor beta

Identifiers

PMID21297990
PMCPMC3030581
OpenAlexW1968127119

What OpenQuestion 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 OpenQuestion graph.