Evidence map›Paper›PMID 25146392›Full record

ArticleJournal of cell science2014

Fibronectin matrix assembly is essential for cell condensation during chondrogenesis.

Purva Singh, Jean E Schwarzbauer

Abstract read
In one paragraph

Article in Journal of cell science, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

29 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Mutations in fibronectin dysregulate chondrogenesis in skeletal dysplasia.Cellular and molecular life sciences : CMLS · 2024
    Article
  5. Potential Targeting Mechanisms for Bone-Directed Therapies.International journal of molecular sciences · 2024
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Hypoxia Modulates Regenerative Potential of Fetal Stem Cells.Applied sciences (Basel, Switzerland) · 2022
    Article
  12. Review
  13. High-impactScience advances · 2021
    Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Purva SinghDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544-1014, USA.
Jean E SchwarzbauerDepartment of Molecular Biology, Princeton University, Princeton, NJ 08544-1014, USA jschwarz@princeton.edu.
Princeton University · US

Funding

Molecular Analysis of Extracellular Matrix AssemblyR01CA160611 · NCI · PRINCETON UNIVERSITY · PI SCHWARZBAUER, JEAN E · 2012 to 2017
$1.6M
NCI NIH HHS CA160611NCI NIH HHS R01 CA160611
6 · The paper itself

Abstract

Mesenchymal cell condensation is the initiating event in endochondral bone formation. Cell condensation is followed by differentiation into chondrocytes, which is accompanied by induction of chondrogenic gene expression. Gene mutations involved in chondrogenesis cause chondrodysplasias and other skeletal defects. Using mesenchymal stem cells (MSCs) in an in vitro chondrogenesis assay, we found that knockdown of the diastrophic dysplasia (DTD) sulfate transporter (DTDST, also known as SLC26A2), which is required for normal cartilage development, blocked cell condensation and caused a significant reduction in fibronectin matrix. Knockdown of fibronectin with small interfering RNAs (siRNAs) also blocked condensation. Fibrillar fibronectin matrix was detected prior to cell condensation, and its levels increased during and after condensation. Inhibition of fibronectin matrix assembly by use of the functional upstream domain (FUD) of adhesin F1 from Streptococcus pyogenes prevented cell condensation by MSCs and also by the chondrogenic cell line ATDC5. Our data show that cell condensation and induction of chondrogenesis depend on fibronectin matrix assembly and DTDST, and indicate that this transporter is required earlier in chondrogenesis than previously appreciated. They also raise the possibility that certain of the skeletal defects in DTD patients might derive from the link between DTDST, fibronectin matrix and condensation.

Indexed as

ChondrogenesisAdhesins, BacterialAnion Transport ProteinsCell DifferentiationCell LineChondrocytesDwarfismFibronectinsHumansMesenchymal Stem CellsRNA, Small InterferingSulfate TransportersAdhesins, BacterialAnion Transport ProteinsFibronectinsRNA, Small InterferingSLC26A2 protein, humanSulfate TransportersChondrogenesisCondensationDiastrophic dysplasia sulfate transporterDTDFibronectin matrix assembly

Identifiers

PMID25146392
PMCPMC4197087
OpenAlexW2109587420

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.