Evidence map›Paper›PMID 31842918›Full record

ArticleCell communication and signaling : CCS2019

N-methyl-D-aspartate (NMDA) receptor expression and function is required for early chondrogenesis.

Csaba Matta, Tamás Juhász, János Fodor, Tibor Hajdú, Éva Katona, Csilla Szűcs-Somogyi, Roland Takács, Judit Vágó, Tamás Oláh, Ádám Bartók and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cell communication and signaling : CCS, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

12 citing papers in PubMed, 18 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Potential Targeting Mechanisms for Bone-Directed Therapies.International journal of molecular sciences · 2024
    Review
  5. Review
  6. Review
  7. Article
  8. CaInternational journal of molecular sciences · 2023
    Review
  9. Review
  10. Article
  11. Review
  12. 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

14 authors at 2 institutions in 2 countries.

Csaba MattaDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. matta.csaba@med.unideb.hu.ORCID 0000-0002-9678-7420
Tamás JuhászDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
János FodorDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tibor HajdúDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Éva KatonaDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Csilla Szűcs-SomogyiDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Roland TakácsDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Judit VágóDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Tamás OláhDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Ádám BartókDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Zoltan VargaDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Gyorgy PanyiDepartment of Biophysics and Cell Biology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
László CsernochDepartment of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
Róza ZákányDepartment of Anatomy, Histology and Embryology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary. roza@anat.med.unideb.hu.
University of Debrecen · HUSemmelweis University · HU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIn vitro chondrogenesis depends on the concerted action of numerous signalling pathways, many of which are sensitive to the changes of intracellular Ca

methodsWe studied the role of glutamatergic signalling during the course of in vitro chondrogenesis in high density chondrifying cell cultures using single cell fluorescent calcium imaging, patch clamp, transient gene silencing, and western blotting.

resultsHere we show that key components of the glutamatergic signalling pathways are functional during in vitro chondrogenesis in a primary chicken chondrogenic model system. We also present the full glutamate receptor subunit mRNA and protein expression profile of these cultures. This is the first study to report that NMDA-mediated signalling may act as a key factor in embryonic limb bud-derived chondrogenic cultures as it evokes intracellular Ca

conclusionsWe propose a key role for NMDARs during the transition of chondroprogenitor cells to cartilage matrix-producing chondroblasts.

Indexed as

AnimalsCalciumCell ProliferationCells, CulturedCell SurvivalChickensChondrogenesisGlutamic AcidN-MethylaspartateReceptors, N-Methyl-D-AspartateSignal TransductionCalciumGlutamic AcidN-MethylaspartateReceptors, N-Methyl-D-AspartateChondrocyteChondrogenesisGlutamate signallingGlycineNMDARN-methyl-D-aspartate receptorSingle cell calcium imagingsiRNA

Identifiers

PMID31842918
PMCPMC6915923
OpenAlexW2994742285

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.