Evidence map›Paper›PMID 23986258›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

TGF-β signaling protects retinal neurons from programmed cell death during the development of the mammalian eye.

Barbara M Braunger, Stefan Pielmeier, Cora Demmer, Victoria Landstorfer, Daniela Kawall, Natalie Abramov, Marco Leibinger, Ingo Kleiter, Dietmar Fischer, Herbert Jägle and 1 more

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
–field-weighted citation impact, top 96% 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

41 citing papers in PubMed, 1 citations in OpenAlex.

  1. Article
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  5. Article
  6. TGF-β signaling in health, disease, and therapeutics.Signal transduction and targeted therapy · 2024
    Review
  7. Article
  8. Article
  9. Article
  10. Review
  11. Review
  12. Article
  13. Review
  14. Optic neuropathy associated with TGFβ dysregulation in mice with a glaucoma-causative mutation of ADAMTS10.Matrix biology : journal of the International Society for Matrix Biology · 2022
    Article
  15. Article
  16. Article
  17. Retina regeneration: lessons from vertebrates.Oxford open neuroscience · 2022
    Review
  18. Review
  19. Adamts10 controls transforming growth factorFrontiers in molecular biosciences · 2022
    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

11 authors at 4 institutions in 1 country.

Barbara M BraungerInstitute of Human Anatomy and Embryology, University of Regensburg, D-93053 Regensburg, Germany.
Stefan Pielmeier
Cora Demmer
Victoria Landstorfer
Daniela Kawall
Natalie Abramov
Marco Leibinger
Ingo Kleiter
Dietmar Fischer
Herbert Jägle
Ernst R Tamm
University of Regensburg · DEHeinrich Heine University Düsseldorf · DERuhr University Bochum · DEUniversity Hospital Regensburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We investigated the influence of transforming growth factor-β (TGF-β) signaling on developmental programmed cell death in the mouse retina by direct and specific molecular targeting of TGF-β type II receptor (TβRII) and Smad7 in retinal progenitor cells. Mice were generated carrying a conditional deletion of the TβRII in cells that originate from the inner layer of the optic cup. The animals showed a significant decrease of phosphorylated Smad3 in both the central and peripheral retina, which indicates the diminished activity of TGF-β signaling. TβRII deficiency significantly increased the apoptotic death of retinal neurons during embryonic and postnatal development without affecting their proliferation. In contrast, treatment with TGF-β2 inhibited cell death of retinal ganglion cells in dissociated retinal cell cultures, an effect that was blocked by inhibiting the phosphorylation of Smad3. The increase in apoptosis during development resulted in a significant reduction in the number of neurons in adult TβRII-deficient mice. The effect was most pronounced in the inner retina neurons and resulted in functional deficits as determined by electroretinography. In contrast, a conditional deletion of TGF-β-inhibiting Smad7 in retinal neurons significantly enhanced Smad3 phosphorylation and significantly decreased apoptosis of retinal neurons in embryos and pups. Moreover, the number of retinal ganglion cells was significantly higher in Smad7-deficient mice compared with control littermates. TβRII-deficient pups showed a lower level of nerve growth factor (NGF) in its mRNA; however, higher levels were observed in Smad7-deficient pups, which strongly suggests that the protective effects of TGF-β signaling on developmental cell death are mediated through NGF.

Indexed as

ApoptosisAnimalsCell ProliferationEmbryo, MammalianGene DeletionGene Expression Regulation, DevelopmentalMiceNerve Growth FactorPhosphorylationProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIRetinal NeuronsRNA, MessengerSignal TransductionSmad7 ProteinNerve Growth FactorProtein Serine-Threonine KinasesReceptors, Transforming Growth Factor betaReceptor, Transforming Growth Factor-beta Type IIRNA, MessengerSmad7 ProteinSmad7 protein, mouseTransforming Growth Factor beta

Identifiers

PMID23986258
PMCPMC6618509
OpenAlexW783568932

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.