Evidence map›Paper›PMID 28703293›Full record

ArticleGlia2017

BMP- and TGFβ-signaling regulate the formation of Müller glia-derived progenitor cells in the avian retina.

Levi Todd, Isabella Palazzo, Natalie Squires, Ninoshka Mendonca, Andy J Fischer

Open access · greenAbstract read
In one paragraph

Article in Glia, 2017. 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
4.6field-weighted citation impact, top 5% 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, 69 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Monocyte Invasion into the Retina Restricts the Regeneration of Neurons from Müller Glia.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024
    Article
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  8. Article
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  10. Article
  11. Article
  12. Article
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  14. Review
  15. Article
  16. Article
  17. Article
  18. Retina regeneration: lessons from vertebrates.Oxford open neuroscience · 2022
    Review
  19. Review
  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

5 authors at 1 institution in 1 country.

Levi ToddDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Ave, Columbus, Ohio, 43210.
Isabella PalazzoDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Ave, Columbus, Ohio, 43210.
Natalie SquiresDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Ave, Columbus, Ohio, 43210.
Ninoshka MendoncaDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Ave, Columbus, Ohio, 43210.
Andy J FischerDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Ave, Columbus, Ohio, 43210.ORCID 0000-0001-6123-7405
The Ohio State University · US

Funding

Muller glia: roles in retinal homeostasis and neuronal regenerationR01EY022030 · NEI · OHIO STATE UNIVERSITY · PI FISCHER, ANDY J · 2012 to 2021
$3.5M
NEI NIH HHS R01 EY022030
6 · The paper itself

Abstract

Müller glia-derived progenitor cells (MGPCs) have the capability to regenerate neurons in the retinas of different vertebrate orders. The formation of MGPCs is regulated by a network of cell-signaling pathways. The purpose of this study was to investigate how BMP/Smad1/5/8- and TGFβ/Smad2/3-signaling are coordinated to influence the formation of MGPCs in the chick model system. We find that pSmad1/5/8 is selectively up-regulated in the nuclei of Müller glia following treatment with BMP4, FGF2, or NMDA-induced damage, and this up-regulation is blocked by a dorsomorphin analogue DMH1. By comparison, Smad2/3 is found in the nuclei of Müller glia in untreated retinas, and becomes localized to the cytoplasm following NMDA- or FGF2-treatment. These findings suggest a decrease in TGFβ- and increase in BMP-signaling when MGPCs are known to form. In both NMDA-damaged and FGF2-treated retinas, inhibition of BMP-signaling suppressed the proliferation of MGPCs, whereas inhibition of TGFβ-signaling stimulated the proliferation of MGPCs. Consistent with these findings, TGFβ2 suppressed the formation of MGPCs in NMDA-damaged retinas. Our findings indicate that BMP/TGFβ/Smad-signaling is recruited into the network of signaling pathways that controls the formation of proliferating MGPCs. We conclude that signaling through BMP4/Smad1/5/8 promotes the formation of MGPCs, whereas signaling through TGFβ/Smad2/3 suppresses the formation of MGPCs.

Indexed as

AnimalsAnimals, NewbornBone Morphogenetic Protein 4BromodeoxyuridineCell ProliferationChickensEnzyme InhibitorsEpendymoglial CellsFibroblast Growth Factor 2In Situ Nick-End LabelingN-MethylaspartateReceptors, Transforming Growth Factor betaRetinaRNA, MessengerSignal TransductionSmad Proteins1-(3-dimethylaminopropyl)-3-ethylureaBMP4 protein, humanBone Morphogenetic Protein 4BromodeoxyuridineEnzyme InhibitorsFibroblast Growth Factor 2N-MethylaspartateReceptors, Transforming Growth Factor betaRNA, MessengerSmad ProteinsUreaBMP-signalingMuller gliaregenerationretinaretinal gliaretina regenerationTGFβ-signaling

Identifiers

PMID28703293
PMCPMC5628513
OpenAlexW2735318647

What Socratic holds

Textmetadata
LicenceTDM
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 Socratic graph.