Evidence map›Paper›PMID 23362023›Full record

ArticleGlia2013

EGF stimulates Müller glial proliferation via a BMP-dependent mechanism.

Yumi Ueki, Thomas A Reh

Open access · greenAbstract read
In one paragraph

Article in Glia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

48 citing papers in PubMed, 70 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. A 3D Astrocyte Microenvironment Model Enables Rapid CaAdvanced healthcare materials · 2026
    Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. Cell-Based Therapies: Strategies for Regeneration.Cold Spring Harbor perspectives in medicine · 2023
    Review
  13. Review
  14. Article
  15. Advances in the study of Müller glia reprogramming in mammals.Frontiers in cellular neuroscience · 2023
    Review
  16. Article
  17. Review
  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.

Yumi UekiDepartment of Biological Structure, University of Washington, Seattle, Washington 98195, USA.
Thomas A Reh
University of Washington · US

Funding

Vision Research CoreP30EY001730 · NEI · UNIVERSITY OF WASHINGTON · PI MAUREEN E NEITZ · 1985 to 2026
$23.5M
Supplement to EY021482 to carry out a screen for retinal regeneration using CRISPR-Cas9 gene activation.R01EY021482 · NEI · UNIVERSITY OF WASHINGTON · PI THOMAS A REH · 2011 to 2026
$6.3M
NEI NIH HHS 1R01EY021482NEI NIH HHS P30 EY001730NEI NIH HHS P30EY01730NEI NIH HHS R01 EY021482
6 · The paper itself

Abstract

Müller glia, the major type of glia in the retina, are mitotically quiescent under normal conditions, though they can be stimulated to proliferate in some pathological states. Among these stimuli, EGF is known to be a potent mitogen for Müller glia. However, the signaling pathways required for EGF-mediated proliferation of Müller glia are not clearly understood. In this study, postnatal day 12 (P12) or adult trp53(-/-) mouse retinas were explanted and cultured in the presence of EGF to stimulate Müller glial proliferation. Treatment with signaling inhibitors showed that activation of both MEK/ERK1/2 and PI3K/AKT pathways is required for EGF-induced proliferation of Müller glia. Interestingly, BMP/Smad1/5/8 activation downstream of PI3K/AKT signaling was also necessary for robust Müller glial proliferation, though activation of BMP/Smad1/5/8 signaling alone failed to stimulate their proliferation. In dissociated Müller glial culture, treatment with EGF induced the upregulation of Bmp7, and this upregulation was blocked significantly by co-treatment with the BMP inhibitor dorsomorphin, suggesting that BMP/Smad1/5/8 activation is mediated at least in part by an autocrine mechanism in Müller glia. A better understanding of how BMP/Smad1/5/8 signaling is involved in glial proliferation may have important implications for proliferative disorders, as well as for retinal regeneration in mammalian retinas.

Indexed as

Cell ProliferationAnimalsBone Morphogenetic Protein 7Cells, CulturedEpidermal Growth FactorMiceMice, Inbred C57BLMice, KnockoutNeurogliaPyrazolesPyrimidinesRetinabmp7 protein, mouseBone Morphogenetic Protein 7dorsomorphinEpidermal Growth FactorPyrazolesPyrimidines

Identifiers

PMID23362023
PMCPMC4007577
OpenAlexW1580312135

What OpenQuestion holds

Textmetadata
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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.