Evidence map›Paper›PMID 25085975›Full record

ArticleDevelopment (Cambridge, England)2014

Glucocorticoid receptors in the retina, Müller glia and the formation of Müller glia-derived progenitors.

Donika Gallina, Christopher Zelinka, Andy J Fischer

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing 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

56 citing papers in PubMed, 84 citations in OpenAlex.

  1. Article
  2. Article
  3. The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025
    Review
  4. Review
  5. Microglia response and function in a chronic model of photoreceptor damage.Frontiers in cell and developmental biology · 2025
    Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Circadian rhythm of intraocular pressure.The journal of physiological sciences : JPS · 2024
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Review
  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

3 authors at 1 institution in 1 country.

Donika GallinaDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210, USA.
Christopher ZelinkaDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210, USA.
Andy J FischerDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210, USA fischer.412@osu.edu.
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 EY022030-02NEI NIH HHS R01 EY022030
6 · The paper itself

Abstract

Identification of the signaling pathways that influence the reprogramming of Müller glia into neurogenic retinal progenitors is key to harnessing the potential of these cells to regenerate the retina. Glucocorticoid receptor (GCR) signaling is commonly associated with anti-inflammatory responses and GCR agonists are widely used to treat inflammatory diseases of the eye, even though the cellular targets and mechanisms of action in the retina are not well understood. We find that signaling through GCR has a significant impact upon the ability of Müller glia to become proliferating Müller glia-derived progenitor cells (MGPCs). The primary amino acid sequence and pattern of GCR expression in the retina is highly conserved across vertebrate species, including chickens, mice, guinea pigs, dogs and humans. In all of these species we find GCR expressed by the Müller glia. In the chick retina, we find that GCR is expressed by progenitors in the circumferential marginal zone (CMZ) and is upregulated by Müller glia in acutely damaged retinas. Activation of GCR signaling inhibits the formation of MGPCs and antagonizes FGF2/MAPK signaling in the Müller glia. By contrast, we find that inhibition of GCR signaling stimulates the formation of proliferating MGPCs in damaged retinas, and enhances the neuronal differentiation while diminishing glial differentiation. Given the conserved expression pattern of GCR in different vertebrate retinas, we propose that the functions and mechanisms of GCR signaling are highly conserved and are mediated through the Müller glia. We conclude that GCR signaling directly inhibits the formation of MGPCs, at least in part, by interfering with FGF2/MAPK signaling.

Indexed as

AnimalsCell ProliferationDexamethasoneEpendymoglial CellsFibroblast Growth Factor 2HumansMAP Kinase Signaling SystemMicrogliaN-MethylaspartateReceptors, GlucocorticoidRetinaRetinal Pigment EpitheliumSignal TransductionStem CellsTOR Serine-Threonine KinasesDexamethasoneFibroblast Growth Factor 2N-MethylaspartateReceptors, GlucocorticoidTOR Serine-Threonine KinasesChickGlucocorticoidsMouseMüller gliaRegenerationRetina

Identifiers

PMID25085975
PMCPMC4199119
OpenAlexW2133415315

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.