Evidence map›Paper›PMID 27068108›Full record

ArticleDevelopment (Cambridge, England)2016

mTor signaling is required for the formation of proliferating Müller glia-derived progenitor cells in the chick retina.

Christopher P Zelinka, Leo Volkov, Zachary A Goodman, Levi Todd, Isabella Palazzo, William A Bishop, Andy J Fischer

Open access · greenAbstract read
In one paragraph

Article in Development (Cambridge, England), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

45 citing papers in PubMed, 72 citations in OpenAlex.

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  19. Retina regeneration: lessons from vertebrates.Oxford open neuroscience · 2022
    Review
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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

7 authors at 1 institution in 1 country.

Christopher P ZelinkaDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210-1239, USA.
Leo VolkovDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210-1239, USA.
Zachary A GoodmanDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210-1239, USA.
Levi ToddDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210-1239, USA.
Isabella PalazzoDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210-1239, USA.
William A BishopDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210-1239, USA.
Andy J FischerDepartment of Neuroscience, College of Medicine, The Ohio State University, 4190 Graves Hall, 333 West 10th Avenue, Columbus, OH 43210-1239, USA andrew.fischer@osumc.edu.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

We investigate the roles of mTor signaling in the formation of Müller glia-derived progenitor cells (MGPCs) in the chick retina. During embryonic development, pS6 (a readout of active mTor signaling) is present in early-stage retinal progenitors, differentiating amacrine and ganglion cells, and late-stage progenitors or maturing Müller glia. By contrast, pS6 is present at low levels in a few scattered cell types in mature, healthy retina. Following retinal damage, in which MGPCs are known to form, mTor signaling is rapidly activated in Müller glia. Inhibition of mTor in damaged retinas prevented the accumulation of pS6 in Müller glia and reduced numbers of proliferating MGPCs. Inhibition of mTor had no effect on MAPK signaling or on upregulation of the stem cell factor Klf4, whereas Pax6 upregulation was significantly reduced. Inhibition of mTor potently blocked the MGPC-promoting effects of Hedgehog, Wnt and glucocorticoid signaling in damaged retinas. In the absence of retinal damage, insulin, IGF1 and FGF2 induced pS6 in Müller glia, and this was blocked by mTor inhibitor. In FGF2-treated retinas, in which MGPCs are known to form, inhibition of mTor blocked the accumulation of pS6, the upregulation of Pax6 and the formation of proliferating MGPCs. We conclude that mTor signaling is required, but not sufficient, to stimulate Müller glia to give rise to proliferating progenitors, and the network of signaling pathways that drive the formation of MGPCs requires activation of mTor.

Indexed as

Signal TransductionAnimalsCell MovementCell NucleusCell ProliferationChickensEpendymoglial CellsFibroblast Growth Factor 2InsulinInsulin-Like Growth Factor IInsulin-Like Growth Factor IIMAP Kinase Signaling SystemModels, BiologicalNeurogliaN-MethylaspartatePAX6 Transcription FactorFibroblast Growth Factor 2InsulinInsulin-Like Growth Factor IInsulin-Like Growth Factor IIN-MethylaspartatePAX6 Transcription FactorPhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktPTEN PhosphohydrolaseSirolimusTOR Serine-Threonine KinasesmTorMüller gliaProgenitorRegenerationRetina

Identifiers

PMID27068108
PMCPMC4920162
OpenAlexW2329189651

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.