Evidence map›Paper›PMID 23136411›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2012

Conditional Müllercell ablation causes independent neuronal and vascular pathologies in a novel transgenic model.

Weiyong Shen, Marcus Fruttiger, Ling Zhu, Sook H Chung, Nigel L Barnett, Joshua K Kirk, SoRa Lee, Nathan J Coorey, Murray Killingsworth, Larry S Sherman and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 156 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
156citing papers in PubMed, 1 pooled it
7.1field-weighted citation impact, top 2% 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

156 citing papers in PubMed, 1 synthesis or guideline pooled it, 269 citations in OpenAlex.

  1. Pooled it
  2. Trial
  3. Trial
  4. Trial
  5. Article
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    Article
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  19. Review
  20. Review

96 more citing papers are in PubMed but not listed here.

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 6 institutions in 3 countries.

Weiyong ShenSave Sight Institute, The University of Sydney, Sydney 2000, Australia. weiyong.shen@sydney.edu.au
Marcus Fruttiger
Ling Zhu
Sook H Chung
Nigel L Barnett
Joshua K Kirk
SoRa Lee
Nathan J Coorey
Murray Killingsworth
Larry S Sherman
Mark C Gillies
University of Sydney · AUOregon Health & Science University · USQueensland Eye Institute · AUUniversity College London · GBUNSW Sydney · AUWestern Sydney University · AU

Funding

YR 50 PROJ- ROBERTS PRIMATE ISLETP51RR000163 · NCRR · OREGON REGIONAL PRIMATE RESEARCH CENTER · PI OJEDA, SERGIO R · 1985 to 2011
$140.8M
NCRR NIH HHS P51 RR000163
6 · The paper itself

Abstract

Müller cells are the major glia of the retina that serve numerous functions essential to retinal homeostasis, yet the contribution of Müller glial dysfunction to retinal diseases remains largely unknown. We have developed a transgenic model using a portion of the regulatory region of the retinaldehyde binding protein 1 gene for conditional Müller cell ablation and the consequences of primary Müller cell dysfunction have been studied in adult mice. We found that selective ablation of Müller cells led to photoreceptor apoptosis, vascular telangiectasis, blood-retinal barrier breakdown and, later, intraretinal neovascularization. These changes were accompanied by impaired retinal function and an imbalance between vascular endothelial growth factor-A (VEGF-A) and pigment epithelium-derived factor. Intravitreal injection of ciliary neurotrophic factor inhibited photoreceptor injury but had no effect on the vasculopathy. Conversely, inhibition of VEGF-A activity attenuated vascular leak but did not protect photoreceptors. Our findings show that Müller glial deficiency may be an important upstream cause of retinal neuronal and vascular pathologies in retinal diseases. Combined neuroprotective and anti-angiogenic therapies may be required to treat Müller cell deficiency in retinal diseases and in other parts of the CNS associated with glial dysfunction.

Indexed as

AnimalsApoptosisBlood-Retinal BarrierCiliary Neurotrophic FactorEye ProteinsMiceMice, TransgenicNerve Growth FactorsNeurogliaPhotoreceptor CellsPigment Epithelium-Derived FactorRetinaRetinal NeovascularizationRetinal TelangiectasisRetinal VesselsSerpinsCiliary Neurotrophic FactorEye ProteinsNerve Growth FactorsPigment Epithelium-Derived FactorSerpinsVascular Endothelial Growth Factor A

Identifiers

PMID23136411
PMCPMC4014009
OpenAlexW2030814182

What OpenQuestion 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 OpenQuestion graph.