Evidence map›Paper›PMID 20861490›Full record

ArticleInvestigative ophthalmology & visual science2011

RhoA inactivation prevents photoreceptor axon retraction in an in vitro model of acute retinal detachment.

Aurora Maria Fontainhas, Ellen Townes-Anderson

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
0.9field-weighted citation impact, top 27% 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

27 citing papers in PubMed, 53 citations in OpenAlex.

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  10. Coming of Age for the Photoreceptor Synapse.Investigative ophthalmology & visual science · 2021
    Article
  11. Article
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  14. Rho kinase inhibitors-a review on the physiology and clinical use in Ophthalmology.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2019
    Review
  15. Article
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  18. Sema3A Reduces Sprouting of Adult Rod Photoreceptors In Vitro.Investigative ophthalmology & visual science · 2017
    Article
  19. Article
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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

2 authors at 1 institution in 1 country.

Aurora Maria FontainhasIntegrative Neurosciences Program, Graduate School of Biomedical Sciences, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA.
Ellen Townes-Anderson
Rutgers, The State University of New Jersey · US

Funding

PLASTICITY AND REGENERATION OF RETINAL SYNAPSESR01EY012031 · NEI · UNIV OF MED/DENT OF NJ-NJ MEDICAL SCHOOL · PI TOWNES-ANDERSON, ELLEN S · 1998 to 2010
$3.1M
NEI NIH HHS EY 012031NEI NIH HHS R01 EY012031
6 · The paper itself

Abstract

purposeAn early injury response to retinal detachment is disruption of synaptic connectivity between photoreceptors and second-order neurons. Most dramatic is the retraction of rod cell axons and their terminals away from the outer synaptic layer and toward their cell bodies. This study tested whether axonal retraction in detached retina was due to the activation of the small GTPase RhoA and was preventable using RhoA antagonists.

methodsRetinal detachments were created in in vitro preparations of porcine eyecups. RhoA activation was determined with a Rhotekin binding assay. To block axon retraction, drugs were applied to neural retinal explants either before or after detachment from the retinal pigment epithelium. Presynaptic movement was quantified by image analysis of double-labeled retinas examined with confocal microscopy.

resultsActive RhoA increases transiently after detachment followed by morphologic evidence of axonal retraction over the next 24 hours. Pretreating the retina with a RhoA antagonist, CT-04, or a Rho kinase inhibitor, Y27632, at multiple concentrations significantly inhibited axonal retraction. Reducing calcium influx through L-type calcium channels with nicardipine also blocked retraction. To create a more plausible therapeutic scenario, drug treatments were delayed and applied after retinal detachment. The Rho kinase inhibitor, but not nicardipine, significantly blocked rod axonal retraction when applied up to 6 hours after detachment.

conclusionsThus, RhoA and downstream Rho kinase activity constitute part of the mechanism that produces rod axonal retraction in retinal explants. Treatments that manipulate RhoA signaling may promote synaptic stability after retinal detachment.

Indexed as

Models, BiologicalAnimalsAxonsCalciumCalcium Channel BlockersEnzyme InhibitorsFemaleFluorescent Antibody Technique, IndirectMaleMicroscopy, ConfocalNeuronal PlasticityNicardipinePhotoreceptor Cells, VertebrateRetinal DetachmentRetinal NeuronsRetinal Pigment EpitheliumCalciumCalcium Channel BlockersEnzyme InhibitorsNicardipinerhoA GTP-Binding Protein

Identifiers

PMID20861490
PMCPMC3053299
OpenAlexW1997257234

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.