Evidence map›Paper›PMID 24065807›Full record

ArticleInvestigative ophthalmology & visual science2013

Optic nerve inflammation and demyelination in a rodent model of nonarteritic anterior ischemic optic neuropathy.

Bernard J Slater, Fernandino L Vilson, Yan Guo, Daniel Weinreich, Shelly Hwang, Steven L Bernstein

Open access · hybridAbstract readComparative Study
In one paragraph

Article in Investigative ophthalmology & visual science, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed, 1 pooled it
1.5field-weighted citation impact, top 18% 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

23 citing papers in PubMed, 1 synthesis or guideline pooled it, 37 citations in OpenAlex.

  1. Pooled it
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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

6 authors at 1 institution in 1 country.

Bernard J SlaterDepartment of Ophthalmology and Visual Sciences, University of Maryland-Baltimore, Baltimore, Maryland.
Fernandino L Vilson
Yan Guo
Daniel Weinreich
Shelly Hwang
Steven L Bernstein
University of Maryland, Baltimore · US

Funding

Mechanisms of Optic Nerve Stroke NeuroprotectionR01EY015304 · NEI · UNIVERSITY OF MARYLAND BALTIMORE · PI BERNSTEIN, STEVEN L · 2004 to 2018
$4.7M
Preclinical analysis of ischemic optic nerve treatmentR01EY019529 · NEI · UNIVERSITY OF MARYLAND BALTIMORE · PI BERNSTEIN, STEVEN L · 2009 to 2013
$2.2M
NEI NIH HHS EY-015304NEI NIH HHS EY-019529NEI NIH HHS R01 EY015304NEI NIH HHS R01 EY019529
6 · The paper itself

Abstract

purposeOptic nerve (ON) ischemia associated with nonarteric anterior ischemic optic neuropathy (NAION) results in axon and myelin damage. Myelin damage activates the intraneural Ras homolog A (RhoA), contributing to axonal regeneration failure. We hypothesized that increasing extrinsic macrophage activity after ON infarct would scavenge degenerate myelin and improve postischemic ON recovery. We used the cytokine granulocyte-macrophage colony-stimulating factor (GM-CSF) to upregulate ON macrophage activity, and evaluated GM-CSF's effects after ON ischemia in the NAION rodent model (rAION).

methodsFollowing rAION induction, GM-CSF was administered via intraventricular injection. Retinal ganglion cell (RGC) stereologic analysis was performed 1 month postinduction. The retinae and optic nerve laminae of vehicle- and GM-CSF-treated animals were examined immunohistochemically and ultrastructurally using transmission electron microscopy (TEM). RhoA activity was analyzed using a rhotekin affinity immunoanalysis and densitometry. Isolated ONs were analyzed functionally ex vivo by compound action potential (CAP) analysis.

resultsRodent NAION produces ON postinfarct demyelination and myelin damage, functionally demonstrable by CAP analysis and ultrastructurally by TEM. Granulocyte-macrophage colony-stimulating factor increased intraneural inflammation, activating and recruiting endogenous microglia, with only a moderate amount of exogenous macrophage recruitment. Treatment with GM-CSF reduced postinfarct intraneural RhoA activity, but did not neuroprotect RGCs after rAION.

conclusionsSudden ON ischemia results in previously unrecognized axonal demyelination, which may have a clinically important role in NAION-related functional defects and recovery. Granulocyte-macrophage colony-stimulating factor is not neuroprotective when administered directly to the optic nerve following ON ischemia, and does not improve axonal regeneration. It dramatically increases ON-microglial activation and recruitment.

Indexed as

AnimalsDemyelinating DiseasesDensitometryDisease Models, AnimalGranulocyte-Macrophage Colony-Stimulating FactorMaleMicrogliaMicroscopy, Electron, TransmissionOptic NerveOptic NeuritisOptic Neuropathy, IschemicRatsRats, Sprague-DawleyRetinal Ganglion CellsUp-RegulationGranulocyte-Macrophage Colony-Stimulating FactorGM-CSFimmune regulationmacrophagesmicroglianaionoptic nerve ischemiapostinfarct demyelinationrodent models

Identifiers

PMID24065807
PMCPMC3854773
OpenAlexW1975473487

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.