Evidence map›Paper›PMID 20621651›Full record

ArticleExperimental eye research2010

Axonal degeneration, regeneration and ganglion cell death in a rodent model of anterior ischemic optic neuropathy (rAION).

Cheng Zhang, Yan Guo, Bernard J Slater, Neil R Miller, Steven L Bernstein

Open access · greenAbstract read
In one paragraph

Article in Experimental eye research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% 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

32 citing papers in PubMed, 1 synthesis or guideline pooled it, 54 citations in OpenAlex.

  1. Pooled it
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  12. Analysis of Macular Microperimetry Characteristics in Non-Arteritic Anterior Ischemic Optic Neuropathy.Medical science monitor : international medical journal of experimental and clinical research · 2020
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  20. Biocompatibility of intravitreal injection of human mesenchymal stem cells in immunocompetent rabbits.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2018
    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

5 authors at 3 institutions in 2 countries.

Cheng ZhangWilmer Eye Institute, Johns Hopkins Hospital, 600 N Wolfe Street, Baltimore, MD 21287, USA.
Yan Guo
Bernard J Slater
Neil R Miller
Steven L Bernstein
University of Maryland, Baltimore · USFirst Affiliated Hospital of Zhengzhou University · CNJohns Hopkins Hospital · 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 R01 EY015304NEI NIH HHS R01 EY019529
6 · The paper itself

Abstract

Using laser-induced photoactivation of intravenously administered rose Bengal in rats, we generated an ischemic infarction of the intrascleral portion of the optic nerve (ON) comparable to that which occurs in humans to investigate optic nerve axon degenerative events following optic nerve infarct and the potential for axon re-growth. Animals were euthanized at different times post infarct. Axon degeneration was evaluated with SMI312 immunolabeling, and GAP-43 immunostaining was used to identify axon regeneration. Terminal dUTP nick end labeling (TUNEL) was used to evaluate retinal ganglion cell (RGC) death. There was significant axon structural disruptinot ion at the anterior intrascleral portion of the ON by 3d post-infarct, extending to the posterior ON by 7d post-stroke. Destruction of normal axon structure and massive loss of axon fibers occurred by 2 weeks. GAP-43 immunoreactivity occurred in the anterior ON by 7d post-infarct, lasting 3-4 weeks, without extension past the primary ischemic lesion. TUNEL-positive cells in the RGC layer appeared by 7d post-insult. These results indicate that following induction of ischemic optic neuropathy, significant axon damage occurs by 3d post-infarct, with later neuronal death. Post-stroke adult rat retinal ganglion cells attempt to regenerate their axons, but this effort is restricted to the unmyelinated region of the anterior ON. These responses are important in understanding pathologic process that underlies human non-arteritic anterior ischemic optic neuropathy (NAION) and may guide both the appropriate treatment of NAION and the window of opportunity for such treatment.

Indexed as

ApoptosisDisease Models, AnimalAnimalsAxonsFluorescent Antibody Technique, IndirectGAP-43 ProteinInfarctionIn Situ Nick-End LabelingNerve DegenerationNerve RegenerationNeurofilament ProteinsOptic NerveOptic Neuropathy, IschemicRatsRats, Sprague-DawleyRetinal Ganglion CellsGAP-43 ProteinNeurofilament ProteinsRose Bengal

Identifiers

PMID20621651
PMCPMC2907443
OpenAlexW1999453116

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.