Evidence map›Paper›PMID 27126275›Full record

ArticleJournal of neuroinflammation2016

Retinal glial responses to optic nerve crush are attenuated in Bax-deficient mice and modulated by purinergic signaling pathways.

Caitlin E Mac Nair, Cassandra L Schlamp, Angela D Montgomery, Valery I Shestopalov, Robert W Nickells

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing papers in PubMed
4.5field-weighted citation impact, top 5% 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

52 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
  2. Neuroinflammation in glaucoma: a myriad of cellular pathways and players.Mammalian genome : official journal of the International Mammalian Genome Society · 2026
    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

5 authors at 1 institution in 1 country.

Caitlin E Mac NairDepartment of Ophthalmology and Visual Sciences, University of Wisconsin, 571A Medical Sciences-1300 University Ave, Madison, WI, 53706, USA.
Cassandra L SchlampDepartment of Ophthalmology and Visual Sciences, University of Wisconsin, 571A Medical Sciences-1300 University Ave, Madison, WI, 53706, USA.
Angela D MontgomeryDepartment of Ophthalmology and Visual Sciences, University of Wisconsin, 571A Medical Sciences-1300 University Ave, Madison, WI, 53706, USA.
Valery I ShestopalovDepartment of Ophthalmology, University of Miami Miller School of Medicine, 900 N.W. 17th Street, Miami, FL, 33136, USA.
Robert W NickellsDepartment of Ophthalmology and Visual Sciences, University of Wisconsin, 571A Medical Sciences-1300 University Ave, Madison, WI, 53706, USA. nickells@wisc.edu.
University of Miami · US

Funding

UW Vision Research Core - Administrative CoreP30EY016665 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI ROBERT W NICKELLS · 2005 to 2026
$12.6M
The molecular mechanism of retinal ganglion cell deathR01EY012223 · NEI · UNIVERSITY OF WISCONSIN-MADISON · PI NICKELLS, ROBERT W · 2005 to 2017
$6.3M
The Role of Pannexin 1 Pathway in Ocular Hypertension Injury of Retinal Ganglion CellsR01EY021517 · NEI · UNIVERSITY OF MIAMI SCHOOL OF MEDICINE · PI SHESTOPALOV, VALERY I · 2012 to 2020
$3.1M
Graduate Training In Cellular And Molecular Pathogenesis Of Human DiseasesT32GM081061 · NIGMS · UNIVERSITY OF WISCONSIN-MADISON · PI FABRY, ZSUZSANNA · 2010 to 2019
$1.8M
NEI NIH HHS P30 EY016665NEI NIH HHS R01 EY012223NEI NIH HHS R01 EY021517NIGMS NIH HHS T32 GM081061
6 · The paper itself

Abstract

backgroundRetinal ganglion cell (RGC) soma death is a consequence of optic nerve damage, including in optic neuropathies like glaucoma. The activation of the innate immune network in the retina after nerve damage has been linked to RGC pathology. Since the eye is immune privileged, innate immune functions are the responsibility of the glia, specifically the microglia, astrocytes, and Müller cells that populate the retina. Glial activation, leading to the production of inflammatory cytokines, is a hallmark feature of retinal injury resulting from optic nerve damage and purported to elicit secondary degeneration of RGC somas.

methodsA mouse model of optic nerve crush (ONC) was used to study retinal glial activation responses. RGC apoptosis was blocked using Bax-deficient mice. Glial activation responses were monitored by quantitative PCR and immunofluorescent labeling in retinal sections of activation markers. ATP signaling pathways were interrogated using P2X receptor agonists and antagonists and Pannexin 1 (Panx1)-deficient mice with RGC-specific deletion.

resultsONC induced activation of both macroglia and microglia in the retina, and both these responses were dramatically muted if RGC death was blocked by deletion of the Bax gene. Macroglial, but not microglial, activation was modulated by purinergic receptor activation. Release of ATP after optic nerve damage was not mediated by PANX1 channels in RGCs.

conclusionsRGC death in response to ONC plays a principal stimulatory role in the retinal glial activation response.

Indexed as

Animalsbcl-2-Associated X ProteinDisease Models, AnimalFluorescent Antibody TechniqueMiceMice, KnockoutNerve CrushNeurogliaOptic Nerve InjuriesRetinal Ganglion CellsReverse Transcriptase Polymerase Chain ReactionSignal Transductionbcl-2-Associated X ProteinBAXMacrogliaMicrogliaNeuroinflammationOptic nerve damageP2X ReceptorPANX1Retinal ganglion cell

Identifiers

PMID27126275
PMCPMC4850653
OpenAlexW2343444117

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.