Evidence map›Paper›PMID 19643015›Full record

ArticleBMC neuroscience2009

Differential response of C57BL/6J mouse and DBA/2J mouse to optic nerve crush.

Justin P Templeton, Mohamed Nassr, Felix Vazquez-Chona, Natalie E Freeman-Anderson, William E Orr, Robert W Williams, Eldon E Geisert

Open access · goldAbstract readComparative Study
In one paragraph

Article in BMC neuroscience, 2009. 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
3.2field-weighted citation impact, top 9% 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, 45 citations in OpenAlex.

  1. Pooled it
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  6. Review
  7. Chemokine CCL5 promotes robust optic nerve regeneration and mediates many of the effects of CNTF gene therapy.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
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  11. The genetic dissection ofMolecular vision · 2018
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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

7 authors at 1 institution in 1 country.

Justin P TempletonDepartment of Ophthalmology, University of Tennessee Health Science Center, Memphis TN, 38163, USA. Jtemplet@utmem.edu
Mohamed Nassr
Felix Vazquez-Chona
Natalie E Freeman-Anderson
William E Orr
Robert W Williams
Eldon E Geisert
University of Tennessee Health Science Center · US

Funding

CORE--MOLECULAR BIOLOGYP30EY013080 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI JOHNSON, DIANNA AMMONS · 2000 to 2010
$3.7M
Modulators of Retinal InjuryR01EY017841 · NEI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI GEISERT, ELDON E · 2007 to 2016
$3.0M
NEI NIH HHS EY13080NEI NIH HHS P30 EY013080NEI NIH HHS R01 EY017841NEI NIH HHS R01EY017841
6 · The paper itself

Abstract

backgroundRetinal ganglion cell (RGC) death is the final consequence of many blinding diseases, where there is considerable variation in the time course and severity of RGC loss. Indeed, this process appears to be influenced by a wide variety of genetic and environmental factors. In this study we explored the genetic basis for differences in ganglion cell death in two inbred strains of mice.

resultsWe found that RGCs are more susceptible to death following optic nerve crush in C57BL/6J mice (54% survival) than in DBA/2J mice (62% survival). Using the Illumina Mouse-6 microarray, we identified 1,580 genes with significant change in expression following optic nerve crush in these two strains of mice. Our analysis of the changes occurring after optic nerve crush demonstrated that the greatest amount of change (44% of the variance) was due to the injury itself. This included changes associated with ganglion cell death, reactive gliosis, and abortive regeneration. The second pattern of gene changes (23% of the variance) was primarily related to differences in gene expressions observed between the C57BL/6J and DBA/2J mouse strains. The remaining changes in gene expression represent interactions between the effects of optic nerve crush and the genetic background of the mouse. We extracted one genetic network from this dataset that appears to be related to tissue remodeling. One of the most intriguing sets of changes included members of the crystallin family of genes, which may represent a signature of pathways modulating the susceptibility of cells to death.

conclusionDifferential responses to optic nerve crush between two widely used strains of mice were used to define molecular networks associated with ganglion cell death and reactive gliosis. These results form the basis for our continuing interest in the modifiers of retinal injury.

Indexed as

Nerve CrushAnimalsAstrocytesCell CountCell Culture TechniquesCell SurvivalCerebral CortexGene Expression ProfilingGenetic Predisposition to DiseaseImmunohistochemistryMiceMice, Inbred C57BLMice, Inbred DBANeuronsOligonucleotide Array Sequence AnalysisOptic Nerve Injuries

Identifiers

PMID19643015
PMCPMC2727955
OpenAlexW2039797538

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.