Evidence map›Paper›PMID 22064993›Full record

ArticleInvestigative ophthalmology & visual science2012

Involvement of EphB/Ephrin-B signaling in axonal survival in mouse experimental glaucoma.

Christine T Fu, David Sretavan

Open access · bronzeAbstract read
In one paragraph

Article in Investigative ophthalmology & visual science, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 34% 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

11 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. The Role of Autophagy in Eye Diseases.Life (Basel, Switzerland) · 2021
    Review
  6. Article
  7. Article
  8. Article
  9. Optic neuritis in neuromyelitis optica.Progress in retinal and eye research · 2013
    Article
  10. Inactivation of the microRNA-183/96/182 cluster results in syndromic retinal degeneration.Proceedings of the National Academy of Sciences of the United States of America · 2013
    Article
  11. Ectopic vesicular glutamate release at the optic nerve head and axon loss in mouse experimental glaucoma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012
    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

2 authors at 1 institution in 1 country.

Christine T FuDepartment of Ophthalmology, University of California, San Francisco, San Francisco, California 94143, USA.
David Sretavan
University of California, San Francisco · US

Funding

Rapid-Prototyping and Design CoreP30EY002162 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI LAKKARAJU, APARNA · 1985 to 2024
$16.8M
MOLECULAR DEVELOPMENT OF CENTRAL RETINAL PATHWAYSR01EY010688 · NEI · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI SRETAVAN, DAVID W · 1994 to 2015
$5.1M
NEI NIH HHS EY010688NEI NIH HHS EY02162NEI NIH HHS P30 EY002162NEI NIH HHS R01 EY010688
6 · The paper itself

Abstract

purposeTo examine the functional significance of EphB/ephrin-B upregulation in mouse experimental glaucoma.

methodsIn a loss-of-function approach, mouse mutants lacking EphB2 (EphB2(-/-)) or EphB3 (EphB3(-/-)) protein, and mutants expressing EphB2 truncated in the C-terminus (EphB2(lacZ/lacZ)) were subjected to laser-induced ocular hypertension (LIOH), an experimental mouse model of glaucoma. The number of optic nerve axons was counted in paraphenylenediamine (PPD)-stained sections and compared between EphB mutants and wild type littermates. In a gain-of-function approach, retina/optic nerve explants obtained from LIOH-treated animals were exposed to EphB2-Fc recombinant proteins or Fc control proteins. Tissue sections through the optic nerve head (ONH) were labeled with neuron-specific anti-tubulin β-III antibody to determine axonal integrity.

resultsBoth EphB2 and EphB3 null mutant mice exhibited more severe axonal degeneration than wild type littermates after treatment with LIOH. Mutant mice in which the C-terminal portion of EphB2 is truncated had an intermediate phenotype. Application of EphB2-Fc recombinant protein to LIOH-treated optic nerve explants resulted in greater sparing of tubulin β-III-containing retinal ganglion cell (RGC) axons.

conclusionsThese results provide genetic evidence in mice that both EphB/ephrin-B forward and reverse signaling feed into an endogenous pathway to moderate the effects of glaucomatous insult on RGC axons. LIOH-induced axon loss is maintained in retina/optic nerve explants after removal from an ocular hypertensive environment. Exogenous application of EphB2 protein enhances RGC axon survival in explants, suggesting that modulation of Eph/ephrin signaling may be of therapeutic interest.

Indexed as

Disease Models, AnimalAnimalsAxonsCell SurvivalColoring AgentsEphrin-B2Ephrin-B3GlaucomaIntraocular PressureMiceMice, KnockoutMicroscopy, ConfocalNerve DegenerationOcular HypertensionOptic Nerve DiseasesOrgan Culture Techniques4-phenylenediamineColoring AgentsEphrin-B2Ephrin-B3PhenylenediaminesRecombinant Fusion Proteins

Identifiers

PMID22064993
PMCPMC3292385
OpenAlexW2018844391

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.