Evidence map›Paper›PMID 16554460›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2006

EphB3: an endogenous mediator of adult axonal plasticity and regrowth after CNS injury.

Xiao Liu, Elizabeth Hawkes, Tatsuto Ishimaru, Tony Tran, David W Sretavan

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
2.9field-weighted citation impact, top 8% 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

34 citing papers in PubMed, 82 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Exploring Optic Nerve Axon Regeneration.Current neuropharmacology · 2017
    Review
  9. Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. 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
  15. Article
  16. Myelin-derived ephrinB3 restricts axonal regeneration and recovery after adult CNS injury.Proceedings of the National Academy of Sciences of the United States of America · 2012
    Article
  17. Article
  18. Article
  19. Article
  20. Chemical priming for spinal cord injury: a review of the literature. Part I-factors involved.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2011
    Review
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.

Xiao LiuProgram in Neuroscience, Department of Ophthalmology, University of California, San Francisco, California 94143, USA.
Elizabeth Hawkes
Tatsuto Ishimaru
Tony Tran
David W Sretavan
University of California, San Francisco · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endogenous mechanisms underlying the remodeling of neuronal circuitry after mammalian CNS injury or disease remain primarily unknown. Here, we investigated axonal plasticity after optic nerve injury and found that macrophages recruited into the injury site and adult retinal ganglion cell (RGC) axons, which undergo injury-induced sprouting and terminal remodeling, were linked by their respective expression of a ligand and receptor pair active in axon guidance. Recruited macrophages specifically upregulated mRNA encoding the guidance molecule EphB3 and expressed EphB proteins capable of binding Ephrin B molecules in vivo and in vitro. Injured adult RGC axons in turn expressed EphrinB3, a known receptor for EphB3, and RGC axons bound recombinant EphB3 protein injected into the optic nerve. In vitro, EphB3 supported adult RGC axon outgrowth, and axons turned toward a source of this guidance molecule. In vivo, both reduction of EphB3 function in adult heterozygous animals and loss of function in homozygous animals greatly decreased RGC axon re-extension or sprouting after optic nerve injury. Comparisons of axon re-extension in EphB3 null and wild-type littermates showed that this loss of axonal plasticity was not attributable to a difference in intrinsic axon growth potential. Rather, the results indicated an essential role for local optic nerve-derived EphB3 in regulating adult RGC axon plasticity after optic nerve injury. Of note, the loss of EphB3 did not affect the ability of injured RGC axons to elaborate complex terminal branching, suggesting that additional EphB3-independent mechanisms governed adult axon branching triggered by CNS damage.

Indexed as

AnimalsCell CommunicationDisease Models, AnimalDown-RegulationEphrin-B3FemaleGrowth ConesMacrophagesMaleMiceMice, KnockoutMice, Mutant StrainsMice, TransgenicNerve Growth FactorsNerve RegenerationNeuronal PlasticityEphrin-B3Nerve Growth FactorsReceptor, EphB3RNA, Messenger

Identifiers

PMID16554460
PMCPMC6674090
OpenAlexW2056450593

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.