Evidence map›Paper›PMID 12657687›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003

Macrophage-derived factors stimulate optic nerve regeneration.

Yuqin Yin, Qi Cui, Yiming Li, Nina Irwin, Dietmar Fischer, Alan R Harvey, Larry I Benowitz

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 223 papers.

0numbers the graph read from it
0cells of the map it votes in
223citing papers in PubMed
8.9field-weighted citation impact, top 1% 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

223 citing papers in PubMed, 541 citations in OpenAlex.

  1. Article
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  4. Review
  5. The rAAV2-ND1 gene therapy for Leber hereditary optic neuropathy.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025
    Article
  6. Review
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  19. Article
  20. Role of microglia/macrophage polarisation in intraocular diseases (Review).International journal of molecular medicine · 2024
    Review

163 more citing papers are in PubMed but not listed here.

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 4 institutions in 2 countries.

Yuqin YinLaboratories for Neuroscience Research in Neurosurgery, Children's Hospital, Boston, Massachusetts 02115, USA.
Qi Cui
Yiming Li
Nina Irwin
Dietmar Fischer
Alan R Harvey
Larry I Benowitz
Boston Children's Hospital · USHarry Perkins Institute of Medical Research · AUHarvard University · USUniversity of Western Australia · AU

Funding

MOLECULAR BASES OF NEURONAL CONNECTIVITYR01EY005690 · NEI · MC LEAN HOSPITAL (BELMONT, MA) · PI BENOWITZ, LARRY IRA · 1985 to 2012
$4.7M
NEI NIH HHS EY05690NEI NIH HHS R01 EY005690
6 · The paper itself

Abstract

After optic nerve injury in mature mammals, retinal ganglion cells (RGCs) are normally unable to regenerate their axons and undergo delayed apoptosis. However, if the lens is damaged at the time of nerve injury, many RGCs survive axotomy and regenerate their axons into the distal optic nerve. Lens injury induces macrophage activation, and we show here that factors secreted by macrophages stimulate RGCs to regenerate their axons. When macrophages were activated by intravitreal injections of Zymosan, a yeast cell wall preparation, the number of RGC axons regenerating into the distal optic nerve was even greater than after lens injury. These effects were further enhanced if Zymosan was injected 3 d after nerve crush. In a grafting paradigm, intravitreal Zymosan increased the number of RGCs that regenerated their axons through a 1.5 cm peripheral nerve graft twofold relative to uninjected controls and threefold if injections were delayed 3 d. In cell culture, media conditioned by activated macrophages stimulated adult rat RGCs to regenerate their axons; this effect was potentiated by a low molecular weight factor that is constitutively present in the vitreous humor. After gel-filtration chromatography, macrophage-derived proteins > or =30 kDa were found to be toxic to RGCs, whereas proteins <30 kDa reversed this toxicity and promoted axon regeneration. The protein(s) that stimulated axon growth is distinct from identified polypeptide trophic factors that were tested. Thus, macrophages produce proteins with both positive and negative effects on RGCs, and the effects of macrophages can be optimized by the timing of their activation.

Indexed as

AnimalsAxonsCell CountCulture Media, ConditionedFluorescent DyesGAP-43 ProteinGrowth SubstancesImmunohistochemistryMacrophage ActivationMacrophagesMaleMolecular WeightNerve CrushNerve RegenerationOptic NervePeripheral NervesCulture Media, ConditionedFluorescent DyesGAP-43 ProteinGrowth SubstancesReceptors, InterferonZymosan

Identifiers

PMID12657687
PMCPMC6742044
OpenAlexW2135551394

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.