Evidence map›Paper›PMID 36971369›Full record

ArticleDevelopment (Cambridge, England)2023

Post-injury born oligodendrocytes incorporate into the glial scar and contribute to the inhibition of axon regeneration.

Jian Xing, Agnieszka Lukomska, Bruce A Rheaume, Juhwan Kim, Muhammad S Sajid, Ashiti Damania, Ephraim F Trakhtenberg

Open access · hybridAbstract read
In one paragraph

Article in Development (Cambridge, England), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
4.0field-weighted citation impact, top 6% 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

14 citing papers in PubMed, 20 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Review
  5. The neuroimmune interface in retinal regeneration.Progress in retinal and eye research · 2025
    Review
  6. Dual role of complement in neuronal repair.Frontiers in immunology · 2025
    Review
  7. Article
  8. Article
  9. Review
  10. Article
  11. Article
  12. Article
  13. Article
  14. 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

7 authors at 1 institution in 1 country.

Jian XingDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.
Agnieszka LukomskaDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.
Bruce A RheaumeDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.
Juhwan KimDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.
Muhammad S SajidDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.
Ashiti DamaniaDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.
Ephraim F TrakhtenbergDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Avenue, Farmington, CT 06030, USA.ORCID 0000-0003-2844-4191
University of Connecticut · US

Funding

Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacityR01EY029739 · NEI · UNIVERSITY OF CONNECTICUT SCH OF MED/DNT · PI TRAKHTENBERG, FELIKS EPHRAIM · 2019 to 2023
$2.1M
NEI NIH HHS R01 EY029739
6 · The paper itself

Abstract

Failure of central nervous system projection neurons to spontaneously regenerate long-distance axons underlies irreversibility of white matter pathologies. A barrier to axonal regenerative research is that the axons regenerating in response to experimental treatments stall growth before reaching post-synaptic targets. Here, we test the hypothesis that the interaction of regenerating axons with live oligodendrocytes, which were absent during developmental axon growth, contributes to stalling axonal growth. To test this hypothesis, first, we used single cell RNA-seq (scRNA-seq) and immunohistology to investigate whether post-injury born oligodendrocytes incorporate into the glial scar after optic nerve injury. Then, we administered demyelination-inducing cuprizone and stimulated axon regeneration by Pten knockdown (KD) after optic nerve crush. We found that post-injury born oligodendrocyte lineage cells incorporate into the glial scar, where they are susceptible to the demyelination diet, which reduced their presence in the glial scar. We further found that the demyelination diet enhanced Pten KD-stimulated axon regeneration and that localized cuprizone injection promoted axon regeneration. We also present a resource for comparing the gene expression of scRNA-seq-profiled normal and injured optic nerve oligodendrocyte lineage cells.

Indexed as

AxonsDemyelinating DiseasesCuprizoneGliosisHumansNerve RegenerationOligodendrogliaRetinal Ganglion CellsCuprizoneAxon regenerationOligodendrocytesOptic nerve injuryRetinal ganglion cell

Identifiers

PMID36971369
PMCPMC10163352
OpenAlexW4361003981

What Socratic 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 Socratic graph.