Evidence map›Paper›PMID 26298667›Full record

ArticleMolecular neurobiology2016

Inhibitory Injury Signaling Represses Axon Regeneration After Dorsal Root Injury.

Fernando M Mar, Anabel R Simões, Inês S Rodrigo, Mónica M Sousa

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed, 1 pooled it
1.1field-weighted citation impact, top 27% 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

17 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
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  5. Article
  6. Function of GSK‑3 signaling in spinal cord injury (Review).Experimental and therapeutic medicine · 2023
    Review
  7. Unleashing Intrinsic Growth Pathways in Regenerating Peripheral Neurons.International journal of molecular sciences · 2022
    Review
  8. Review
  9. Review
  10. Article
  11. Article
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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

4 authors at 2 institutions in 1 country.

Fernando M MarInstituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200, Porto, Portugal.
Anabel R SimõesInstituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200, Porto, Portugal.
Inês S RodrigoInstituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200, Porto, Portugal.
Mónica M SousaInstituto de Investigação e Inovação em Saúde, Universidade do Porto, 4200, Porto, Portugal. msousa@ibmc.up.pt.
i3S - Instituto de Investigação e Inovação em Saúde, Universidade do Porto · PTUniversidade do Porto · PT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Following injury to peripheral axons, besides increased cyclic adenosine monophosphate (cAMP), the positive injury signals extracellular-signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and signal transducer and activator of transcription 3 (STAT-3) are locally activated and retrogradely transported to the cell body, where they induce a pro-regenerative program. Here, to further understand the importance of injury signaling for successful axon regeneration, we used dorsal root ganglia (DRG) neurons that have a central branch without regenerative capacity and a peripheral branch that regrows after lesion. Although injury to the DRG central branch (dorsal root injury (DRI)) activated ERK, JNK, and STAT-3 and increased cAMP levels, it did not elicit gain of intrinsic growth capacity nor the ability to overcome myelin inhibition, as occurred after peripheral branch injury (sciatic nerve injury (SNI)). Besides, gain of growth capacity after SNI was independent of ERK and cAMP. Antibody microarrays of dynein-immunoprecipitated axoplasm from rats with either DRI or SNI revealed a broad differential activation and transport of signals after each injury type and further supported that ERK, JNK, STAT-3, and cAMP signaling pathways are minor contributors to the differential intrinsic axon growth capacity of both injury models. Increased levels of inhibitory injury signals including GSK3β and ROCKII were identified after DRI, not only in axons but also in DRG cell bodies. In summary, our work shows that activation and transport of positive injury signals are not sufficient to promote increased axon growth capacity and that differential modulation of inhibitory molecules may contribute to limited regenerative response.

Indexed as

AnimalsAxonsCells, CulturedFemaleGanglia, SpinalGlycogen Synthase Kinase 3 betaMaleMiceNerve RegenerationRatsRats, Wistarrho-Associated KinasesSciatic NeuropathySignal TransductionGlycogen Synthase Kinase 3 betaGsk3b protein, ratrho-Associated KinasesAxon regenerationDorsal root gangliaGSK3βInjury signalingROCKII

Identifiers

PMID26298667
OpenAlexW1619557239

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.