Evidence map›Paper›PMID 27716282›Full record

ArticleMolecular neurodegeneration2016

Spinal cord injury induces astroglial conversion towards neuronal lineage.

Harun Najib Noristani, Jean Charles Sabourin, Hassan Boukhaddaoui, Emilie Chan-Seng, Yannick Nicolas Gerber, Florence Evelyne Perrin

Abstract read
In one paragraph

Article in Molecular neurodegeneration, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

31 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  5. Neural regeneration research · 2024
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  16. Gsx1 promotes locomotor functional recovery after spinal cord injury.Molecular therapy : the journal of the American Society of Gene Therapy · 2021
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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

6 authors.

Harun Najib NoristaniUniversity of Montpellier, Montpellier, F-34095, France.
Jean Charles SabourinIntegrative Biology of Neurodegeneration", IKERBASQUE Basque Foundation for Science and Neuroscience Department, University of the Basque Country, E-48013, Bilbao, Spain.
Hassan BoukhaddaouiINSERM U1051, F-34095, Montpellier, France.
Emilie Chan-SengIntegrative Biology of Neurodegeneration", IKERBASQUE Basque Foundation for Science and Neuroscience Department, University of the Basque Country, E-48013, Bilbao, Spain.
Yannick Nicolas GerberUniversity of Montpellier, Montpellier, F-34095, France.
Florence Evelyne PerrinUniversity of Montpellier, Montpellier, F-34095, France. florence.perrin@inserm.fr.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeurons have intrinsic capability to regenerate after lesion, though not spontaneously. Spinal cord injury (SCI) causes permanent neurological impairments partly due to formation of a glial scar that is composed of astrocytes and microglia. Astrocytes play both beneficial and detrimental roles on axonal re-growth, however, their precise role after SCI is currently under debate.

methodsWe analyzed molecular changes in astrocytes at multiple stages after two SCI severities using cell-specific transcriptomic analyses.

resultsWe demonstrate that astrocyte response after injury depends on both time after injury and lesion severity. We then establish that injury induces an autologous astroglial transdifferentiation where over 10 % of astrocytes express classical neuronal progenitor markers including βIII-tubulin and doublecortin with typical immature neuronal morphology. Lineage tracing confirmed that the origin of these astrocytes is resident mature, rather than newly formed astrocytes. Astrocyte-derived neuronal progenitors subsequently express GABAergic, but not glutamatergic-specific markers. Furthermore, we have identified the neural stem cell marker fibroblast growth factor receptor 4 (Fgfr4) as a potential autologous modulator of astrocytic transdifferentiation following SCI. Finally, we establish that astroglial transdifferentiation into neuronal progenitors starts as early as 72 h and continues to a lower degrees up to 6 weeks post-lesion.

conclusionWe thus demonstrate for the first time autologous injury-induced astroglial conversion towards neuronal lineage that may represent a therapeutic strategy to replace neuronal loss and improve functional outcomes after central nervous system injury.

Indexed as

Cell LineageAnimalsAstrocytesCell ProliferationCells, CulturedCell TransdifferentiationDisease Models, AnimalGlial Fibrillary Acidic ProteinMiceMicrogliaNeural Stem CellsSpinal Cord InjuriesGlial Fibrillary Acidic ProteinAstrocytesAstrogliosisCell specific transcriptomicSpinal cord injuryTransdifferentiation

Identifiers

PMID27716282
PMCPMC5052929

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Registered trials

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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.