Evidence map›Paper›PMID 25458895›Full record

ArticleStem cell reports2014

Sox2-mediated conversion of NG2 glia into induced neurons in the injured adult cerebral cortex.

Christophe Heinrich, Matteo Bergami, Sergio Gascón, Alexandra Lepier, Francesca Viganò, Leda Dimou, Bernd Sutor, Benedikt Berninger, Magdalena Götz

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 172 papers.

0numbers the graph read from it
0cells of the map it votes in
172citing papers in PubMed
15.2field-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

172 citing papers in PubMed, 331 citations in OpenAlex.

  1. Review
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  5. Phosphorylation and DNA damage resolution coordinate SOX2-mediated reprogramming in vivo.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  6. iScience · 2026
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112 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

9 authors at 3 institutions in 2 countries.

Christophe HeinrichPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany; INSERM U836, University Grenoble Alpes, Grenoble Institute of Neurosciences, 38000 Grenoble, France.
Matteo BergamiPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany.
Sergio GascónPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, National Research Center for Environment and Health, 85764 Neuherberg, Germany.
Alexandra LepierPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany.
Francesca ViganòPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany.
Leda DimouPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, National Research Center for Environment and Health, 85764 Neuherberg, Germany.
Bernd SutorPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany.
Benedikt BerningerPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany; Institute of Physiological Chemistry, University Medical Center, Johannes Gutenberg University Mainz, 55128 Mainz, Germany; Focus Program Translational Neuroscience, Johannes Gutenberg University Mainz, 55131 Mainz, Germany. Electronic address: berningb@uni-mainz.de.
Magdalena GötzPhysiological Genomics, Institute of Physiology, Ludwig-Maximilians University Munich, 80336 Munich, Germany; Institute for Stem Cell Research, National Research Center for Environment and Health, 85764 Neuherberg, Germany; Munich Cluster for Systems Neurology (SyNergy), 80336 Munich, Germany. Electronic address: magdalena.goetz@helmholtz-muenchen.de.
Ludwig-Maximilians-Universität München · DEUniversité Grenoble Alpes · FRUniversity Medical Center of the Johannes Gutenberg University Mainz · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The adult cerebral cortex lacks the capacity to replace degenerated neurons following traumatic injury. Conversion of nonneuronal cells into induced neurons has been proposed as an innovative strategy toward brain repair. Here, we show that retrovirus-mediated expression of the transcription factors Sox2 and Ascl1, but strikingly also Sox2 alone, can induce the conversion of genetically fate-mapped NG2 glia into induced doublecortin (DCX)(+) neurons in the adult mouse cerebral cortex following stab wound injury in vivo. In contrast, lentiviral expression of Sox2 in the unlesioned cortex failed to convert oligodendroglial and astroglial cells into DCX(+) cells. Neurons induced following injury mature morphologically and some acquire NeuN while losing DCX. Patch-clamp recording of slices containing Sox2- and/or Ascl1-transduced cells revealed that a substantial fraction of these cells receive synaptic inputs from neurons neighboring the injury site. Thus, NG2 glia represent a potential target for reprogramming strategies toward cortical repair.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsCell ProliferationCell TransdifferentiationCellular ReprogrammingCerebral CortexDoublecortin ProteinGene ExpressionMiceNeurogliaNeuronsSOXB1 Transcription FactorsSynaptic PotentialsAscl1 protein, mouseBasic Helix-Loop-Helix ProteinsDcx protein, mouseDoublecortin ProteinSOXB1 Transcription Factors

Identifiers

PMID25458895
PMCPMC4264057
OpenAlexW2017830127

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.