Evidence map›Paper›PMID 25564492›Full record

ArticleBrain : a journal of neurology2015

Gain of Olig2 function in oligodendrocyte progenitors promotes remyelination.

Amélie Wegener, Cyrille Deboux, Corinne Bachelin, Magali Frah, Christophe Kerninon, Danielle Seilhean, Matthias Weider, Michael Wegner, Brahim Nait-Oumesmar

Open access · bronzeAbstract read
In one paragraph

Article in Brain : a journal of neurology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
3.4field-weighted citation impact, top 8% 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

94 citing papers in PubMed, 160 citations in OpenAlex.

  1. Article
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  7. Temporal Transcriptional Regulation of Human Neuronal Differentiation via Forward Programming.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  8. Article
  9. Article
  10. Article
  11. Spinal Cord Injury Remyelination: Pathways to Therapies.International journal of molecular sciences · 2025
    Review
  12. Genes · 2025
    Article
  13. Article
  14. Pretreatment with oleuropein protects the neonatal brain from hypoxia-ischemia by inhibiting apoptosis and neuroinflammation.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2025
    Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Review
  20. Article

34 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 6 institutions in 2 countries.

Amélie Wegener1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France.
Cyrille Deboux1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France.
Corinne Bachelin1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France.
Magali Frah1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France.
Christophe Kerninon1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France.
Danielle Seilhean1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France.
Matthias Weider1 Inserm, U 1127, F-75013, Paris, France.
Michael Wegner1 Inserm, U 1127, F-75013, Paris, France.
Brahim Nait-Oumesmar1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France 1 Inserm, U 1127, F-75013, Paris, France brahim.nait_oumesmar@upmc.fr.
Centre National de la Recherche Scientifique · FRFriedrich-Alexander-Universität Erlangen-Nürnberg · DEInserm · FRInstitut du Cerveau · FRPitié-Salpêtrière Hospital · FRSorbonne Université · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The basic helix-loop-helix transcription factor Olig2 is a key determinant for the specification of neural precursor cells into oligodendrocyte progenitor cells. However, the functional role of Olig2 in oligodendrocyte migration and differentiation remains elusive both during developmental myelination and under demyelinating conditions of the adult central nervous system. To decipher Olig2 functions, we generated transgenic mice (TetOlig2:Sox10(rtTA/+)) overexpressing Olig2 in Sox10(+) oligodendroglial cells in a doxycycline inducible manner. We show that Olig2 overexpression increases the generation of differentiated oligodendrocytes, leading to precocious myelination of the central nervous system. Unexpectedly, we found that gain of Olig2 function in oligodendrocyte progenitor cells enhances their migration rate. To determine whether Olig2 overexpression in adult oligodendrocyte progenitor cells promotes oligodendrocyte regeneration for myelin repair, we induced lysophosphatidylcholine demyelination in the corpus callosum of TetOlig2:Sox10(rtTA/+) and control mice. We found that Olig2 overexpression enhanced oligodendrocyte progenitor cell differentiation and remyelination. To assess the relevance of these findings in demyelinating diseases, we also examined OLIG2 expression in multiple sclerosis lesions. We demonstrate that OLIG2 displays a differential expression pattern in multiple sclerosis lesions that correlates with lesion activity. Strikingly, OLIG2 was predominantly detected in NOGO-A(+) (now known as RTN4-A) maturing oligodendrocytes, which prevailed in active lesion borders, rather than chronic silent and shadow plaques. Taken together, our data provide proof of principle indicating that OLIG2 overexpression in oligodendrocyte progenitor cells might be a possible therapeutic mechanism for enhancing myelin repair.

Indexed as

AnimalsAnimals, NewbornBasic Helix-Loop-Helix ProteinsCell DifferentiationCells, CulturedDemyelinating DiseasesDisease Models, AnimalDoxycyclineEmbryo, MammalianGene Expression RegulationLysophosphatidylcholinesMiceMice, Inbred C57BLMice, TransgenicMultiple SclerosisMyelin SheathBasic Helix-Loop-Helix ProteinsDoxycyclineLysophosphatidylcholinesNerve Tissue ProteinsOlig2 protein, mouseOligodendrocyte Transcription Factor 2Sox10 protein, mouseSOXE Transcription Factorsmultiple sclerosisOlig2oligodendrocyteremyelinationtetracycline system

Identifiers

PMID25564492
PMCPMC4441088
OpenAlexW2062159906

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.