Evidence map›Paper›PMID 31566924›Full record

ArticleEMBO molecular medicine2019

Disruption of Sema3A/Plexin-A1 inhibitory signalling in oligodendrocytes as a therapeutic strategy to promote remyelination.

Fabien Binamé, Lucas D Pham-Van, Caroline Spenlé, Valérie Jolivel, Dafni Birmpili, Lionel A Meyer, Laurent Jacob, Laurence Meyer, Ayikoé G Mensah-Nyagan, Chrystelle Po and 3 more

Open access · goldAbstract read
In one paragraph

Article in EMBO molecular medicine, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed, 1 pooled it
2.3field-weighted citation impact, top 12% 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

18 citing papers in PubMed, 1 synthesis or guideline pooled it, 35 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
  14. Semaphorins in Adult Nervous System Plasticity and Disease.Frontiers in synaptic neuroscience · 2021
    Review
  15. Review
  16. Review
  17. Article
  18. 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

13 authors at 2 institutions in 1 country.

Fabien BinaméINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Lucas D Pham-VanINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Caroline SpenléINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Valérie JolivelINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Dafni BirmpiliINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Lionel A MeyerINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Laurent JacobINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Laurence MeyerINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Ayikoé G Mensah-NyaganINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Chrystelle PoInstitut de Physique Biologique, Faculté de Médecine, Strasbourg University, Strasbourg, France.
Michaël Van der HeydenINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Guy RousselINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.
Dominique BagnardINSERM U1119 Biopathology of Myelin, Neuroprotection, Therapeutic Strategy, Labex Medalis, Fédération de Médecine Translationnelle de Strasbourg, Strasbourg University, Strasbourg, France.ORCID 0000-0002-5261-902X
Inserm · FRInstitut de Physique · FR

Funding

Agence Nationale de la Recherche (ANR) Labex Medalis- MEDALIS-DBA-2016INSERMMinistère de la Recherche ACI JC#5327PlexremyelSATT Conectus
6 · The paper itself

Abstract

Current treatments in multiple sclerosis (MS) are modulating the inflammatory component of the disease, but no drugs are currently available to repair lesions. Our study identifies in MS patients the overexpression of Plexin-A1, the signalling receptor of the oligodendrocyte inhibitor Semaphorin 3A. Using a novel type of peptidic antagonist, we showed the possibility to counteract the Sema3A inhibitory effect on oligodendrocyte migration and differentiation in vitro when antagonizing Plexin-A1. The use of this compound in vivo demonstrated a myelin protective effect as shown with DTI-MRI and confirmed at the histological level in the mouse cuprizone model of induced demyelination/remyelination. This effect correlated with locomotor performances fully preserved in chronically treated animals. The administration of the peptide also showed protective effects, leading to a reduced severity of demyelination in the context of experimental autoimmune encephalitis (EAE). Hence, the disruption of the inhibitory microenvironmental molecular barriers allows normal myelinating cells to exert their spontaneous remyelinating capacity. This opens unprecedented therapeutic opportunity for patients suffering a disease for which no curative options are yet available.

Indexed as

RemyelinationSignal TransductionAnimalsBrainCell LineCell MovementCell ProliferationDisease Models, AnimalMagnetic Resonance ImagingMice, Inbred C57BLMultiple SclerosisNerve Tissue ProteinsOligodendrogliaReceptors, Cell SurfaceSemaphorin-3ANerve Tissue ProteinsPLXNA1 protein, humanReceptors, Cell SurfaceSEMA3A protein, humanSemaphorin-3Amultiple sclerosismyelinationoligodendrocytePlexinSemaphorin

Identifiers

PMID31566924
PMCPMC6835579
OpenAlexW2977771295

What OpenQuestion 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 OpenQuestion graph.