Evidence map›Paper›PMID 28899916›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017

GD1a Overcomes Inhibition of Myelination by Fibronectin via Activation of Protein Kinase A: Implications for Multiple Sclerosis.

Jing Qin, Arend H Sikkema, Kristine van der Bij, Jenny C de Jonge, Karin Klappe, Vera Nies, Johan W Jonker, Jan Willem Kok, Dick Hoekstra, Wia Baron

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed, 1 pooled it
2.6field-weighted citation impact, top 11% 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

26 citing papers in PubMed, 1 synthesis or guideline pooled it, 40 citations in OpenAlex.

  1. Pooled it
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  14. Remyelination in Multiple Sclerosis: Findings in the Cuprizone Model.International journal of molecular sciences · 2022
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 1 institution in 1 country.

Jing QinDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and.
Arend H SikkemaDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and.
Kristine van der BijDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and.ORCID 0000-0002-7920-1213
Jenny C de JongeDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and.
Karin KlappeDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and.
Vera NiesCenter for Liver, Digestive and Metabolic Diseases, Department of Pediatrics, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, The Netherlands.
Johan W JonkerCenter for Liver, Digestive and Metabolic Diseases, Department of Pediatrics, University of Groningen, University Medical Center Groningen, 9713 GZ, Groningen, The Netherlands.
Jan Willem KokDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and.
Dick HoekstraDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and.
Wia BaronDepartment of Cell Biology, University of Groningen, University Medical Center Groningen, 9713 AV, Groningen, The Netherlands, and w.baron@umcg.nl.
University Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Remyelination failure by oligodendrocytes contributes to the functional impairment that characterizes the demyelinating disease multiple sclerosis (MS). Since incomplete remyelination will irreversibly damage axonal connections, treatments effectively promoting remyelination are pivotal in halting disease progression. Our previous findings suggest that fibronectin aggregates, as an environmental factor, contribute to remyelination failure by perturbing oligodendrocyte progenitor cell (OPC) maturation. Here, we aim at elucidating whether exogenously added gangliosides (i.e., cell surface lipids with a potential to modulate signaling pathways) could counteract fibronectin-mediated inhibition of OPC maturation. Exclusive exposure of rat oligodendrocytes to GD1a, but not other gangliosides, overcomes aggregated fibronectin-induced inhibition of myelin membrane formation,

Indexed as

AnimalsAxonsCells, CulturedCuprizoneCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinDemyelinating DiseasesEnzyme ActivationFibronectinsGangliosidesMaleMiceMultiple SclerosisMyelin SheathNeural Stem CellsOligodendrogliaCuprizoneCyclic AMP-Dependent Protein KinasesCyclic AMP Response Element-Binding ProteinFibronectinsganglioside, GD1aGangliosidesfibronectingangliosidemultiple sclerosisoligodendrocyteremyelination

Identifiers

PMID28899916
PMCPMC6596593
OpenAlexW2754161393

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.