Evidence map›Paper›PMID 25589163›Full record

ArticleActa neuropathologica communications2014

Transcript profiling of different types of multiple sclerosis lesions yields FGF1 as a promoter of remyelination.

Hema Mohan, Anita Friese, Stefanie Albrecht, Markus Krumbholz, Christina L Elliott, Ariel Arthur, Ramesh Menon, Cinthia Farina, Andreas Junker, Christine Stadelmann and 8 more

Open access · goldAbstract read
In one paragraph

Article in Acta neuropathologica communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed, 1 pooled it
1.6field-weighted citation impact, top 17% 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

30 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Neuroprotective Effect ofCurrent pharmaceutical biotechnology · 2024
    Article
  6. Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. Oligodendrocyte-specific deletion of FGFR2 ameliorates MOGBrain pathology (Zurich, Switzerland) · 2021
    Article
  14. Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. 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

18 authors at 9 institutions in 5 countries.

Hema MohanInstitute of Clinical Neuroimmunology, Ludwig Maximilian University Munich, Marchioninistraße 15, D-81377, Munich, Germany. hema.mohan@ukmuenster.de.
Anita FrieseInstitute of Clinical Neuroimmunology, Ludwig Maximilian University Munich, Marchioninistraße 15, D-81377, Munich, Germany. anita.friese@web.de.
Stefanie AlbrechtInstitute of Neuropathology, University Hospital Münster, Münster, Germany. stefanie.albrecht@ukmuenster.de.
Markus KrumbholzInstitute of Clinical Neuroimmunology, Ludwig Maximilian University Munich, Marchioninistraße 15, D-81377, Munich, Germany. markus.krumbholz@med.uni-muenchen.de.
Christina L ElliottDivision of Clinical Neurosciences, University of Glasgow, Glasgow, UK. Christina.Elliott@glasgow.ac.uk.
Ariel ArthurDivision of Clinical Neurosciences, University of Glasgow, Glasgow, UK. ariel.arthur@gmail.com.
Ramesh MenonDivision of Neuroscience, Institute of Experimental Neurology (INSpe), San Raffaele Scientific Institute, Milan, Italy. menon.ramesh@hsr.it.
Cinthia FarinaDivision of Neuroscience, Institute of Experimental Neurology (INSpe), San Raffaele Scientific Institute, Milan, Italy. farina.cinthia@hsr.it.
Andreas JunkerInstitute for Neuropathology, Göttingen, Germany. andreas.junker@med.uni-goettingen.de.
Christine StadelmannInstitute for Neuropathology, Göttingen, Germany. cstadelmann@med.uni-goettingen.de.
Susan C BarnettDivision of Clinical Neurosciences, University of Glasgow, Glasgow, UK. Susan.Barnett@glasgow.ac.uk.
Inge HuitingaThe Netherlands Brain Bank, Netherlands Institute for Neuroscience, Amsterdam, Netherlands. i.huitinga@nin.knaw.nl.
Hartmut WekerleMax Planck Institute of Neurobiology, Hertie Senior Professorship, Martinsried, Germany. Hartmut.Wekerle@med.uni-muenchen.de.
Reinhard HohlfeldInstitute of Clinical Neuroimmunology, Ludwig Maximilian University Munich, Marchioninistraße 15, D-81377, Munich, Germany. Reinhard.Hohlfeld@med.uni-muenchen.de.
Hans LassmannCenter for Brain Research, Medical University of Vienna, Vienna, Austria. hans.lassmann@meduniwien.ac.at.
Tanja KuhlmannInstitute of Neuropathology, University Hospital Münster, Münster, Germany. Tanja.Kuhlmann@ukmuenster.de.
Chris LiningtonDivision of Clinical Neurosciences, University of Glasgow, Glasgow, UK. Christopher.Linington@glasgow.ac.uk.
Edgar MeinlInstitute of Clinical Neuroimmunology, Ludwig Maximilian University Munich, Marchioninistraße 15, D-81377, Munich, Germany. edgar.meinl@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DEUniversity of Glasgow · GBEuropean Neuroscience Institute Göttingen · DENeuroscience Institute · ITUniversity Hospital Münster · DEMax Planck Institute of Neurobiology · DEMedical University of Vienna · ATMunich Cluster for Systems Neurology · DENetherlands Institute for Neuroscience · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Chronic demyelination is a pathological hallmark of multiple sclerosis (MS). Only a minority of MS lesions remyelinates completely. Enhancing remyelination is, therefore, a major aim of future MS therapies. Here we took a novel approach to identify factors that may inhibit or support endogenous remyelination in MS. We dissected remyelinated, demyelinated active, and demyelinated inactive white matter MS lesions, and compared transcript levels of myelination and inflammation-related genes using quantitative PCR on customized TaqMan Low Density Arrays. In remyelinated lesions, fibroblast growth factor (FGF) 1 was the most abundant of all analyzed myelination-regulating factors, showed a trend towards higher expression as compared to demyelinated lesions and was significantly higher than in control white matter. Two MS tissue blocks comprised lesions with adjacent de- and remyelinated areas and FGF1 expression was higher in the remyelinated rim compared to the demyelinated lesion core. In functional experiments, FGF1 accelerated developmental myelination in dissociated mixed cultures and promoted remyelination in slice cultures, whereas it decelerated differentiation of purified primary oligodendrocytes, suggesting that promotion of remyelination by FGF1 is based on an indirect mechanism. The analysis of human astrocyte responses to FGF1 by genome wide expression profiling showed that FGF1 induced the expression of the chemokine CXCL8 and leukemia inhibitory factor, two factors implicated in recruitment of oligodendrocytes and promotion of remyelination. Together, this study presents a transcript profiling of remyelinated MS lesions and identified FGF1 as a promoter of remyelination. Modulation of FGF family members might improve myelin repair in MS.

Indexed as

AnimalsAstrocytesBrainCells, CulturedFibroblast Growth Factor 1Gene Expression ProfilingHumansInterleukin-8Leukemia Inhibitory FactorMiceMice, Inbred C57BLMultiple SclerosisMyelin SheathOligodendrogliaRats, Sprague-DawleyRats, WistarCXCL8 protein, humanFibroblast Growth Factor 1Interleukin-8Leukemia Inhibitory FactorRNA, Messenger

Identifiers

PMID25589163
PMCPMC4359505
OpenAlexW2156341134

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.