Evidence map›Paper›PMID 31953424›Full record

ArticleScientific reports2020

TLR3 agonists induce fibronectin aggregation by activated astrocytes: a role of pro-inflammatory cytokines and fibronectin splice variants.

Inge Werkman, Arend H Sikkema, Joris B Versluijs, Jing Qin, Pascal de Boer, Wia Baron

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Cellular fibronectin exacerbates α-synuclein aggregation via integrin alpha4beta1 mediated PARP1 and SCD elevation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Article
  5. Review
  6. Article
  7. A novelFrontiers in cellular neuroscience · 2024
    Article
  8. Article
  9. Review
  10. Article
  11. Macroglial diversity: white and grey areas and relevance to remyelination.Cellular and molecular life sciences : CMLS · 2021
    Review
  12. Review
  13. Article
  14. 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

6 authors at 1 institution in 1 country.

Inge Werkman *Department of Biomedical Sciences of Cells & Systems, section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Arend H Sikkema *Department of Biomedical Sciences of Cells & Systems, section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Joris B VersluijsDepartment of Biomedical Sciences of Cells & Systems, section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Jing QinDepartment of Biomedical Sciences of Cells & Systems, section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Pascal de BoerDepartment of Biomedical Sciences of Cells & Systems, section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands.
Wia BaronDepartment of Biomedical Sciences of Cells & Systems, section Molecular Neurobiology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands. w.baron@umcg.nl.ORCID http://orcid.org/0000-0002-6673-4766
University Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic demyelinating disease of the central nervous system which eventually results in axonal loss mainly due to failure of remyelination. Previously we have shown that the persistent presence of stable astrocyte-derived fibronectin aggregates in MS lesions impairs OPC differentiation, and thereby remyelination. Here we set out to discern whether and, if so, how inflammatory mediators as present in MS lesions trigger astrocytes to form fibronectin aggregates. Our findings revealed that in slice cultures only upon demyelination, the TLR3 agonist Poly(I:C) evoked astrocytes to form fibronectin aggregates. Consistently, pro-inflammatory cytokine-pretreated astrocytes were more susceptible to Poly(I:C)-induced fibronectin aggregation, indicating that astrocytes form fibronectin aggregates upon a double hit by inflammatory mediators. The underlying mechanism involves disrupted fibronectin fibrillogenesis at the cell surface as a result of a cytokine-induced increase in relative mRNA levels of EIIIA

Indexed as

AnimalsAstrocytesCell AdhesionExtracellular SpaceFibronectinsGray MatterHumansPoly I-CProtein AggregatesProtein IsoformsRatsToll-Like Receptor 3White MatterFibronectinsPoly I-CProtein AggregatesProtein IsoformsToll-Like Receptor 3

Identifiers

PMID31953424
PMCPMC6969115
OpenAlexW2999616751

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.