Evidence map›Paper›PMID 25329699›Full record

ArticleThe Journal of clinical investigation2014

Axonally derived matrilin-2 induces proinflammatory responses that exacerbate autoimmune neuroinflammation.

Anna Jonas, Stefan Thiem, Tanja Kuhlmann, Raimund Wagener, Attila Aszodi, Cameron Nowell, Karin Hagemeier, Louise Laverick, Victoria Perreau, Vilija Jokubaitis and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 21% 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

25 citing papers in PubMed, 1 synthesis or guideline pooled it, 38 citations in OpenAlex.

  1. Pooled it
  2. Article
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024
    Review
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Interleukin 38 alleviates aortic valve calcification by inhibition of NLRP3.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  15. Monocytes augment inflammatory responses in human aortic valve interstitial cells via βInflammation research : official journal of the European Histamine Research Society ... [et al.] · 2022
    Article
  16. Article
  17. White Matter Stroke Induces a Unique Oligo-Astrocyte Niche That Inhibits Recovery.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  18. Article
  19. Article
  20. Matrilin-2 is a novel prognostic marker in osteosarcoma.International journal of clinical and experimental pathology · 2019
    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

14 authors at 7 institutions in 3 countries.

Anna Jonas
Stefan Thiem
Tanja Kuhlmann
Raimund Wagener
Attila Aszodi
Cameron Nowell
Karin Hagemeier
Louise Laverick
Victoria Perreau
Vilija Jokubaitis
Ben Emery
Trevor Kilpatrick
Helmut Butzkueven
Melissa Gresle
The University of Melbourne · AUThe Royal Melbourne Hospital · AULudwig Cancer Research · AUUniversity Hospital Münster · DEFlorey Institute of Neuroscience and Mental Health · AULudwig-Maximilians-Universität München · DEUniversity of Cologne · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In patients with multiple sclerosis (MS) and mice with experimental autoimmune encephalomyelitis (EAE), inflammatory axonal injury is a major determinant of disability; however, the drivers of this injury are incompletely understood. Here, we used the EAE model and determined that the extracellular matrix protein matrilin-2 (MATN2) is an endogenous neuronal molecule that is regulated in association with inflammatory axonal injury. Compared with WT mice, mice harboring a deletion of Matn2 exhibited reduced disease severity and axon damage following induction of EAE. Evaluation of neuron-macrophage cocultures revealed that exogenous MATN2 specifically signals through TLR4 and directly induces expression of proinflammatory genes in macrophages, promoting axonal damage. Moreover, the MATN2-induced proinflammatory response was attenuated greatly in macrophages from Myd88 KO mice. Examination of brain sections from patients with MS revealed that MATN2 is expressed in lesions but not in normal-appearing white matter. Together, our results indicate that MATN2 is a deleterious endogenous neuroaxonal injury response signal that activates innate immune cells and could contribute to early axonal damage in CNS inflammatory diseases like MS.

Indexed as

AnimalsAxonsCells, CulturedCoculture TechniquesEncephalomyelitis, Autoimmune, ExperimentalFemaleHumansImmunity, InnateInflammation MediatorsMacrophagesMaleMatrilin ProteinsMice, Inbred C57BLMice, KnockoutMotor CortexSignal TransductionInflammation MediatorsMatn2 protein, mouseMatrilin ProteinsTlr4 protein, mouseToll-Like Receptor 4

Identifiers

PMID25329699
PMCPMC4347228
OpenAlexW2000648415

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.