Evidence map›Paper›PMID 27550808›Full record

ArticleMolecular and cellular biology2016

Microglia-induced activation of non-canonical Wnt signaling aggravates neurodegeneration in demyelinating disorders.

Takeshi Shimizu, Ron Smits, Kazuhiro Ikenaka

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.6field-weighted citation impact, top 16% 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

12 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Review
  6. Effects of Wnt5a overexpression in spinal cord injury.Journal of cellular and molecular medicine · 2021
    Article
  7. Article
  8. Article
  9. Review
  10. Article
  11. Brain injury and neural stem cells.Neural regeneration research · 2018
    Review
  12. 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

3 authors at 3 institutions in 2 countries.

Takeshi ShimizuDivision of Neurobiology and Bioinformatics, National Institute for Physiological Sciences, 5-1 Higashiyama Myodaiji Okazaki, Aichi 444-8787, Japan Department of Physiological Sciences, School of Life Sciences, SOKENDAI; (The Graduate University for Advanced Studies), Okazaki 444-8787, Japan shimizu@nips.ac.jp.
Ron SmitsDepartment of Gastroenterology and Hepatology, Erasmus MC University Medical Center Rotterdam, 's-Gravendijkwal 230, 3015 CE Rotterdam, The Netherlands.
Kazuhiro IkenakaDivision of Neurobiology and Bioinformatics, National Institute for Physiological Sciences, 5-1 Higashiyama Myodaiji Okazaki, Aichi 444-8787, Japan Department of Physiological Sciences, School of Life Sciences, SOKENDAI; (The Graduate University for Advanced Studies), Okazaki 444-8787, Japan.
Erasmus MC · NLNational Institute for Physiological Sciences · JPThe Graduate University for Advanced Studies, SOKENDAI · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Oligodendrocytes are myelinating cells of the central nervous system. Multiple sclerosis (MS) is a demyelinating disease characterized by both myelin loss and neuronal degeneration. However, the molecular mechanisms underlying neuronal degeneration in demyelinating disorders are not fully understood. In the experimental autoimmune encephalomyelitis (EAE) demyelinating mouse model of MS, inflammatory microglia produce cytokines including interleukin-1β (IL-1β). Since microglia and non-canonical Wnt signaling components in neurons, such as the co-receptor Ror2, were observed in the spinal cord of EAE mice, we postulated that the interplay between activated microglia and spinal neurons under EAE conditions is mediated through non-canonical Wnt signaling. EAE treatment up-regulated in vivo expression of non-canonical Wnt signaling components in spinal neurons through microglial activation. In accordance with the neuronal degeneration detected in the EAE spinal cord in vivo, co-culture of spinal neurons with microglia or the application of recombinant IL-1β up-regulated non-canonical Wnt signaling, and induced neuronal cell death, which was suppressed by the inhibition of the Wnt-Ror2 pathway. Ectopic non-canonical Wnt signaling aggravated the demyelinating pathology in another MS mouse model due to Wnt5a-induced neurodegeneration. The linkage between activated microglia and neuronal Wnt-Ror2 signaling may provide a possible candidate target for therapeutic approaches to demyelinating disorders.

Identifiers

PMID27550808
PMCPMC5064219
OpenAlexW2515107329

What OpenQuestion holds

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Registered trials

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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.