Evidence map›Paper›PMID 34344859›Full record

ArticleCell death & disease2021

Interleukin-17A regulates ependymal cell proliferation and functional recovery after spinal cord injury in mice.

Hisao Miyajima, Takahide Itokazu, Shogo Tanabe, Toshihide Yamashita

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 23% 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

13 citing papers in PubMed, 21 citations in OpenAlex.

  1. Regional Molecular Diversity in Chronic Spinal Cord Injury.Cellular and molecular neurobiology · 2026
    Article
  2. Review
  3. Repurposing of Chemokine Antagonists for Combined Phase-Resolved Spinal Cord Injury Treatment.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026
    Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Review
  12. Article
  13. Review
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

4 authors at 1 institution in 1 country.

Hisao MiyajimaDepartment of Molecular Neuroscience, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan.
Takahide ItokazuDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan. t.itokazu@molneu.med.osaka-u.ac.jp.ORCID 0000-0003-2977-7190
Shogo TanabeDepartment of Molecular Neuroscience, Graduate School of Medicine, Osaka University, Suita, Japan.
Toshihide YamashitaDepartment of Molecular Neuroscience, Graduate School of Frontier Biosciences, Osaka University, Suita, Japan. yamashita@molneu.med.osaka-u.ac.jp.ORCID 0000-0003-4559-7018
The University of Osaka · JP

Funding

Japan Agency for Medical Research and Development (AMED) 18gm1210005h0001
6 · The paper itself

Abstract

Ependymal cells have been suggested to act as neural stem cells and exert beneficial effects after spinal cord injury (SCI). However, the molecular mechanism underlying ependymal cell regulation after SCI remains unknown. To examine the possible effect of IL-17A on ependymal cell proliferation after SCI, we locally administrated IL-17A neutralizing antibody to the injured spinal cord of a contusion SCI mouse model, and revealed that IL-17A neutralization promoted ependymal cell proliferation, which was paralleled by functional recovery and axonal reorganization of both the corticospinal tract and the raphespinal tract. Further, to test whether ependymal cell-specific manipulation of IL-17A signaling is enough to affect the outcomes of SCI, we generated ependymal cell-specific conditional IL-17RA-knockout mice and analyzed their anatomical and functional response to SCI. As a result, conditional knockout of IL-17RA in ependymal cells enhanced both axonal growth and functional recovery, accompanied by an increase in mRNA expression of neurotrophic factors. Thus, Ependymal cells may enhance the regenerative process partially by secreting neurotrophic factors, and IL-17A stimulation negatively regulates this beneficial effect. Molecular manipulation of ependymal cells might be a viable strategy for improving functional recovery.

Indexed as

Recovery of FunctionAnimalsAntibodies, NeutralizingBehavior, AnimalCell ProliferationEpendymaFemaleInterleukin-17MiceMice, Inbred C57BLMice, TransgenicMotor ActivityNerve Growth FactorsNeurogenesisReceptors, Interleukin-17RNA, MessengerAntibodies, NeutralizingIl17ra protein, mouseInterleukin-17Nerve Growth FactorsReceptors, Interleukin-17RNA, MessengerTamoxifen

Identifiers

PMID34344859
PMCPMC8333070
OpenAlexW3190605318

What Socratic 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 Socratic graph.