Evidence map›Paper›PMID 32564090›Full record

ArticleCerebral cortex (New York, N.Y. : 1991)2020

Olig2-Induced Semaphorin Expression Drives Corticospinal Axon Retraction After Spinal Cord Injury.

Masaki Ueno, Yuka Nakamura, Hiroshi Nakagawa, Jesse K Niehaus, Mari Maezawa, Zirong Gu, Atsushi Kumanogoh, Hirohide Takebayashi, Qing Richard Lu, Masahiko Takada and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in Cerebral cortex (New York, N.Y. : 1991), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing 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

16 citing papers in PubMed, 24 citations in OpenAlex.

  1. Semaphorins and Their Role in Neuropathic Pain.Life (Basel, Switzerland) · 2026
    Review
  2. Article
  3. Review
  4. Review
  5. Article
  6. Article
  7. Article
  8. Article
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  10. Altered plasma membrane abundance of the sulfatide-binding protein NF155 links glycosphingolipid imbalances to demyelination.Proceedings of the National Academy of Sciences of the United States of America · 2023
    Article
  11. Single Nuclei Analyses Reveal Transcriptional Profiles and Marker Genes for Diverse Supraspinal Populations.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  12. Article
  13. Article
  14. Review
  15. Modulation of Both Intrinsic and Extrinsic Factors Additively Promotes Rewiring of Corticospinal Circuits after Spinal Cord Injury.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Article
  16. 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

11 authors at 6 institutions in 2 countries.

Masaki UenoDepartment of System Pathology for Neurological Disorders, Brain Research Institute, Niigata University, Niigata 951-8585, Japan.
Yuka NakamuraDepartment of System Pathology for Neurological Disorders, Brain Research Institute, Niigata University, Niigata 951-8585, Japan.
Hiroshi NakagawaSystems Neuroscience Section, Primate Research Institute, Kyoto University, Inuyama 484-8506, Japan.
Jesse K NiehausDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Mari MaezawaDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Zirong GuDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Atsushi KumanogohDepartment of Respiratory Medicine, Allergy and Rheumatic Diseases, Graduate School of Medicine, Osaka University, Suita 565-0871, Japan.
Hirohide TakebayashiDivision of Neurobiology and Anatomy, Graduate School of Medical and Dental Sciences, Niigata University, Niigata 951-8510, Japan.
Qing Richard LuDivision of Experimental Hematology and Cancer Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Masahiko TakadaSystems Neuroscience Section, Primate Research Institute, Kyoto University, Inuyama 484-8506, Japan.
Yutaka YoshidaDivision of Developmental Biology, Cincinnati Children's Hospital Medical Center, Cincinnati, OH 45229, USA.
Cincinnati Children's Hospital Medical Center · USKyoto University · JPNiigata University · JPJapan Science and Technology Agency · JPMIND Research Institute · USOsaka University · JP

Funding

CENTER FOR NEUROANATOMY WITH NEUROTROPIC VIRUSES: COMPARATIVE MEDICINEP40RR018604 · NCRR · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI STRICK, PETER · 2004 to 2011
$6.5M
Synapse elimination in the central nervous systemR01NS093002 · NINDS · WINIFRED MASTERSON BURKE MED RES INST · PI YOSHIDA, YUTAKA · 2015 to 2024
$4.6M
A novel combinatorial approach to restore motor function after spinal cord injuryR01NS100772 · NINDS · WINIFRED MASTERSON BURKE MED RES INST · PI YOSHIDA, YUTAKA · 2017 to 2021
$1.9M
NCRR NIH HHS P40 RR018604NINDS NIH HHS R01 NS093002NINDS NIH HHS R01 NS100772
6 · The paper itself

Abstract

Axon regeneration is limited in the central nervous system, which hinders the reconstruction of functional circuits following spinal cord injury (SCI). Although various extrinsic molecules to repel axons following SCI have been identified, the role of semaphorins, a major class of axon guidance molecules, has not been thoroughly explored. Here we show that expression of semaphorins, including Sema5a and Sema6d, is elevated after SCI, and genetic deletion of either molecule or their receptors (neuropilin1 and plexinA1, respectively) suppresses axon retraction or dieback in injured corticospinal neurons. We further show that Olig2+ cells are essential for SCI-induced semaphorin expression, and that Olig2 binds to putative enhancer regions of the semaphorin genes. Finally, conditional deletion of Olig2 in the spinal cord reduces the expression of semaphorins, alleviating the axon retraction. These results demonstrate that semaphorins function as axon repellents following SCI, and reveal a novel transcriptional mechanism for controlling semaphorin levels around injured neurons to create zones hostile to axon regrowth.

Indexed as

AnimalsAxonsGene Expression RegulationMiceMice, Inbred C57BLNerve RegenerationOligodendrocyte Transcription Factor 2Pyramidal TractsSemaphorinsSpinal Cord InjuriesOlig2 protein, mouseOligodendrocyte Transcription Factor 2Semaphorinsaxon diebackcorticospinal tractOlig2semaphorinspinal cord injury

Identifiers

PMID32564090
PMCPMC8179623
OpenAlexW3035987722

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.