Evidence map›Paper›PMID 25652774›Full record

ArticleScientific reports2015

Crmp4 deletion promotes recovery from spinal cord injury by neuroprotection and limited scar formation.

Jun Nagai, Yoshiteru Kitamura, Kazuki Owada, Naoya Yamashita, Kohtaro Takei, Yoshio Goshima, Toshio Ohshima

Abstract read
In one paragraph

Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
–field-weighted citation impact
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

22 citing papers in PubMed.

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  15. Plexina2 and CRMP2 Signaling Complex Is Activated by Nogo-A-Liganded Ngr1 to Restrict Corticospinal Axon Sprouting after Trauma.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
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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

7 authors.

Jun Nagai1] Department of Life Science and Medical Bioscience, Graduate School of Advanced Science and Engineering, TWIns, Waseda University, Tokyo, 162-8480 Japan [2] Research Fellow of Japan Society for the Promotion of Science.
Yoshiteru KitamuraDepartment of Life Science and Medical Bioscience, Graduate School of Advanced Science and Engineering, TWIns, Waseda University, Tokyo, 162-8480 Japan.
Kazuki OwadaDepartment of Life Science and Medical Bioscience, Graduate School of Advanced Science and Engineering, TWIns, Waseda University, Tokyo, 162-8480 Japan.
Naoya YamashitaDepartment of Molecular Pharmacology and Neurobiology, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan.
Kohtaro TakeiDepartment of Medical Life Science, Graduate School of Medical Life Science, Yokohama City University, Yokohama, 236-0004, Japan.
Yoshio GoshimaDepartment of Molecular Pharmacology and Neurobiology, Graduate School of Medicine, Yokohama City University, Yokohama 236-0004, Japan.
Toshio OhshimaDepartment of Life Science and Medical Bioscience, Graduate School of Advanced Science and Engineering, TWIns, Waseda University, Tokyo, 162-8480 Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Axonal outgrowth inhibitors and scar formation are two major obstacles to central nervous system (CNS) repair. No target molecule that regulates both axonal growth and scarring has been identified. Here we identified collapsin response mediator protein 4 (CRMP4), a common mediator of inhibitory signals after neural injury, as a crucial factor that contributes to both axonal growth inhibition and scarring after spinal cord injury (SCI). We found increases in the inhibitory and toxic forms of CRMP4 in injured spinal cord. Notably, CRMP4 expression was evident in inflammatory cells as well as in neurons after spinal cord transection. Crmp4-/- mice displayed neuroprotection against SCI and reductions in inflammatory response and scar formation. This permissive environment for axonal growth due to CRMP4 deletion restored locomotor activity at an unusually early phase of healing. These results suggest that deletion of CRMP4 is a unique therapeutic strategy that overcomes two obstacles to CNS repair after SCI.

Indexed as

Gene DeletionAnimalsApoptosisAxonsCicatrixDemyelinating DiseasesDisease Models, AnimalGene ExpressionInflammationMiceMice, KnockoutMicrotubulesMotor ActivityMotor NeuronsNerve Tissue ProteinsNeurogliaDpysl3 protein, mouseNerve Tissue Proteins

Identifiers

PMID25652774
PMCPMC4317684

What OpenQuestion holds

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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.