Evidence map›Paper›PMID 29959434›Full record

ArticleScientific reports2018

The extent of extra-axonal tissue damage determines the levels of CSPG upregulation and the success of experimental axon regeneration in the CNS.

Juhwan Kim, Muhammad S Sajid, Ephraim F Trakhtenberg

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 29% 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

20 citing papers in PubMed, 30 citations in OpenAlex.

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  16. Glycosylation in Axonal Guidance.International journal of molecular sciences · 2021
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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

3 authors at 1 institution in 1 country.

Juhwan KimDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT, 06030, USA.
Muhammad S SajidDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT, 06030, USA.
Ephraim F TrakhtenbergDepartment of Neuroscience, University of Connecticut School of Medicine, 263 Farmington Ave., Farmington, CT, 06030, USA. trakhtenberg@uchc.edu.ORCID 0000-0003-2844-4191
University of Connecticut · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The failure of mature central nervous system (CNS) projection neurons to regenerate axons over long distances drastically limits the recovery of functions lost after various CNS injuries and diseases. Although a number of manipulations that stimulate some degree of axon regeneration that overcomes the inhibitory environment after CNS injury have been discovered, the extent of regeneration remains very limited, emphasizing the need for improved therapies. Regenerating axons need nerve tissue environment capable of supporting their growth, and severe extra-axonal tissue damage and remodeling after injury may disrupt such environment. Here, we used traumatic injury to the mouse optic nerve as a model system to investigate how the extent of extra-axonal tissue damage affects experimental axon regeneration. Axon regeneration was stimulated by the shRNA-mediated knockdown (KD) of Pten gene expression in the retinal ganglion cells, and the extent of extra-axonal tissue damage was varied by changing the duration of optic nerve crush. Although no axons were spared using either 1 or 5 seconds crush, we found that Pten KD-stimulated axon regeneration was significantly reduced in 5 seconds compared with 1 second crush. The more severe extra-axonal tissue damage did not cause tissue atrophy, but led to significantly higher upregulation of axon growth-inhibiting chondroitin sulfate proteoglycan (CSPG) in the glial scar and also enlarged glial scar size, compared with less severely damaged tissue. Thus, the success of axon-regenerating approaches that target neuronal intrinsic mechanisms of axon growth is dependent on the preservation of appropriate extra-axonal tissue environment, which may need to be co-concurrently repaired by tissue remodeling methods.

Indexed as

Nerve RegenerationAnimalsAxonsCentral Nervous SystemChondroitin Sulfate ProteoglycansMaleMiceNeurogliaPTEN PhosphohydrolaseRetinal Ganglion CellsUp-RegulationChondroitin Sulfate ProteoglycansPTEN PhosphohydrolasePten protein, mouse

Identifiers

PMID29959434
PMCPMC6026156
OpenAlexW2810105483

What Socratic holds

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LicenceCC BY
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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 Socratic graph.