Evidence map›Paper›PMID 29760175›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2018

Modulation of Receptor Protein Tyrosine Phosphatase Sigma Increases Chondroitin Sulfate Proteoglycan Degradation through Cathepsin B Secretion to Enhance Axon Outgrowth.

Amanda Phuong Tran, Sapna Sundar, Meigen Yu, Bradley T Lang, Jerry Silver

Abstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 44 papers.

0numbers the graph read from it
0cells of the map it votes in
44citing 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

44 citing papers in PubMed.

  1. Review
  2. Review
  3. Neuronal Axon Generation/Regeneration Regulated by Sulfated Glycans.Advances in experimental medicine and biology · 2026
    Review
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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

5 authors.

Amanda Phuong TranDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106 and.
Sapna SundarDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106 and.
Meigen YuDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106 and.
Bradley T LangBioEnterprise, Cleveland, Ohio 44106.
Jerry SilverDepartment of Neurosciences, Case Western Reserve University School of Medicine, Cleveland, Ohio 44106 and jxs10@case.edu.ORCID 0000-0001-5002-2599

Funding

FACTORS AFFECTING REGENERATION THRU THE GLIAL SCARR01NS025713 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI SILVER, JERRY · 1988 to 2016
$3.1M
Factors Affecting Regeneration Through the Glial ScarR37NS025713 · NINDS · CASE WESTERN RESERVE UNIVERSITY · PI SILVER, JERRY · 2005 to 2011
$2.7M
NINDS NIH HHS R01 NS025713NINDS NIH HHS R37 NS025713
6 · The paper itself

Abstract

Severed axon tips reform growth cones following spinal cord injury that fail to regenerate, in part, because they become embedded within an inhibitory extracellular matrix. Chondroitin sulfate proteoglycans (CSPGs) are the major axon inhibitory matrix component that is increased within the lesion scar and in perineuronal nets around deafferented neurons. We have recently developed a novel peptide modulator (intracellular sigma peptide) of the cognate receptor of CSPGs, protein tyrosine phosphatase σ (RPTPσ), which has been shown to markedly improve sensorimotor function, micturition, and coordinated locomotor behavior in spinal cord contused rats. However, the mechanism(s) underlying how modulation of RPTPσ mediates axon outgrowth through inhibitory CSPGs remain unclear. Here, we describe how intracellular sigma peptide modulation of RPTPσ induces enhanced protease Cathepsin B activity. Using DRG neurons from female Sprague Dawley rats cultured on an aggrecan/laminin spot assay and a combination of biochemical techniques, we provide evidence suggesting that modulation of RPTPσ regulates secretion of proteases that, in turn, relieves CSPG inhibition through its digestion to allow axon migration though proteoglycan barriers. Understanding the mechanisms underlying RPTPσ modulation elucidates how axon regeneration is impaired by proteoglycans but can then be facilitated following injury.

Indexed as

AnimalsCathepsin BCells, CulturedChondroitin Sulfate ProteoglycansFemaleNerve RegenerationNeuronal OutgrowthRatsRats, Sprague-DawleyReceptor-Like Protein Tyrosine Phosphatases, Class 2Cathepsin BChondroitin Sulfate ProteoglycansCtsb protein, ratReceptor-Like Protein Tyrosine Phosphatases, Class 2axon regenerationcathepsin BCSPGDRGproteaseRPTPσ

Identifiers

PMID29760175
PMCPMC5990985

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.