Evidence map›Paper›PMID 32959171›Full record

ArticleMolecular neurobiology2021

Dual Specificity Phosphatases Support Axon Plasticity and Viability.

Ambika Chandrasekhar, Prashanth Komirishetty, Aparna Areti, Anand Krishnan, Douglas W Zochodne

Abstract read
PubMed Publisher
In one paragraph

Article in Molecular neurobiology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
0.7field-weighted citation impact, top 35% 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

9 citing papers in PubMed, 13 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. The Role of Protocadherin γ in Adult Sensory Neurons and Skin Reinnervation.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  7. Review
  8. Unleashing Intrinsic Growth Pathways in Regenerating Peripheral Neurons.International journal of molecular sciences · 2022
    Review
  9. Article
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 at 1 institution in 1 country.

Ambika ChandrasekharNeuroscience and Mental Health Institute and Division of Neurology, Department of Medicine, University of Alberta, 7-132A Clinical Sciences Building, 11350-83 Ave, Edmonton, AB, T6G 2G3, Canada.
Prashanth KomirishettyNeuroscience and Mental Health Institute and Division of Neurology, Department of Medicine, University of Alberta, 7-132A Clinical Sciences Building, 11350-83 Ave, Edmonton, AB, T6G 2G3, Canada.
Aparna AretiNeuroscience and Mental Health Institute and Division of Neurology, Department of Medicine, University of Alberta, 7-132A Clinical Sciences Building, 11350-83 Ave, Edmonton, AB, T6G 2G3, Canada.
Anand KrishnanNeuroscience and Mental Health Institute and Division of Neurology, Department of Medicine, University of Alberta, 7-132A Clinical Sciences Building, 11350-83 Ave, Edmonton, AB, T6G 2G3, Canada.
Douglas W ZochodneNeuroscience and Mental Health Institute and Division of Neurology, Department of Medicine, University of Alberta, 7-132A Clinical Sciences Building, 11350-83 Ave, Edmonton, AB, T6G 2G3, Canada. zochodne@ualberta.ca.ORCID http://orcid.org/0000-0003-1692-5983
University of Alberta · CA

Funding

CIHR FRN148675
6 · The paper itself

Abstract

In peripheral neuropathies, axonal degeneration (AxD) impairs the prognosis for recovery. Here, we describe a role for dual specificity phosphatases (DUSPs; MAP kinase phosphatases, MKPs), in supporting autonomous axon plasticity and viability. Both DUSPs 1 and 4 were identified within intact or axotomized sensory neurons. Knockdown of DUSP 1 or 4 independently or combined impaired neurite outgrowth in adult dissociated sensory neurons. Furthermore, adult sensory neurons with DUSP knockdown were rendered sensitive to axonopathy in vitro following exposure to low, subtoxic TrpV1 (transient receptor potential cation channel subfamily V member 1) activation by capsaicin, an intervention normally supportive of growth. This was not prevented by concurrent DLK (dual leucine zipper kinase) knockdown. Ex vivo neurofilament dissolution was heightened by DUSP inhibition within explanted nerves. In vivo DUSP knockdown or inhibition was associated with more rapid loss of motor axon excitability. The addition of SARM1 (sterile alpha and TIR motif containing 1) siRNA abrogated DUSP1 and 4 mediated loss of excitability. DUSP knockdown accelerated neurofilament breakdown and there was earlier morphological evidence of myelinated axon degeneration distal to axotomy. Taken together, the findings identify a key role for DUSPs in supporting axon plasticity and survival.

Indexed as

Neuronal PlasticityAnimalsAxonsAxotomyCell SurvivalDual-Specificity PhosphatasesGanglia, SpinalIntermediate FilamentsMaleMAP Kinase Kinase KinasesNerve DegenerationNeuronal OutgrowthNeuroprotectionRatsRats, Sprague-DawleySensory Receptor CellsDual-Specificity PhosphatasesMAP Kinase Kinase Kinasesmitogen-activated protein kinase kinase kinase 12Axonal degenerationDual specificity phosphatasesMAP kinase phosphatases

Identifiers

PMID32959171
OpenAlexW3087404207

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.